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$\"Bio-Rad$ 关注我们 Bio-rad LinkedIn Bio-rad Antibodies LinkedIn Bio-rad YouTube Bio-rad Antibodies YouTube Bio-rad Twitter Bio-rad Antibodies Twitter Bio-rad Facebook Bio-rad Antibodies Facebook Bio-rad Instagram Bio-rad Pinterest关于 Bio-RadBioradiations联系我们SustainabilityLab CrunchesNewsroomCareersInvestor RelationsFooter Home|商标|网站条款|网络安全|无障碍网页|条款与条件|隐私© 2023 Bio-Rad Laboratories, Inc.美国Immunofluorescence staining of a mouse lymph node cryosection with Rat anti Mouse CD68 antibody, clone FA11 (MCA1957), green in A and Rat anti Mouse CD8 antibody, clone YTS105.18 (MCA1108), red in B. C is the merged image with nuclei counterstained blue using DAPI. Low power Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957GA) used for the identification of microglia in mouse brain by immunofluorescence.Image caption:CB2 receptors are expressed in microglial cells and do not accumulate in A plaques of APPswe/PS1 E9 mice. A representative confocal image of staining for CB2 receptors (green, H60 antibody) in the cortex of 12 mo-old transgenic mice. (B) An overlap of red (CD68) and blue (DAPI) channels for the image shown in A. Note a characteristic gathering of activated microglia around an amyloid plaque (marked by an asterisk). (C) An overlap of channels shown in A-B. Note that areas with high CB2 intensities overlap with CD68-positive areas. White rectangle shows an example of areas used for quantifications presented in E-F. Scale bar is 15 m. (D) Quantification of CB2 densities (integrated intensities/area) in CD68-positive and –negative areas. 26 areas like that shown in A-C were used for the quantification (n = 2 transgenic mice). Asterisk indicates a significant difference between CD68+ and CD68- areas (one-way ANOVA, p 0.0001). (E) A scatterplot of CB2 and DAPI intensities as a function of distance from the center of an A plaque with radius 10 μm. Note low CB2 signal in the core of the plaque. CB2 and DAPI intensities were normalized ( ) to a maximum signal on each channel. An example of an area used for calculations is shown by a white rectangle in C. (F) Quantification of CB2 signal at different distances from a plaque center. 4–6 slices of z stacks from five plaques (range of radiuses 7–15 m) were used in one-way ANOVA. Asterisks indicate a significant increase (p 0.0001, post-hoc test) in CB2 intensities as compared to the core of plaques (radius ≤ 7 m).From: Savonenko AV, Melnikova T, Wang Y, Ravert H, Gao Y, Koppel J, et al. (2015)Cannabinoid CB2 Receptors in a Mouse Model of A Amyloidosis: Immunohistochemical Analysis and Suitability as a PET Biomarker of Neuroinflammation.PLoS ONE 10(6): e0129618.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 used for the identification of microglia in mouse brain by immunofluorescence.Image caption:Comparison of CB2 immunoreactivity in neurons, activated microglia and astrocytes. (A) Representative confocal images from the cortex of 12 mo-old non-transgenic (NTG) and APPswe/PS1 E9 transgenic (AD) mice stained with a CB2 receptor antibody (H60sc; left columns; green) and markers for neurons (NeuN, far red), activated microglia (CD68, red), and astrocytes (GFAP, far red). Brain slides were counterstained with DAPI shown with a grey pseudo color. Note substantial micro- and astro-gliosis in the cortex of the AD mouse brain. In the NTG mice, CD68+ and/or GFAP+ areas were rare (indicated in the upper right panel by an arrowhead and arrow, respectively). (B) Quantification of densities (+-SEM) for CB2 receptor immunoreactivity (integrated intensities/area) in areas positive for NeuN, CD68, and GFAP markers. Densities were averaged over 22 (AD) and 14 (NTG) images of the cortex as shown in A (n = 2 mice per genotype). Single and double asterisks indicate a significant difference between NTG and AD groups as a result of LSD post-hoc test with p levels 0.01 and 0.0001, respectively. Arcs indicate non-significant (NS) differences. Single and double pound signs (p levels 0.05 and 0.001) indicate markers that correspond to the highest CB2 density in the NTG (blue sign) or AD (red sign) groups (LSD post-hoc test). Solid black line at the level of 4,930 shows average densities for the background. (C) An example of NeuN (blue), CD68 (red), and GFAP (green) masks from the AD image shown in A. NeuN masks were drawn by hand as shown in Fig 2C; masks for CD68 and GFAP were created by a threshold function. Black area represents background. Scale is 15 m.From: Savonenko AV, Melnikova T, Wang Y, Ravert H, Gao Y, Koppel J, et al. (2015)Cannabinoid CB2 Receptors in a Mouse Model of A Amyloidosis: Immunohistochemical Analysis and Suitability as a PET Biomarker of Neuroinflammation.PLoS ONE 10(6): e0129618.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 (MCA1957) used for the detection of macrophages in mouse brain by immunohistochemistry on cryostat sections.Image caption:Primed innate immune response in the brain following a systemic bacterial infection. Phenotypic changes after intracerebral injection of 100 pg of LPS in naïve mice (A, B, E, F, I, J, M, N) or mice pretreated with SL3261 (C, D, G, H, K, L, O, P). Representative images of immune marker expression (CD11c (A-D), CD68 (E-H), MHCII (I-L) in the injected hemisphere (B, D, F, H, J, L, N, P) or contralateral site are shown. Panels M-P show a double immunofluorescent stain for MHCII (green) and laminin (red). n=5 animals per group, black scale bar=50 m, white scale bar=75 m.From: P ntener U, Booth SG, Perry VH, Teeling JL.Long-term impact of systemic bacterial infection on the cerebral vasculature and microglia.J Neuroinflammation. 2012 Jun 27;9:146.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 (MCA1957) used for the detection of macrophages in mouse by flow cytometry.Image caption:F4/80 and either CD11b or CD68 expression of whole liver MNCs. Liver MNCs were obtained from CD, HFD, HCD and HFCD mice and expression of F4/80 either with CD11b or CD68 were examined. The numbers were the means SE from four mice in each group. F4/80 positive gate was determined by using the isotype control Ab.From: Nakashima H, Ogawa Y, Shono S, Kinoshita M, Nakashima M, et al. (2013)Activation of CD11b+ Kupffer Cells/Macrophages as a Common Cause for Exacerbation of TNF/Fas-Ligand-Dependent Hepatitis in Hypercholesterolemic Mice.PLoS ONE 8(1): e49339.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 (MCA1957) used for the detection of macrophages in mouse by flow cytometry.Image caption:The expression of CD68 and CD11b by liver F4/80+ Kupffer cells. Liver MNCs were obtained from CD, HFD, HCD and HFCD mice, and Kupffer cells gated by F4/80 were analyzed for their expression levels of CD68 and CD11b. CD68 positive gate was determined by using the isotype control Ab. The numbers are the means SE from six to eight mice in each group. *P 0.05 vs. CD and HFD.From: Nakashima H, Ogawa Y, Shono S, Kinoshita M, Nakashima M, et al. (2013)Activation of CD11b+ Kupffer Cells/Macrophages as a Common Cause for Exacerbation of TNF/Fas-Ligand-Dependent Hepatitis in Hypercholesterolemic Mice.PLoS ONE 8(1): e49339.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 (MCA1957GA) used for the detection of macrophages in mouse aortic root tissue by immunohistochemistry on cryostat sections.Image caption:Immunohistochemical analysis of mouse atherosclerotic lesions. Representative aortic root sections immunostained for the foam cell marker CD68 (A), VCAM-1 (B), or Masson trichrome blue stain for collagen content (C). Original magnification, 40×. Note abundant immunostaining for foam cell marker, CD68 (brown), VCAM-1 adhesion molecules (also brown), and presence of collagen αblue) within lesion in baseline and AAV.TBG.nLacZ injected Ldlr-/-Apobec1-/-animals.From: Kassim SH, Li H, Vandenberghe LH, Hinderer C, Bell P, et al. (2010)Gene Therapy in a Humanized Mouse Model of Familial Hypercholesterolemia Leads to Marked Regression of Atherosclerosis.PLoS ONE 5(10): e13424. This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 (MCA1957) used for the detection of macrophages in mouse by flow cytometry.Image caption:Phenotype of pancreatic macrophages. (A) Identification of macrophage subsets in pancreas of CX3CR1GFP/+ C56BL/6 mice. Pancreatic single cell suspensions were gated on FSC-A vs FSC-W and CD45+. Histograms show receptor expression profile of CX3CR1hiLYVE-1− (green line) and CX3CR1loLYVE-1+ (red line) macrophages. (B) Sorted CX3CR1loLYVE-1+ and CX3CR1hiLYVE-1− macrophages spun onto glass slides and stained with Wright s stain. 1000× magnification. (C) mRNA expression profile of chemokine receptors, chemokines and VEGFs in pancreatic macrophage subsets. mRNA levels examined by qRT-PCR in duplicate or triplicate. 6–7 mice/group, data representative of 2–4 separate experiments.From: Yin N, Zhang N, Lal G, Xu J, Yan M, et al. (2011)Lymphangiogenesis Is Required for Pancreatic Islet Inflammation and Diabetes.PLoS ONE 6(11): e28023.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 (MCA1957GA) used for the detection of macrophages in mouse pancreas by immunofluorescence.Image caption:Interaction of LEC and pancreatic macrophages. (A) CX3CR1hi macrophages, LYVE-1+ macrophages, CD11b−-lymphocytes and LEC were sorted from pancreatic single cell suspensions of CX3CR1GFP/+ mice. Co-cultured CX3CR1hi macrophages-CFSE, LYVE-1+ macrophages-eFlour670, or lymphocytes-CFSE with/without LEC on Matrigel for 5 days. Scale bars: 60 m. 100× magnification. (B) Immunofluorescent staining of CD68 and LYVE-1 in pancreas from C57BL/6 mice. Scale bars: 160 m. 50× magnification. (C) Sorted CX3CR1hi macrophages labeled with CFSE and co-cultured with LEC (left upper panel) or without LEC (left lower panel) for 5 days, and stained for CD11b (red) and LYVE-1 (yellow). Scale bars: 10 m. 630× magnification. Right panel, quantitative analysis, total cells from 5 fields (1344×1024 pixels) were counted. All data representative of 2 to 4 separate experiments.From: Yin N, Zhang N, Lal G, Xu J, Yan M, et al. (2011)Lymphangiogenesis Is Required for Pancreatic Islet Inflammation and Diabetes.PLoS ONE 6(11): e28023.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 (MCA1957) used for the detection of macrophages in mouse pancreas by immunofluorescence.Image caption:Macrophages infiltrate into inflamed islets. MLDS treated BALB/c mice received sunitinib, or anti-VEGFR3 mAb starting from the first STZ injection 3 days. (A) Immunofluorescent analysis of CD68+LYVE-1+ (yellow arrows) and CD68+LYVE-1− (red arrows) macrophage subsets migrating near islets. 200× magnification. Scale bars: 30 m. (B) Quantitative analysis of CD68+LYVE-1+ and CD68+LYVE-1− cells surrounding islets. Each symbol represents one islet. 43–52 islets/group, 4–5 slides/mice, 3 mice/group. *** P 0.001. Mean ± SD.From: Yin N, Zhang N, Lal G, Xu J, Yan M, et al. (2011)Lymphangiogenesis Is Required for Pancreatic Islet Inflammation and Diabetes.PLoS ONE 6(11): e28023.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 used for the detection of macrophages in mouse brain by immunohistochemistry on formain fixed, paraffin embedded tissue.Image caption:Iminosugar-based GCS inhibitors decrease the number of brain CD68 positive cells. (A) CD68 immunolabeling of brain stem from 28, 56, 84 and 112 day old Sandhoff mice, untreated or treated with either Genz-529468 or NB-DNJ. Dark brown cells are positive for CD68; scale bar = 50 m. (B) Quantification of CD68+ cell counts in the brain stem, cerebellum, hippocampus and thalamus of 112 day old drug-treated Sandhoff mice (n = 4–5 mice per group). Cell counts are presented relative to those in untreated Sandhoff mice. Statistics are between untreated and treated Sandhoff mice, and were determined using the Graphpad Prism software t test; * = p 0.05. Error bars indicate SEM.From: Ashe KM, Bangari D, Li L, Cabrera-Salazar MA, Bercury SD, et al. (2011)Iminosugar-Based Inhibitors of Glucosylceramide Synthase Increase Brain Glycosphingolipids and Survival in a Mouse Model of Sandhoff Disease.PLoS One. 2011;6(6):e21758.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 used for the detection of macrophages in mouse atherosclerotic plaques by immunofluorescence.Image caption:Impact of SOCS-1 deficiency on atherosclerotic plaque composition A. Atherosclerotic plaques from Socs-1−/− triple-KO (Socs-1−/−) mice showed an increased CD68 (red);iNOS (green) double-positive cell content. B. CD68 (red); CD206 (green) double-positive cells were hardly detected. C. Atherosclerotic plaques from Socs-1−/−triple-KO (Socs-1−/−) mice contained slightly more MOMA-2 (red); Ly-6C (green) double-positive cells after 4 weeks of HCD as well as D. a higher number of Ly-6G positive cells (scale bar A–C: 20 m, scale bar D:50 m). N = 5–7 animals per group.From: Grothusen C, Schuett H, Hillmer A, Lumpe S, Grote K, et al. (2012)Role of Suppressor of Cytokine Signaling-1 In Murine Atherosclerosis.PLoS ONE 7(12): e51608.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 used for the detection of macrophages in mouse vacscular tissue by immunofluorescence.Image caption:CD68 positive macrophages/monocytes cells can be seen within early developing neointima in some mice. Sections from the same two mice shown in Figure 6 were stained with antibodies to CD68 (white). Left panels show mTomato (red)/mEGFP (green) co-stained sections and in the right panels are the same sections visualized for mEGFP (green) and CD68 (white). CD68-positive cells can be seen within the neointima of vessels from the mouse shown in the upper panels but not in the vessels of the mouse shown in the lower panels. Nuclei were visualized by staining with DAPI (blue). All images are shown at the same magnification with the scale bar shown in the bottom left panel representing 50 m.From: Herring BP, Hoggatt AM, Burlak C, Offermanns S.Previously differentiated medial vascular smooth muscle cells contribute to neointima formation following vascular injury.Vasc Cell. 2014 Oct 1;6:21.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 (MCA1957) used for the detection of macrophages in mouse lung and liver by immunohistochemistry on formalin fixed, paraffin embedded tissues.Image caption:Histology in 9V/9V/GCStg and 9V/null/GCStg mice. (A) The lung and liver sections from 9-wk old 9V/9V (row 1), 9V/9V/GCStg (row 2), 9V/null (row 3) and 9V/null/GCStg (row 4) were processed for H&E and CD68 antibody staining as indicated. Large and pale storage cells were observed in H&E stained lung and liver sections (arrows). The macrophages were indicated by anti-CD68 immunostaining (brown). Images were captured by Zeiss microscope with Spot Advance software. Scale bar was 40 m for all images. (B) The distribution and density of macrophages in 9V/null/GCStg lung and liver immunostained by anti-CD68 antibody (brown). Scale bar was 40 m for both images. (C) CD68 positive cells (CD68+) in 9V/9V/GCStg and 9V/null/GCStg lungs had significantly more CD68 stained macrophages than 9V/9V and 9V/null at 9 wks of age, respectively. The data present number of cells per image of total 5−15 images/mouse, 3 mice per genotype. Results with error bars are mean S.E. The p values were from Student's t-test.From: Barnes S, Xu Y-H, Zhang W, Liou B, Setchell KDR, et al. (2014)Ubiquitous Transgene Expression of the Glucosylceramide-Synthesizing Enzyme Accelerates Glucosylceramide Accumulation and Storage Cells in a Gaucher Disease Mouse Model.PLoS ONE 9(12): e116023.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA!957GA) used for the detection of infiltrating macrophages in mouse kidney by immunohistochemistry on paraffin embedded material.Image caption:Reduction in cellular infiltration and inflammatory markers in UUO kidneys exposed to telmisartan or PXS64. Untreated UUO kidneys showed increased F4/80, CD68 and CD45 positively stained cells as compared to the sham operated control animals. PXS64 significantly reduced F4/80 and CD45 positive stained cells (Fig. 6C and E) with a trend to a reduction in CD68 cells, although this was not statistically significant (Fig. 6D). Telmisartan treated kidneys showed a reduction in F4/80 positive cells but no difference in CD45 or CD68 stained cells, suggesting a differential action of PXS64 and telmisartan in modifying cellular infiltration. Results are presented as mean showed (n = 8, *P 0.05 vs. UUO, ** P 0.01 vs. UUO). Magnification x 400.From: Zhang J, Wong MG, Wong M, Gross S, Chen J, et al. (2015)A Cationic-Independent Mannose 6-Phosphate Receptor Inhibitor (PXS64) Ameliorates Kidney Fibrosis by Inhibiting Activation of Transforming Growth Factor- 1.PLoS ONE 10(2): e0116888.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 used for the detection of macrophages in murine cervical lymph nodes by immunofluorescence.Image caption:Brucella and fluorescent microspheres in the CLN localize in cells positive for CD68 and low or negative for CD11c. (A) C57BL/6 mice were fed by oral gavage with 0.2 m yellow green fluorescent microspheres. After 3 days, they were sacrificed and CLN processed for immunofluorescence microscopy. (B) Cells with internal beads from experiments as shown in (A) were quantified as to their expression of CD11c and CD68. At least 100 bead-containing cells per experiment were counted. (C) Mice infected by the oral route with 109 B. melitensis per mouse were sacrificed at day 8, CLN prepared for immunofluorescence analysis as described above and (D) the number of infected cells positive for either marker was determined. All available cuts from the CLN of one mouse were analyzed. Data shown represents mean and standard deviation of three independent experiments. Bars: 10 m.From: von Bargen K, Gagnaire A, Arce-Gorvel V, de Bovis B, Baudimont F, Chasson L, et al. (2015)Cervical Lymph Nodes as a Selective Niche for Brucella during Oral Infections.PLoS ONE 10(4): e0121790.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used for the identification of macrophages in atherosclerotic lesions by immunofluorescence.Image caption:Macrophage and VSMC accumulation is reduced in uPAR-/-/LDLR-/-. (A) Representative Mac-3 immunostaining and (B) %-Mac-3-positive lesion per lesion area. (C) Representative anti-SMC immunostaining and (D) % anti-SMC-positive lesion per lesion area. (E) PCNA/CD68 double staining excludes differences in macrophage proliferation in the lesions. (F) Macrophage apoptosis was not responsible for the differences in macrophage content as evidenced by cleaved caspase 3 staining. Mean SEM, n = 8. *P 0.05, **P 0.01, ***P 0.001. A/C: Bar = 250 m, E/F Bar = 100 m SMA: alpha smooth-muscle-actin, PCNA: Proliferating-Cell-Nuclear-Antigen, cC3: cleaved caspase-3, DAPI: 4′,6-Diamidin-2-phenylindol.From:Larmann J, Jurk K, Janssen H, M ller M, Herzog C, Lorenz A, et al. (2015)Hepatic Overexpression of Soluble Urokinase Receptor (uPAR) Suppresses Diet-Induced Atherosclerosis in Low-Density Lipoprotein Receptor-Deficient (LDLR-/-) Mice.PLoS ONE 10(8): e0131854.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957GA) used for the identification of macrophages in atherosclerotic lesions by immunohistochemistry on cryosections.Image caption:Guide-wire injury induced intimal hyperplasia. Mice were subjected to guide wire injury of the internal carotid artery after hypercholesterolemia had been induced. (A) Representative Micrographs of carotid artery lesions in the injured and the contralateral artery. GWI induced concentric lesions did not differ in (B) size or (C) lipid content. (D) Macrophage recruitment did occur, but (E) differences between uPAR-deficient and uPAR-wild-type lesions were not observed in this model. Additionally, no differences between uPAR+/+ and uPAR-/- animals were observable with respect to (F-G) VSMC content of the lesions. No relevant lesion formation was observed in the contralateral sham vessels. (H) Proliferating cells in atherosclerotic lesions are mainly non-VSMC. The amount of proliferating VSMC appears similar for the two genotypes. A, D, F: Bar = 250 m, H: Bar: 50 m, mean SEM, n = 8. n.s.: not significant, SMA: alpha smooth-muscle-actin, DAPI: 4′,6-Diamidin-2-phenylindol, GWI: guide-wire injury, L: left, R: right, PCNA: Proliferating Cell Nuclear Antigen.From:Larmann J, Jurk K, Janssen H, M ller M, Herzog C, Lorenz A, et al. (2015)Hepatic Overexpression of Soluble Urokinase Receptor (uPAR) Suppresses Diet-Induced Atherosclerosis in Low-Density Lipoprotein Receptor-Deficient (LDLR-/-) Mice.PLoS ONE 10(8): e0131854.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957GA) used for the identification of macrophages in atherosclerotic lesions by immunofluorescence.Image caption:Hepatic overexpression of soluble full-length uPAR inhibits atherosclerotic lesion development and macrophage accumulation in LDLR-/- mice. A, Immunostaining for the c-myc-tag revealed expression of soluble uPAR in the livers of mice after hydrodynamic transfection. Bar = 100 m B. Oil red-O staining of aortic valve cryosections. Bar = 250 m C. Atherosclerotic lesion size was assessed as % total aortic sinus lumen area occupied. D, Representative CD68 immunostaining and E. % CD68-positive lesion area. F, Representative anti- SMC immunostaining and G. % anti- SMA-positive lesion area. Bar = 250 m, Mean SEM, n = 6/8. *Pet al. (2015)Hepatic Overexpression of Soluble Urokinase Receptor (uPAR) Suppresses Diet-Induced Atherosclerosis in Low-Density Lipoprotein Receptor-Deficient (LDLR-/-) Mice.PLoS ONE 10(8): e0131854.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Biotin conjugated Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957B) used for the assessment of CD68 expression on Kuppfer cells by flow cytometry. Image caption:The flow cytometric analysis of liver F4/80+CD11b+ cells and F4/80+CD68+ cells three days after Sham operated or PHx mice(A). The changes in the proportions of F4/80+CD11b+ cells in the remnant livers (B). The changes in the proportions of F4/80+CD68+ cells in the remnant livers (C). The percentages of F4/80+CD11b+ cells which are indicated by red dots and F4/80+CD68+ cells indicated by blue dots are the representative data from four to six mice (A). The percentages of each cellular population at the indicated time points are shown as the means SE (B, C). (*P .05 vs Sham).From: Nishiyama K, Nakashima H, Ikarashi M, Kinoshita M, Nakashima M, Aosasa S, et al. (2015)Mouse CD11b+Kupffer Cells Recruited from Bone Marrow Accelerate Liver Regeneration after Partial Hepatectomy.PLoS ONE 10(9): e0136774.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957)used for the identification of inflammatory macrophages at the site of tibial fracture by immunofluorescenceImage caption:Bone fracture increased CD68+ macrophages in the peri-infarct region. (A) Image illustrates infarct core (Core), infarct border (dotted line) and the peri-infarct region (P.I.). (B) Quantification of CD68+ cells. *: P = 0.004, compared to stroke-only group. (C) Representative images of anti-CD68 antibody-stained sections. BF + 6hS: mice that received tibia fracture 6 hours before pMCAO; BF+1dS: mice that received tibia fracture 24 hours before pMCAO. Scale bars: 50 m. N = 6. From: Wang L, Kang S, Zou D, Zhan L, Li Z, Zhu W, et al. (2016)Bone Fracture Pre-Ischemic Stroke Exacerbates Ischemic Cerebral Injury in Mice. PLoS ONE 11(4): e0153835.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA11 (MCA1957) used for the identification of macrophages and microglia in unfixed cryosections by immunofluorescence.Image caption:Engulfment of fibrillar A by BMDM and primary microglia AA schematic shows 10‐μm cryosections of unfixed brain from 6‐month‐old APP/PS1 mice, which show a high amyloid plaque burden (right panel with methoxy‐X04 staining), were incubated with antibody for 1 h, followed by adding BMDM or primary microglia on top of the sections. After 24 h incubation, sections were analyzed by immunostaining or immunoblotting.BmAb11 but not the isotype control (IC) co‐localized with methoxy‐X04. Scale bar: 10 m.C, DBMDM (C) or primary microglia (D) were cultured on cryosections pre‐incubated with mAb11 (1 g/ml). After 24 h, sections were processed for immunostaining using antibody against CD68 to identify myeloid cells and methoxy‐X04 staining to visualize A . Note that both cell types internalize A into intracellular vesicles (right panels show enlargement of insets). Scale bar: 10 m.From: Xiang X, Werner G, Bohrmann B, Liesz A, Mazaheri F, Capell A, Feederle R, Knuesel I, Kleinberger G, Haass C.TREM2 deficiency reduces the efficacy of immunotherapeutic amyloid clearance.EMBO Mol Med. 2016 Sep 1;8(9):992-1004.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA11 (MCA1957) used for the identification of macrophages in post stroke infarcts by immunohistochemistry on frozen tissue sections.Image caption:Immune cell composition in infarcts at the stage of liquefactive necrosis in humans and mice. a Representative images of CD3+ T-lymphocyte, CD20+ B-lymphocyte, and CD68+ macrophage/microglia infiltration in human infarcts at the stage of liquefactive necrosis. Scale bars, 10 m (human, CD3 and CD20 images) and 30 m (human, CD68 image). b Quantification of CD4+ and CD8+ T-lymphocyte, and CD20+ B-lymphocyte infiltration into the infarcts. c Representative images of CD3+ T-lymphocytes, B220+ B-lymphocytes, and CD68+ macrophages/microglia in the infarcts of C57BL/6 and BALB/c mice at 7 weeks post-stroke. Scale bar,100 m. d Higher magnification images of CD68+ macrophages/microglia in the infarct to reveal individual cells. Scale bar, 25 m. e Quantification of CD3+ T-lymphocyte infiltration, B220+ B-lymphocyte infiltration, and CD68 immunostaining in mouse infarcts. ****p Published customer image: Rat anti Mouse CD68 antibody, clone FA11 (MCA1957) used for the identification of macrophages in post stroke infarcts by immunohistochemistry on frozen tissue sections.Image caption:Impact of age on the chronic inflammatory response to stroke in C57BL/6 mice. a Comparison of the levels of 25 cytokines and chemokines in infarcts at the stage of liquefactive necrosis dissected from 3-month old and 18-month old C57BL/6 mice at 7 weeks post-stroke. Data are expressed as a fold-change relative to age matched sham control values. Data represent mean SEM. There is no significant difference in the overall cytokine and chemokine profile at the stage of liquefactive necrosis between 3-month old and 18-month old mice by two-way ANOVA. Cytokines and chemokines that are significantly different between the 3-month old and 18-month old mice corrected for multiple comparisons are denoted by an asterisk (*p 0.05 versus 3-month old mice). b Representative images of CD3+ T-lymphocytes, B220+ B-lymphocytes, and CD68+ macrophages/microglia in the infarcts of 3-month old and 18-month old C57BL/6 mice at 7 weeks post-stroke. Scale bar, 50 m. Red dotted lines indicate locations of the glial scar in each image. c Quantification of CD3+ T-lymphocyte and B220+ B-lymphocyte infiltration into the mouse infarcts.From: Nguyen TV, Frye JB, Zbesko JC, Stepanovic K, Hayes M, Urzua A, Serrano G, Beach TG, Doyle KP.Acta Neuropathol Commun. 2016 Sep 6;4(1):100.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Alexaflour 488 conjugated Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957A488) used for visualisation of CD68 expressing cells in brain lesions by immunofluorescence and purified Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to assess CD68 expression in similar lesions by western blotting.Image caption:Analysis of M/M phenotypic markers at different time points after dMCAO. a Coronal sections of the lesioned hemispheres of the inhibitor and control mice brains, at seven (two upper rows of panels) and 14 days (two lower rows) after dMCAO. The sections were triple-immunostained with anti-Iba-1 (red), anti-CD45 (blue), and anti-CD68 (green) antibodies. Representative merged and single-channel images depict part of the infarct core (I, outlined with white dotted lines) and peri-infarct area of stroke. High magnification images demonstrate distribution of Iba-1, CD45, and CD68 in the glial scar area (right panels). Imaging was performed using Zeiss LSM800 Airyscan confocal microscope, using single-scan and tile-scan image acquisitions. Bars: from left to right: 100 and 10 m. b Quantification of the corrected fluorescence intensity for CD45 and CD68 immunofluorescence staining in the inhibitor (black bars) and control groups (white bar), at 7 and 14 days after dMCAO. N = 5–6 mice per group/per time point, three brain sections per mouse. Error bars: SEM; Student s t test, *p 0.05; **p 0.01. c Representative Western blots and quantification analysis (graphs) of CD206, CD45, CD68, and Iba-1 expression in lysates prepared from the lesioned cortical tissue of the animals from the inhibitor (black bars) and control (white bars) groups, at 7 and 14 days after dMCAO. Graphs: optical density of each band was normalized to -actin (loading control). N = 5–6 mice per group/per time point. Error bars: SEM; Student s t test, *p 0.05From: Pena-Philippides JC, Caballero-Garrido E, Lordkipanidze T, Roitbak T.In vivo inhibition of miR-155 significantly alters post-stroke inflammatory response.J Neuroinflammation. 2016 Nov 9;13(1):287.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 used for the identification of infiltrating microglia in a murine model of Retinitis pigmentosa by immunofluorescence on vibrotome sections. Image caption:Transient expression of phagocytic molecules and exposure of the \"eat-me” signal phosphatidylserine (PS) in the outer nuclear layer during rod degenerationA–C Microglia infiltrating the ONL demonstrate upregulation of the phagocytic molecule, CD68. Top images in (A) show composites of CD68 (red), Iba1 (green), and DAPI (blue) staining; bottom images show the same field with CD68 staining only. At P18, non-infiltrating microglia expressed low or undetectable levels of CD68, a lysosome-associated membrane protein. At P21–23, microglia infiltrating the ONL strongly upregulated CD68 (arrowheads). At P30, CD68 immunopositivity in ONL microglia decreased and was mostly confined to amoeboid cells in the subretinal space. (B) Magnified view of inset in (A) demonstrates localization of CD68 to microglia phagosomes. (C) CD68 expression (area of immunopositivity as a fraction of the ONL) demonstrated a peaked at P22 and decreased by P30. Scale bar, 20 m.D–F Upregulation of MFG-E8, a secreted glycoprotein that serves as a bridging molecule for phagocytosis receptors, in the ONL. (D) MFG-E8 was low or absent in the ONL at P18, but emerged at P21–23, localizing to photoreceptor cell bodies in a column-like pattern (arrow) and as a punctate signal within infiltrating microglia (arrowhead), before decreasing throughout the ONL at P30. (E) A magnified orthogonal view of the inset from (D) demonstrating punctate MFG-E8 immunopositivity within ONL microglia. (F) Quantification of MFG-E8 expression demonstrated a prominent emergence at P22 and a subsequent decrement by P30. Scale bar, 20 m.G–K Increase in phosphatidylserine (PS) exposure in the ONL during photoreceptor degeneration. (G) At P18, PS immunopositivity is near absent in the ONL, but increased significantly in ONL somata at P21–23, before decreasing at P30. (H) Quantitation of PS exposure by image analysis (by fractional area of PS immunopositivity within the ONL (top), and the mean intensity of PS staining in the ONL (bottom)) demonstrated a transient increase at P22. (I) Co-immunolabeling of rods with rhodopsin at P22 demonstrates that PS exposure was present in a majority of rods (inset shows at high magnification the co-labeling of PS and rhodopsin in multiple rod somata). (J) Conversely, immunolabeling of cones with cone arrestin demonstrates the sparse co-localization of PS in cones (inset shows close juxtaposition but no colocalization of PS and arrestin labeling). (K) Scoring of rhodopsin+ rods and arrestin+ cones for PS co-labeling demonstrates that a large majority of rods, but only a small minority of cones, showed PS exposure (two-sided unpaired t-test, n = 3 animals at P22). Scale bars = 20 m.Data information: Quantitative analyses in (C, F, H, and K) involved three animals at each time point. Column heights and error bars indicate mean SEM.From: Zhao L, Zabel MK, Wang X, Ma W, Shah P, Fariss RN, Qian H, Parkhurst CN, Gan WB, Wong WT.Microglial phagocytosis of living photoreceptors contributes to inherited retinal degeneration.EMBO Mol Med. 2015 Jul 2;7(9):1179-97.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957GA) used for the identification of microglia engulfing rods in the retinal outer nuclear layer (ONL) in a murine model of retinitis pigmentoisa by immunofluorescence. Image caption:Infiltrating microglia phagocytose non-apoptotic photoreceptor rods during rod degenerationA–C Phagocytosis of rods by infiltrating microglia. (A) Representative example of a Iba1+ microglial process extending into the ONL with a phagosome at its terminal end. Each phagosome contained a photoreceptor nucleus (labeled with DAPI, arrow) that was identified as a rod photoreceptor by rhodopsin immunopositivity (superposition of Iba1+ phagosome with rhodopsin+ soma in orthogonal views). (B) Example of an amoeboid microglia in the ONL with multiple phagosomes containing both rhodopsin-positive (arrowhead) and rhodopsin-negative (arrow) nuclei. (C) Rhodopsin+ nuclei can be localized within CD68-positive phagosomes in infiltrating microglia, indicating phagocytic engulfment of rods. Scale bar, 10 m.From: Zhao L, Zabel MK, Wang X, Ma W, Shah P, Fariss RN, Qian H, Parkhurst CN, Gan WB, Wong WT.Microglial phagocytosis of living photoreceptors contributes to inherited retinal degeneration.EMBO Mol Med. 2015 Jul 2;7(9):1179-97.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA11 used for the demonstration of macrophages in murine muscle tissue by immunofluorescence on cryosections. Image caption:Osteopontin deletion in laminin α2 chain-deficient muscle temporarily influences macrophage numbers, but does not change the general character of macrophage-mediated immune response.(a) CD68 immunostaining of 2-week-old dy3K/dy3K and dy3K/OPN triceps muscle reveals increased infiltration of macrophages/monocytes in double knockout muscle. Representative areas of triceps and whole triceps are shown. (a ) Quantification of CD68-stained muscle area confirms significant escalation of macrophage numbers in 2-week-old double knockout mice compared to dy3K/dy3K single knockout mice (p = 0.0317, Mann Whitney) (b) Increase in macrophage numbers in younger double knockout mice is only transient. Three-week-old triceps muscle from both dy3K/dy3K and dy3K/OPN mice show the same appearance when stained against CD68 (top panel, green staining). M1 macrophages are present in both dy3K/dy3K and dy3K/OPN triceps, as demonstrated by immunostaining against iNOS (red, middle panel) and CD68 (merged staining, bottom panel). iNOS is expressed at low levels in vessels in wild-type and osteopontin-deficient muscle. (b ) Quantification of CD68 and iNOS labelling confirms no change of M1 macrophage-mediated immune response upon osteopontin deletion in 3-week-old mice (p = 0.2222 and p = 0.6905, respectively; Mann-Whitney). Five mice from each group were analysed in (a) and (b). Bars: 50 and 100 m.From: Gawlik KI, Holmberg J, Svensson M, Einerborg M, Oliveira BM, Deierborg T, Durbeej M. Potent pro-inflammatory and pro-fibrotic molecules, osteopontin and galectin-3, are not major disease modulators of laminin 2 chain-deficient muscular dystrophy.Sci Rep. 2017 Mar 10;7:44059.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957GA) used for the identifcation of macrophages in kidney sections by immunohistochemistry on cryosections. Image caption:Renal markers of inflammation at Week 32.CD68 representative images at 200x magnification, B. Area (%) of CD68 staining. Results are expressed as mean SEM, N = 4–6. *P 0.05, **P 0.01, ***P 0.001, ****P 0.0001 compared to CC.From: Glastras SJ, Chen H, Tsang M, Teh R, McGrath RT, Zaky A, et al. (2017)The renal consequences of maternal obesity in offspring are overwhelmed by postnatal high fat diet.PLoS ONE 12(2): e0172644.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957GA) used for the demonstration of macrophages in murine peritoneal tissue by immunohistochemistry.Image caption:BIX01294 inhibits monocyte/macrophage infiltration, TGF- 1, and H3K9me1 in mice with peritoneal fibrosis(A) Immunohistochemical staining shows typical CD68 expression in peritoneal tissue of control mice, MGO-injected mice, and MGO-injected mice treated with BIX01294 (original magnification, ×200). (B) Graph indicates the number of CD68-positive cells in the three groups of mice. (C) Immunohistochemical staining shows typical TGF- 1 expression in peritoneal tissue of control mice, MGO-injected mice, and MGO-injected mice treated with BIX01294 (original magnification, ×200). (D) Graph indicates the number of TGF- 1-positive cells in the three groups of mice. (E) Two-color immunohistochemical staining shows that most CD68 cells (brown) are immunoreactive for TGF- 1 (blue-gray) (arrows). (F) TGF- 1 protein levels in mouse PD effluent were quantified by ELISA. ( Data are expressed as the mean SE. Statistical analysis were performed by analysis of variance followed by Tukey s post-hoc test. *P 0.05, n = 5 mice per group.From: Maeda K, Doi S, Nakashima A, Nagai T, Irifuku T, Ueno T, et al. (2017)Inhibition of H3K9 methyltransferase G9a ameliorates methylglyoxal-induced peritoneal fibrosis.PLoS ONE 12(3): e0173706.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Moouse CD68 antibody, clone FA11 (MCA1957)Image caption:Astrogliosis and white matter volume loss in PVL model.Studies of microglial M1 and M2 phenotypes at P15 (10 days after HI) in HI group versus sham.Panel A: Immunostaining for all Microglia (Iba1) in green (top), CD 68 (marker of activated microglia only) in red (middle). Co-localization in yellow indicating amount of activated microglia. Scale Bar = 100 m. Panel B: Immunostaining for Arginase 1 (M2 microglial marker) in green (top); for Microglia (Iba1) in blue (middle); and Co-localization (bottom) indicating the percentage of M2 microglia. Co-localization showed scare M2 microglial phenotype cells in HI group. Scale Bar = 100 m. Panel C: Quantification of CD68/Iba1 per section Panel D: Arginase 1/Iba1 per section. There was significant increase of M1 microglia and a significant reduction of M2 microlgia in HI group. N = 5 animals/group & 4 sections/animal. Bars represent the Mean + SE. **** indicates P 0.0001.From: Zaghloul N, Patel H, Ahmed MN (2017)A model of Periventricular Leukomalacia (PVL) in neonate mice with histopathological and neurodevelopmental outcomes mimicking human PVL in neonates.PLoS ONE 12(4): e0175438.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody (MCA1957) used to indicate macrophages in mouse brain by immunofluorescence (panels A-C-see text below)Image caption:Microglia activation was not observed in the corpus callosum three days after the stimulation at 300 Hz, and also not in sham-treated animals.(A-C) Sham-treated animal: Coronal section of corpus callosum from a showing double channel immunofluorescent labeling with DAPI (A, blue), CD68 (B, red), and the overlay of two channels (C). Left column: Overview image taken with an open pinhole. The dashed and white squares indicate the region of electrode implantation and the region of interest used for counting of oligodendroglial cells, respectively. These regions are shown at a higher magnification in the middle- and right-column images. Note that cell counting area is far away from injury site. ctx = cortex, cc = corpus callosum, cc = hippocampus. Scale bars: 500 m. Middle column: Higher magnification of the area indicated on the left image with the dashed square. The image shows the site of cortical injury caused by electrode implantation. Single confocal plane. Scale bars: 100 m. Right column: Higher magnification of the area indicated on the left image with the white square. The image shows the region of corpus callosum with white dashed line denoting the region of interest where counting of oligodendroglial cells was performed. Single confocal plane. Scale bars: 100 m. (D-F) As in (A-C) but for 300 Hz stimulation. Note that in both sham-treated and stimulated animal CD68-expressing cells are visible only at the injury site, but not in corpus callosum. All images are representative examples. Samples from the group of mice received stimulation at 25 Hz (not shown) followed very similar pattern, i.e. CD68-expressing cells appeared at the injury site, but not in the corpus callosum.From: Citation: Nagy B, Hovhannisyan A, Barzan R, Chen T-J, Kukley M (2017)Different patterns of neuronal activity trigger distinct responses of oligodendrocyte precursor cells in the corpus callosum.PLoS Biol 15(8): e2001993.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody (MCA1957) used to indicate macrophages in mouse brain by immunofluorescence (panels A-C-see text below)Image caption:Microglia activation was not observed in the corpus callosum three days after the stimulation at 300 Hz, and also not in sham-treated animals.(A-C) Sham-treated animal: Coronal section of corpus callosum from a showing double channel immunofluorescent labeling with DAPI (A, blue), CD68 (B, red), and the overlay of two channels (C). Left column: Overview image taken with an open pinhole. The dashed and white squares indicate the region of electrode implantation and the region of interest used for counting of oligodendroglial cells, respectively. These regions are shown at a higher magnification in the middle- and right-column images. Note that cell counting area is far away from injury site. ctx = cortex, cc = corpus callosum, cc = hippocampus. Scale bars: 500 m. Middle column: Higher magnification of the area indicated on the left image with the dashed square. The image shows the site of cortical injury caused by electrode implantation. Single confocal plane. Scale bars: 100 m. Right column: Higher magnification of the area indicated on the left image with the white square. The image shows the region of corpus callosum with white dashed line denoting the region of interest where counting of oligodendroglial cells was performed. Single confocal plane. Scale bars: 100 m. (D-F) As in (A-C) but for 300 Hz stimulation. Note that in both sham-treated and stimulated animal CD68-expressing cells are visible only at the injury site, but not in corpus callosum. All images are representative examples. Samples from the group of mice received stimulation at 25 Hz (not shown) followed very similar pattern, i.e. CD68-expressing cells appeared at the injury site, but not in the corpus callosum.From: Citation: Nagy B, Hovhannisyan A, Barzan R, Chen T-J, Kukley M (2017)Different patterns of neuronal activity trigger distinct responses of oligodendrocyte precursor cells in the corpus callosum.PLoS Biol 15(8): e2001993.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA11 (MCA1957) used to identify macrophages in murine kidney sections by immunohistochemistry on cryostat sections.Image caption:Histology at day 8 after NTN induction. Representative histology from PAS stained sections from Experiment 2, of WT and RIPK3−/− kidney. a) WT b) RIPK3- /−. Immunoperoxidase staining for CD68 in WT and RIPK3−/− kidney showing glomerular macrophage infiltration following the induction of NTN. c) WT d) RIPK3−/−From: Hill NR, Cook HT, Pusey CD, Tarzi RM.RIPK3-deficient mice were not protected from nephrotoxic nephritis.BMC Nephrol. 2018 Mar 14;19(1):61.This is an open access article distributed under the terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11(MCA1957) used to identify lysozomes by immunofluorescence.Image caption:CD68-positive brain myeloid cells after permanent ischemia and simplified scheme of the phagocytic process. Confocal images of the ischemic hemisphere showing cells positive for the lysosomal marker CD68 (red) and for the myeloid cell membrane marker CD11b (green) in the ischemic area at 48 h (a) or 7 days (b) after pMCAo, the latter time showing increased density of CD68-positive cells (nuclei in blue, scale bar = 200 m). Steps leading to phagocytosis include cell targeting by eat-me-signals, recognition by the phagocytic cell, and vesicular trafficking within the phagocyting cell. There, primary lysosomes get close to cell membrane and fuse with phagosomes. The mature lysosomes complete digestion with lysozimes, leaving residual bodies within the cytoplasm or getting back to Golgi. From: Fumagalli S, Fiordaliso F, Perego C, Corbelli A, Mariani A, De Paola M, De Simoni MG.The phagocytic state of brain myeloid cells after ischemia revealed by superresolution structured illumination microscopy.J Neuroinflammation. 2019: 16(1):9.This image is from an open access article distributed under the terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11(MCA1957) used to identify lysozomes by immunofluorescence.Image caption:Confocal microscopy vs. SIM and CD68 SIM dataset validation by image diagnosis. Planar xy view with xz (below) and yz (right) projections of CD11b (green) and CD68 (red) showing merged signal (yellow) by confocal microscopy (a), or signal proximity with no colocalization by SIM (a′). Image overimposition details the different resolutions achieved by confocal microscopy vs. SIM (a′′). Three-dimensional view of the same cell by confocal (b) and SIM (b′). The arrow in (b) show a lysosome (CD68) entirely surrounded by cell membrane (CD11b) in confocal microscopy. SIM yields enough resolution to visualize lysosome proximity to cell mebrane with no fusion (b′, arrow). Scale bars = 2 m. Plot profiles over the lines in a and a′ confirm that SIM, but not confocal microscopy, allows to visualize close, non-overlapping CD11b and CD68 signals. From: Fumagalli S, Fiordaliso F, Perego C, Corbelli A, Mariani A, De Paola M, De Simoni MG.The phagocytic state of brain myeloid cells after ischemia revealed by superresolution structured illumination microscopy.J Neuroinflammation. 2019: 16(1):9.This image is from an open access article distributed under the terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957)used for the identification of microglia in mouse brain by immunofluorescence.Image caption:Localization of CB2 receptors in microglial cells and engulfment synapses. (A) A confocal image of CB2 (green) and CD68 staining (red) centered at the core of an A plaque (marked by an asterisk). Note a region of high intensity for CB2 and CD68 staining around the plaque implying that CB2 receptors are localized in microglial processes surrounding the plaque. Scale 15 m. (B) A magnification of a microglia cell body (red) and its process (red) forming an engulfment synapse on a dense core amyloid plaque (marked by an asterisk, DAPI). Note CB2 receptor staining along the edge of CD68-positive staining and at the engulfment synapse. White boxes indicate areas used for quantifications in C-D. (C-D) Quantification of CB2, CD68, and DAPI signals from the image of a microglia cell body (C) and engulfment synapse (D). The quantification was done using a Plot profile analysis tool (Fiji). Signals were averaged along short axes of boxes shown in B and normalized to a max value (100%) for each channel. Units of X axis are pixels, scale: 11.1 pixels/ m. (E) 3D reconstruction of the engulfment synapse shown in B, D. A z stack of 0.31 m slices (n = 29) was processed by using a background subtraction function and normalization for each of the channels. Surfaces for the plaque (DAPI), microglia process (CD68), and CB2 signal were created by arbitrary thresholding at an upper third of intensity distributions. Note high intensities of CB2 signals are located between CD68 and DAPI surfaces. Insert shows orientation of a 3D window as related to a position of the brain slide.From: Savonenko AV, Melnikova T, Wang Y, Ravert H, Gao Y, Koppel J, et al. (2015)Cannabinoid CB2 Receptors in a Mouse Model of A Amyloidosis: Immunohistochemical Analysis and Suitability as a PET Biomarker of Neuroinflammation.PLoS ONE 10(6): e0129618.This is an open access article distributed under the terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957GA) used for the detection of macrophages in murine kidney using immunohistochemistry on PLP fixed cryosections.Image caption:Representative histological sections from the 3 bone marrow transplant groups with NTN. (A) PAS-stained sections of renal histology. The WT to IL-17-/- group have severe glomerular thrombosis with profound tubular dilatation and casts, significantly more than the other groups. (B) and (C) Immunofluorescence for glomerular deposition of sheep and mouse IgG respectively. There was no difference between the groups. (D) and (E) Representative glomerular staining for CD68 and CD4 respectively. Magnification x400.From: Hamour S, Gan P-Y, Pepper R, Florez Barros F, Wang H-H, O Sullivan K, et al. (2015)Local IL-17 Production Exerts a Protective Role in Murine Experimental Glomerulonephritis.PLoS ONE 10(8): e0136238. This is an open access article distributed under the terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA11 (MCA1957) used for the identification of macrophages in mouse liver by immunohistochemistry on formalin fixed, paraffin tissue sections. Image caption:Expression of F4/80 and CD68 in liver tissue assessed by immunostaining using anti-F4/80 or anti-CD68 antibody.From: Citation: Ibusuki R, Uto H, Oda K, Ohshige A, Tabu K, Mawatari S, et al. (2017)Human neutrophil peptide-1 promotes alcohol-induced hepatic fibrosis and hepatocyte apoptosis.PLoS ONE 12(4): e0174913.This is an open access article distributed under the terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA11 (MCA1957GA) used for the identification of macrophages in vascular smooth muscle by immunohistochemistry on formalin fixed, paraffin embedded tissue sections.Image caption:A-D Representative images and quantifications of macrophages (CD68 staining) (A) T lymphocytes (CD3 staining) (B), apoptotic area as assessed by TUNEL assay (C) and -actin (D) in Ldlr-/- infused either PBS (n = 5), AngII (n = 5) and Ldlr-/-Ido1-/- mice infused with AngII (n = 5) for 7 days. Mean values SEM are shown. *P 0.05, **P 0.001.From: Metghalchi S, Vandestienne M, Haddad Y, Esposito B, Dairou J, Tedgui A, et al. (2018)IDO deficiency prevents AngII-induced vascular smooth muscle cell apoptosis.PLoS ONE 13(3): e0193737.This is an open access article distributed under the terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used for the detection of macrophages in mouse brain by immunofluorescence.Image caption:DCH-paclitaxel exhibits good biocompatibility in healthy CNS in contrast to paclitaxel in Cremophor EL vehicle. A-D. Images of caudate putamen at 1 week after injection into healthy, uninjured tissue of Cremophor EL vehicle (A), Cremophor EL + paclitaxel (B), DCH only (C), or DCH + paclitaxel (D), showing single channel and merged multichannel immunofluorescence for multiple markers of inflammation and gliosis, CD 68, IBA-1 and GFAP. Scale bar, 200 m for all images, D = DCH depot.From: Garrett MC, O’Shea TM, Wollenberg AL, Bernstein AM, Hung D, Staarman B, et al. (2020)Injectable diblock copolypeptide hydrogel provides platform to deliver effective concentrations of paclitaxel to an intracranial xenograft model of glioblastoma.PLoS ONE 15(7): e0219632.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to label macrophages in mouse aortic samples by immunofluorescence.Image caption:Nba2.Yaa mutation in Apoe−/−mice does not affect atherosclerosis lesion size. Representative pictures CD68, iNos and Arginase (Arg) staining in the roots of Apoe−/− or Apoe−/−Nba2.Yaa mice on HCD.From: Santiago-Raber ML, Montecucco F, Vuilleumier N, Miteva K, Baptista D, Carbone F, Pagano S, Roth A, Burger F, Mach F, Brandt KJ.Atherosclerotic plaque vulnerability is increased in mouse model of lupus.Sci Rep. 2020 Oct 27;10(1):18324.doi: 10.1038/s41598-020-74579-8.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used for labeling macrophages in mouseImage caption:Targeted silencing of miR-33 does not influence macrophage and smooth muscle cell content in atherosclerotic lesions. Low density lipoprotein receptor knockout (Ldlr-/-) mice were placed on a western diet (WD) for 3 months, and then switched to a chow diet andreceived anti-miR-33 peptide nucleic acid delivery vector (anti-miR33pHLIP) or scrambled control (SrcpHLIP) at a dose of 1 mg/kg body weight every week for a total of 5 injections. Representative immunofluorescence staining of macrophage (CD68 positive) and smooth muscle cell ( -smooth muscle actin) in cross sections of the aortic root from Ldlr-/- mice injected with anti-miR33pHLIP or SrcpHLIP vectors.From: Xinbo Zhang, Noemi Rotllan, Alberto Canfr n-Duque et al.Targeted suppression of microRNA-33 in lesional macrophages using pH low-insertion peptides (pHLIP) improves atherosclerotic plaque regression, 29 October 2020, PREPRINT (Version 1) available at Research Square10.21203/rs.3.rs-92252/v1This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used for the demonstration of macrophages in murine lungs by immunohistochemistry on formalin fixed, paraffin embedded tissue sections.Image caption:Immunolocalization of macrophages in lung tissue sections from female mice sham surgery (Sham) or ovariectomized (OVX) inoculated with the ATCC 25923 strain of S. aureusem> or saline (Sham Control or OVX Control). (B) Representative photomicrographs of immunolocalization of macrophages (original magnification ×400).From: Souza CLSE, Oliveira HBM, Santos J nior MN, Silva MO, Coqueiro IL, Silva ÍBSD, Campos GB, Silva RAAD, Soares TJ, Oliveira MV, Timenetsky J, Marques LM.Ovarian hormones influence immune response to Staphylococcus aureus infection.Braz J Infect Dis. 2020 Nov 10:S1413-8670(20)30156-2.doi: 10.1016/j.bjid.2020.10.004.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse antibody, clone FA-11 (MCA1957) used for the demonstration of macrophages in murine aortic arches by immunohistochemistry on vibratome sections. Image caption:Histological analyses of atherosclerotic lesions in the aortic valve of 26-week-old low-density lipoprotein receptor knockout (Ldlr-/-) mice. Mice were fed a Western diet with adequate (0.3%; P0.3) or high (1.5%; P1.5) phosphorus levels coupled with adequate (1000 IU; D1000) or low (50 IU; D50) vitamin D levels over a 17-week period. Shown are (c) the percentage of macrophages in the aortic valve lesions and representative images of aortic valve sections that were stained by immunohistochemical staining with CD68 antibodies and haematoxylin.From: Grundmann SM, Schutkowski A, Berger C, Baur AC, K nig B, Stangl GI.High-phosphorus diets reduce aortic lesions and cardiomyocyte size and modify lipid metabolism in Ldl receptor knockout mice.Sci Rep. 2020 Nov 27;10(1):20748.doi: 10.1038/s41598-020-77509-w.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used for the demonstration of macrophages in murine brain by immunofluorescenceImage caption:NF- B modulates microglial activation to an inflammatory, neurotoxic phenotype. a Immunostaining for all microglia (Iba1) in green (top) and CD 68 (marker of activated microglia M1 only) in red (middle). Co-localization in yellow indicating amount of activated microglia at postnatal day 15. * indicates lateral ventricle. From: Zaghloul N, Kurepa D, Bader MY, Nagy N, Ahmed MN.Prophylactic inhibition of NF- B expression in microglia leads to attenuation of hypoxic ischemic injury of the immature brain.J Neuroinflammation. 2020 Dec 1;17(1):365.doi: 10.1186/s12974-020-02031-9.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to stain CD68 expressing cells in murine hippocampus by immunofluorescence on cryosections.Image caption:BF increased the amount of CD68+ cells in the ipsilateral hippocampal CA1 region. (A). Representative microscopic images of CD68+ antibody (red) stained sections. The nuclei were stained with DAPI (Blue). Scale bar: 500 m. (B). Quantification of the number of CD68+ cells. The groups represented by different colors are indicated on the X-axis. N = 6. con: contralateral to stroke injury. ips: ipsilateral to stroke injury. BFS: BF 6 h before stroke.From: Huang J, Lyu H, Huo K, Do Prado LB, Tang C, Wang Z, Li Q, Wong J, Su H.Bone Fracture Enhanced Blood-Brain Barrier Breakdown in the Hippocampus and White Matter Damage of Stroke Mice.Int J Mol Sci. 2020 Nov 11;21(22):8481.doi: 10.3390/ijms21228481.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to identify microglia in mouse brain tissue by immunofluorescence on formalin fixed cryosections. Image caption:Alcohol downregulates the microglial expression of CD68.a). Representative images of the hippocampal sections stained for Iba1 (green), CD68 (red), and DAPI (blue) from pair-fed (PF) and alcohol-fed (EtOH) mice, acquired at × 63 magnification. From: Lowe PP, Morel C, Ambade A, Iracheta-Vellve A, Kwiatkowski E, Satishchandran A, Furi I, Cho Y, Gyongyosi B, Catalano D, Lefebvre E, Fischer L, Seyedkazemi S, Schafer DP, Szabo G.Chronic alcohol-induced neuroinflammation involves CCR2/5-dependent peripheral macrophage infiltration and microglia alterations.J Neuroinflammation. 2020 Oct 9;17(1):296.doi: 10.1186/s12974-020-01972-5. This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to identify macrophages in murine femoral arteries by immunohistochemistry on formalin fixed, paraffin embedded tissue sections.Image caption:Effects of Revacept administration to mice on CD68 expression in femoral artery sections. Immunohistochemistry of femoral artery sections to assess CD68 at 28 days after surgery in mice treated with Revacept or Fc.From: Alberti S, Zhang Q, D\'Agostino I, Bruno A, Tacconelli S, Contursi A, Guarnieri S, Dovizio M, Falcone L, Ballerini P, Münch G, Yu Y, Patrignani P.The antiplatelet agent revacept prevents the increase of systemic thromboxane A2 biosynthesis and neointima hyperplasia.Sci Rep. 2020 Dec 8;10(1):21420.doi: 10.1038/s41598-020-77934-x.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to stain macrophages in murine aortic root by immunohistochemistry on cryostat sections. Image caption:Serum cholesterol lowering leads to phenotypic plaque regression in APOE*3-Leiden.CETP mice.a. Representative images of aortic root sections stained with Oil-red O (ORO), anti-CD68 (for macrophages, M ) on the left. On the right, lesion area was measured on 8 aortic root sections at 50 m intervals starting from valve initiation. Plaque composition was analyzed by quantifying the percent ORO+ and CD68+ and areas within lesions. Data are presented as mean SEM percent change over values in the baseline group to visualize relative changes during plaque progression and regression. *, , p 0.05 denote statistically significant differences between the Ctrl and Base ( ), Statin (*) and Free ( ) groups, respectively, baseline n = 6, other 3 groups n = 8 per group, one-way ANOVA.From: H rdtner C, et al. Inhibition of macrophage proliferation dominates plaque regression in response to cholesterol lowering.Basic Res Cardiol. 2020 Dec 9;115(6):78.doi: 10.1007/s00395-020-00838-4.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to label macrophages in murine renal tissue by immunohistochemistry on formalin fixed, paraffin embedded sections.Image caption:Immunohistochemistry and quantitative analysis for anti-CD68 and anti- -SMA. Anti-CD68 for the a CKD group, b RPC group, and c hiPSC group, magnification of × 40. d Anti-CD68 quantitative analysis for all the three groups. Anti- -SMA for the e CKD group, f RPC group, and g hiPSC group, magnification of × 40. h Anti- -SMA quantitative analysis for all the three groups. *p value 0.05 vs. CKD.From: Ribeiro PC, Lojudice FH, Fernandes-Charpiot IMM, Baptista MASF, de Almeida Araújo S, Mendes GEF, Sogayar MC, Abbud-Filho M, Caldas HC.Therapeutic potential of human induced pluripotent stem cells and renal progenitor cells in experimental chronic kidney disease.Stem Cell Res Ther. 2020 Dec 9;11(1):530.doi: 10.1186/s13287-020-02060-4.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to stain microglia in mouse brain by immunohistochemistry on free floating sections.Image caption:Threshold imaging analysis of sections stained for microglia (CD68) show a significant increase in both the dorsal and ventral horns of the lumbo-sacral cord at early (3MO) and late (7MO) disease states in Ppt1−/− cords compared to WT. From: Nelvagal HR, Hurtado ML, Eaton SL, Kline RA, Lamont DJ, Sands MS, Wishart TM, Cooper JD.Comparative proteomic profiling reveals mechanisms for early spinal cord vulnerability in CLN1 disease.Sci Rep. 2020 Sep 16;10(1):15157.doi: 10.1038/s41598-020-72075-7.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody (MCA1957) used to identify macrophages in mouse atherosclerotic plaques by immunofluorescence on cryostat sections.Image caption:CD68 staining in ApoE-/- mice after 12 weeks with Western Diet.(A) without plaque formation in the aortic arch, (B) with big plaque formation with macrophages inside in the thoracic part of the aorta.From: Riedl KA, Kampf T, Herold V, Behr VC, Bauer WR (2020)Wall shear stress analysis using 17.6 Tesla MRI: A longitudinal study in ApoE-/- mice with histological analysis.PLoS ONE 15(8): e0238112.doi: 10.1371/journal.pone.0238112This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to identify microglia in mouse brain free floating sections by immunohistochemistry.Image caption:Microglial activation, revealed by CD68 immunoreactivity (C), is increased all brain regions for Cln3Q352X mice of both sexes, except for the S1BF of female Cln3Q352X mice. Two-way ANOVA, Fisher’s LSD post-hoc. Mean SEM, *p 0.05; **p 0.01; ****p 0.0001. WT images are representative of female mice. Mutant images are representative for male mice (SubC, CD68) and female mice (GFAP). Scale bar = 100 m.From: Langin L, Johnson TB, Kov cs AD, Pearce DA, Weimer JM.A tailored Cln3Q352X mouse model for testing therapeutic interventions in CLN3 Batten disease.Sci Rep. 2020 Jun 29;10(1):10591.doi: 10.1038/s41598-020-67478-5.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used for the detection of activated micropahe cells in mouse brain sections by immunofluorescence.Image caption:Maximum intensity projections of confocal stacks, showing a representative image of activated myeloid cells around plaques (distance 10 m) and less activated myeloid cells distant from the plaque; scale bar = 25 m. (j) Quantification of the percentage of CD68 + activated myeloid cells close and distant from plaques; n = 3 animals, 4-6 fields of view per animal; 2-way ANOVA with Bonferroni post-hoc test; df = 57; interaction; ***p 0.001.From: Drost N, Houtman J, Cseresny s Z, Niesner R, Rinnenthal JL, Miller KR, Prokop S, Heppner FL.The Amyloid-beta rich CNS environment alters myeloid cell functionality independent of their origin.Sci Rep. 2020 Apr 28;10(1):7152.doi: 10.1038/s41598-020-63989-3.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to illustrate microglia in mouse brain by immunofluorescence.Image caption:Switch in microglial proteomic signatures and increased phagocytosis occur already in pre-symptomatic Npc1−/− mice and precede neuronal loss.Immunostaining of cerebellum of P7 WT and Npc1−/− mice from three independent experiments (n = 3) using antibodies against neuronal markers (green) Calbindin (Purkinje cells, cerebellum), NeuN (cortex) and lysosomal microglial marker CD68 (red) reveal no neurodegeneration in Npc1−/− mice (10×, upper panels). In contrast, CD68 immunoreactivity showed activated Npc1−/− microglia with amoeboid morphology already at this early pathological stage (100×, lower panels). Hoechst was used for nuclear staining (blue). Scale bars: 250 m (10×, left panels) and 25 m (100×, right panels). From: Colombo A, Dinkel L, M ller SA, Sebastian Monasor L, Schifferer M, Cantuti-Castelvetri L, König J, Vidatic L, Bremova-Ertl T, Lieberman AP, Hecimovic S, Simons M, Lichtenthaler SF, Strupp M, Schneider SA, Tahirovic S.Loss of NPC1 enhances phagocytic uptake and impairs lipid trafficking in microglia.Nat Commun. 2021 Feb 24;12(1):1158.doi: 10.1038/s41467-021-21428-5.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to illustrate microglia in mouse brain by immunofluorescence.Image caption:Switch in microglial proteomic signatures and increased phagocytosis occur already in pre-symptomatic Npc1−/− mice and precede neuronal loss.Immunostaining of cortex of P7 WT and Npc1−/− mice from three independent experiments (n = 3) using antibodies against neuronal markers (green) Calbindin (Purkinje cells, cerebellum), NeuN (cortex) and lysosomal microglial marker CD68 (red) reveal no neurodegeneration in Npc1−/− mice (10×, upper panels). In contrast, CD68 immunoreactivity showed activated Npc1−/− microglia with amoeboid morphology already at this early pathological stage (100×, lower panels). Hoechst was used for nuclear staining (blue). Scale bars: 250 m (10×, left panels) and 25 m (100×, right panels). From: Colombo A, Dinkel L, M ller SA, Sebastian Monasor L, Schifferer M, Cantuti-Castelvetri L, K nig J, Vidatic L, Bremova-Ertl T, Lieberman AP, Hecimovic S, Simons M, Lichtenthaler SF, Strupp M, Schneider SA, Tahirovic S.Loss of NPC1 enhances phagocytic uptake and impairs lipid trafficking in microglia.Nat Commun. 2021 Feb 24;12(1):1158.doi: 10.1038/s41467-021-21428-5.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to illustrate microglial expression of CD68 in mouse brain by western blotting.Image caption:Switch in microglial proteomic signatures and increased phagocytosis occur already in pre-symptomatic Npc1−/− mice and precede neuronal loss.Representative immunoblots of acutely isolated microglia from WT mice and Npc1−/− littermates showing increased level of late endosomal/lysosomal markers (NPC2, LAMP1, CTSB, CTSD, CD68, and CD63). Calnexin was used as a loading control.From: Colombo A, Dinkel L, M ller SA, Sebastian Monasor L, Schifferer M, Cantuti-Castelvetri L, K nig J, Vidatic L, Bremova-Ertl T, Lieberman AP, Hecimovic S, Simons M, Lichtenthaler SF, Strupp M, Schneider SA, Tahirovic S.Loss of NPC1 enhances phagocytic uptake and impairs lipid trafficking in microglia.Nat Commun. 2021 Feb 24;12(1):1158.doi: 10.1038/s41467-021-21428-5.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to illustrate microglial expression of CD68 in mouse brain by western blotting.Image caption:Cell autonomous function of NPC1 in microglia.Western blot analysis and corresponding quantification of 8-weeks old Npc1flox/cre+ (Cre+) mice with specific depletion of NPC1 in microglia and their littermate controls Npc1flox/cre− (Cre−). Representative immunoblots showing specific NPC1 depletion in microglia enriched (MG enriched) compared to microglia depleted (MG depleted) fraction of Cre+ microglia. Increased levels of late endosomal/lysosomal markers (LAMP1, CD68, and CD63) could only be detected in MG enriched fraction of Cre+ microglia. GAPDH was used as a loading control.From: Colombo A, Dinkel L, M ller SA, Sebastian Monasor L, Schifferer M, Cantuti-Castelvetri L, K nig J, Vidatic L, Bremova-Ertl T, Lieberman AP, Hecimovic S, Simons M, Lichtenthaler SF, Strupp M, Schneider SA, Tahirovic S.Loss of NPC1 enhances phagocytic uptake and impairs lipid trafficking in microglia.Nat Commun. 2021 Feb 24;12(1):1158.doi: 10.1038/s41467-021-21428-5.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to illustrate microglial expression of CD68 in mouse brain by western blotting.Image caption:Npc1−/− microglia display impairment in myelin turnover.In vitro myelin phagocytosis assay. Cultured primary microglia isolated from P7 mice from three independent experiments (n = 3) were incubated with fluorescently labeled myelin (green) and analyzed. Microglial lysosomes were stained with anti-CD68 antibody (red). Hoechst was used for nuclear staining (blue). At 48 h fluorescently labeled lipid vesicles were observed in WT microglia, indicating myelin turnover. In contrast, Npc1−/− microglia accumulated myelin within the CD68 positive compartments and no fluorescently labeled lipid vesicles were detected. Scale bars: 25 m.From: Colombo A, Dinkel L, M ller SA, Sebastian Monasor L, Schifferer M, Cantuti-Castelvetri L, K nig J, Vidatic L, Bremova-Ertl T, Lieberman AP, Hecimovic S, Simons M, Lichtenthaler SF, Strupp M, Schneider SA, Tahirovic S.Loss of NPC1 enhances phagocytic uptake and impairs lipid trafficking in microglia.Nat Commun. 2021 Feb 24;12(1):1158.doi: 10.1038/s41467-021-21428-5.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to demonstrate macrophages in murine spinal chord tissue by immunofluorescence.Image caption:Fasudil‐modified mononuclear cells (MNCs) inhibit inflammation and improve myelination in spinal cords. Chronic experimental autoimmune encephalomyelitis was induced in C57BL/6 mice with MOG35‐55. Fasudil‐modified MNCs were administrated by bilateral intranasal instillation with 3 × 106 cells/unilateral nasal cavity on day 3 postimmunization (p.i.) and 11 p.i. Phosphate buffered solution (PBS)‐treated MNCs were set up as control in a similar manner. On day 28 p.i., spinal cords were used for immunohistochemistry staining. From: Guo SD, Liu CY, Yu JW, Chai Z, Wang Q, Mi XT, Song GB, Li YH, Yang PW, Feng L, Xiao BG, Ma CG.Nasal delivery of Fasudil-modified immune cells exhibits therapeutic potential in experimental autoimmune encephalomyelitis.Infiltration of CD4+ T cells and CD68+ macrophage. Results are shown as mean SEM of five mice in each group. Differences are analyzed using Student s t‐test. **P 0.01; ***P 0.001CNS Neurosci Ther. 2019 Jun;25(6):783-95.doi: 10.1111/cns.13111.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Rat anti Mouse CD68:Alexa Fluor 488 CD68 antibody, clone FA-11 recognizes mouse macrosialin which is a homolog of human CD68, which is classified as a unique scavenger receptor (ScR) family member. CD68 is considered a pan macrophage marker expressed on the intracellular lysosomes of tissue macrophages. Rat anti Mouse CD68:Alexa Fluor 647 CD68 antibody, clone FA-11 recognizes mouse macrosialin which is a homolog of human CD68, which is classified as a unique scavenger receptor (ScR) family member. CD68 is considered a pan macrophage marker expressed on the intracellular lysosomes of tissue macrophages. Rat anti Mouse CD68:Biotin CD68 antibody, clone FA-11 recognizes mouse macrosialin which is a homolog of human CD68, which is classified as a unique scavenger receptor (ScR) family member. CD68 is considered a pan macrophage marker expressed on the intracellular lysosomes of tissue macrophages. Rat anti Mouse CD68:FITC CD68 antibody, clone FA-11 recognizes mouse macrosialin which is a homolog of human CD68, which is classified as a unique scavenger receptor (ScR) family member. CD68 is considered a pan macrophage marker expressed on the intracellular lysosomes of tissue macrophages. Rat anti Mouse CD68:Endotoxin Low CD68 antibody, clone FA-11 recognizes mouse macrosialin which is a homolog of human CD68, which is classified as a unique scavenger receptor (ScR) family member. CD68 is considered a pan macrophage marker expressed on the intracellular lysosomes of tissue macrophages. Rat anti Mouse CD68 CD68 antibody, clone FA-11 recognizes mouse macrosialin which is a homolog of human CD68, which is classified as a unique scavenger receptor (ScR) family member. CD68 is considered a pan macrophage marker expressed on the intracellular lysosomes of tissue macrophages. Rat anti Mouse CD68:RPE CD68 antibody, clone FA-11 recognizes mouse macrosialin which is a homolog of human CD68, which is classified as a unique scavenger receptor (ScR) family member. CD68 is considered a pan macrophage marker expressed on the intracellular lysosomes of tissue macrophages. Rat anti Mouse CD68:Alexa Fluor 700 CD68 antibody, clone FA-11 recognizes mouse macrosialin which is a homolog of human CD68, which is classified as a unique scavenger receptor (ScR) family member. CD68 is considered a pan macrophage marker expressed on the intracellular lysosomes of tissue macrophages. Rat anti Mouse CD68:Amethyst Orange CD68 antibody, clone FA-11 recognizes mouse macrosialin which is a homolog of human CD68, which is classified as a unique scavenger receptor (ScR) family member. CD68 is considered a pan macrophage marker expressed on the intracellular lysosomes of tissue macrophages. Product Type Monoclonal Antibody Clone FA-11 Isotype IgG2a Rat anti Mouse CD68 antibody, clone FA-11 recognizes mouse macrosialin, a heavily glycosylated transmembrane protein and murine homolog of human CD68, which is classified as a unique scavenger receptor (ScR) family member, due to the presence of a lysosome associated membrane protein (LAMP)-like domain.CD68 is considered a pan macrophage marker, predominantly expressed on the intracellular lysosomes of tissue macrophages/monocytes, including Kupffer cells, microglia, histiocytes and osteoclasts, and is expressed to a lesser extent by dendritic cells and peripheral blood granulocytes. CD68 is expressed by many tumor types including some B cell lymphomas, blastic NK lymphomas, melanomas, granulocytic (myeloid) sarcomas, hairy cell leukemias, and renal, urinary and pancreatic tumors, and can be used in cancer studies to demonstrate the presence/localization of macrophages.Rat anti mouse CD68 antibody, clone FA-11, has been used in many mouse models for the identification of CD68 in immunohistochemical studies, using both frozen and paraffin-embedded tissues (Masaki et al. 2003) and (Devey et al. 2009).Rat anti mouse CD68 antibody, clone FA-11 can be used in flow cytometry to detect intracellular CD68, following permeabilization, and can detect surface macrosialin at low levels in resident mouse peritoneal macrophages which can be enhanced with thioglycollate stimulation. Product Form Purified IgG conjugated to Fluorescein Isothiocyanate Isomer 1 (FITC) - liquid Product Form Purified IgG - liquid Product Form Purified IgG - liquid Product Form Purified IgG conjugated to R. Phycoerythrin (RPE) - lyophilized Product Form Purified IgG conjugated to Alexa Fluor® 700 - liquid Product Form Purified IgG conjugated to Amethyst Orange - liquid Reconstitution Pack Size: 100 TestsReconstitute with 1.0 ml distilled water Pack Size: 25 TestsReconstitute in 0.25 ml disilled water Preparation Purified IgG prepared by affinity chromatography on Protein G from tissue culture supernatant Preparation Purified IgG prepared by affinity chromatography on Protein G from tissue culture supernatant Preparation Purified IgG prepared by affinity chromatography on Protein G from tissue culture supernatant Preparation Purified IgG prepared by affinity chromatography on Protein G from tissue culture supernatant Preparation Purified IgG prepared by affinity chromatography on Protein G from tissue culture supernatant Preparation Purified IgG prepared by affinity chromatography on Protein G from tissue culture supernatant Preparation Purified IgG prepared by affinity chromatography on Protein G from tissue culture supernatant Preparation Purified IgG prepared by affinity chromatography on Protein G from tissue culture supernatant Preparation Purified IgG prepared by affinity chromatography on Protein G from tissue culture supernatant Buffer Solution Phosphate buffered saline Buffer Solution Phosphate buffered saline Buffer Solution Phosphate buffered saline Buffer Solution Phosphate buffered saline Buffer Solution Phosphate buffered saline Buffer Solution Phosphate buffered saline Buffer Solution Phosphate buffered saline Buffer Solution Phosphate buffered saline Buffer Solution Phosphate buffered saline Preservative Stabilisers 0.09%Sodium Azide1%Bovine Serum Albumin Preservative Stabilisers 0.09%Sodium Azide1%Bovine Serum Albumin Preservative Stabilisers 0.09%Sodium Azide1%Bovine Serum Albumin Preservative Stabilisers 0.09%Sodium Azide1%Bovine Serum Albumin Preservative Stabilisers None present Preservative Stabilisers 0.09%Sodium Azide Preservative Stabilisers 0.09%Sodium Azide1%Bovine Serum Albumin5%Sucrose Preservative Stabilisers 0.09%Sodium Azide1%Bovine Serum Albumin Preservative Stabilisers 0.09% Sodium Azide (NaN3) 1% Bovine Serum Albumin Carrier Free Carrier Free Immunogen Purified Concanavalin A acceptor glycoprotein from P815 cell line. Approx. Protein Concentrations IgG concentration 0.05 mg/ml Approx. Protein Concentrations IgG concentration 0.05 mg/ml Approx. Protein Concentrations IgG concentration 0.1mg/ml Approx. Protein Concentrations IgG concentration 0.1mg/ml Approx. Protein Concentrations IgG concentration 1.0mg/ml Approx. Protein Concentrations Pack Size: 0.25 mg, 25 µgIgG concentration 1.0mg/ml Pack Size: 0.1 mgIgG concentration 1.0 mg/ml Approx. Protein Concentrations IgG concentration 0.05 mg/ml Approx. Protein Concentrations IgG concentration 0.1 mg/ml Storage This product is shipped at ambient temperature. It is recommended to aliquot and store at -20 C on receipt. When thawed, aliquot the sample as needed. Keep aliquots at 2-8 C for short term use (up to 4 weeks) and store the remaining aliquots at -20 C.Avoid repeated freezing and thawing as this may denature the antibody. Storage in frost-free freezers is not recommended. This product is photosensitive and should be protected from light. Storage This product is shipped at ambient temperature. It is recommended to aliquot and store at -20 C on receipt. When thawed, aliquot the sample as needed. Keep aliquots at 2-8 C for short term use (up to 4 weeks) and store the remaining aliquots at -20 C.Avoid repeated freezing and thawing as this may denature the antibody. Storage in frost-free freezers is not recommended. This product is photosensitive and should be protected from light. Storage This product is shipped at ambient temperature. It is recommended to aliquot and store at -20 C on receipt. When thawed, aliquot the sample as needed. Keep aliquots at 2-8 C for short term use (up to 4 weeks) and store the remaining aliquots at -20 C.Avoid repeated freezing and thawing as this may denature the antibody. Storage in frost-free freezers is not recommended. Storage This product is shipped at ambient temperature. It is recommended to aliquot and store at -20 C on receipt. When thawed, aliquot the sample as needed. Keep aliquots at 2-8 C for short term use (up to 4 weeks) and store the remaining aliquots at -20 C.Avoid repeated freezing and thawing as this may denature the antibody. Storage in frost-free freezers is not recommended. This product is photosensitive and should be protected from light. Storage Store at -20oC only. This product should be stored undiluted.Storage in frost-free freezers is not recommended. Avoid repeated freezing and thawing as this may denature the antibody. Should this product contain a precipitate we recommend microcentrifugation before use. Storage This product is shipped at ambient temperature. It is recommended to aliquot and store at -20 C on receipt. When thawed, aliquot the sample as needed. Keep aliquots at 2-8 C for short term use (up to 4 weeks) and store the remaining aliquots at -20 C.Avoid repeated freezing and thawing as this may denature the antibody. Storage in frost-free freezers is not recommended. Storage Store at +4oC.DO NOT FREEZE.This product should be stored undiluted. This product is photosensitive and should be protected from light. Should this product contain a precipitate we recommend microcentrifugation before use. Storage This product is shipped at ambient temperature. It is recommended to aliquot and store at -20 C on receipt. When thawed, aliquot the sample as needed. Keep aliquots at 2-8 C for short term use (up to 4 weeks) and store the remaining aliquots at -20 C.Avoid repeated freezing and thawing as this may denature the antibody. Storage in frost-free freezers is not recommended. This product is photosensitive and should be protected from light. Storage This product is shipped at ambient temperature. It is recommended to aliquot and store at -20 C on receipt. When thawed, aliquot the sample as needed. Keep aliquots at 2-8 C for short term use (up to 4 weeks) and store the remaining aliquots at -20 C.Avoid repeated freezing and thawing as this may denature the antibody. Storage in frost-free freezers is not recommended. This product is photosensitive and should be protected from light. Guarantee 12 months from date of despatch Guarantee 12 months from date of despatch Guarantee 12 months from date of despatch Guarantee 12 months from date of despatch Guarantee 12 months from date of despatch Guarantee 12 months from date of despatch Guarantee 12 months from date of despatch Guarantee 12 months from date of despatch Guarantee 12 months from date of despatch GO:0010008 endosome membrane Acknowledgements This product is provided under an intellectual property licence from Life Technologies Corporation. The transfer of this product is contingent on the buyer using the purchase product solely in research, excluding contract research or any fee for service research, and the buyer must not sell or otherwise transfer this product or its components for (a) diagnostic, therapeutic or prophylactic purposes; (b) testing, analysis or screening services, or information in return for compensation on a per-test basis; (c) manufacturing or quality assurance or quality control, or (d) resale, whether or not resold for use in research. For information on purchasing a license to this product for purposes other than as described above, contact Life Technologies Corporation, 5791 Van Allen Way, Carlsbad CA 92008 USA or outlicensing@thermofisher.com Acknowledgements This product is provided under an intellectual property licence from Life Technologies Corporation. The transfer of this product is contingent on the buyer using the purchase product solely in research, excluding contract research or any fee for service research, and the buyer must not sell or otherwise transfer this product or its components for (a) diagnostic, therapeutic or prophylactic purposes; (b) testing, analysis or screening services, or information in return for compensation on a per-test basis; (c) manufacturing or quality assurance or quality control, or (d) resale, whether or not resold for use in research. For information on purchasing a license to this product for purposes other than as described above, contact Life Technologies Corporation, 5791 Van Allen Way, Carlsbad CA 92008 USA or outlicensing@thermofisher.com Acknowledgements This product is provided under an intellectual property licence from Life Technologies Corporation. The transfer of this product is contingent on the buyer using the purchase product solely in research, excluding contract research or any fee for service research, and the buyer must not sell or otherwise transfer this product or its components for (a) diagnostic, therapeutic or prophylactic purposes; (b) testing, analysis or screening services, or information in return for compensation on a per-test basis; (c) manufacturing or quality assurance or quality control, or (d) resale, whether or not resold for use in research. For information on purchasing a license to this product for purposes other than as described above, contact Life Technologies Corporation, 5791 Van Allen Way, Carlsbad CA 92008 USA or outlicensing@thermofisher.com Regulatory For research purposes only This product has been reported to work in the following applications. This information is derived from testing within our laboratories, peer-reviewed publications or personal communications from the originators. Please refer to references indicated for further information. For general protocol recommendations, please visit the antibody protocols page. 1 Membrane permeabilisation is required for this application. Bio-Rad recommends the use of Leucoperm (Product Code BUF09) for this purpose.The Fc region of monoclonal antibodies may bind non-specifically to cells expressing low affinity Fc receptors. This may be reduced by using SeroBlock FcR (Product Code BUF041) 1 Membrane permeabilisation is required for this application. Bio-Rad recommends the use of Leucoperm (Product Code BUF09) for this purpose.The Fc region of monoclonal antibodies may bind non-specifically to cells expressing low affinity Fc receptors. This may be reduced by using SeroBlock FcR (Product Code BUF041A) 1 Membrane permeabilisation is required for this application. Bio-Rad recommends the use of Leucoperm (Product Code BUF09) for this purpose.The Fc region of monoclonal antibodies may bind non-specifically to cells expressing low affinity Fc receptors. This may be reduced by using SeroBlock FcR (Product Code BUF041). 1 Membrane permeabilisation is required for this application. Bio-Rad recommends the use of Leucoperm (Product Code BUF09) for this purpose.2This product may require antigen retrieval using heat treatment prior to staining of paraffin sections.Sodium citrate buffer pH 6.0 is recommended for this purpose. See Martin-Manso for details. Staining has also been achieved without antigen retrieval, see Lu for details.3 Non-reducing conditions recommended. 1 Membrane permeabilisation is required for this application. Bio-Rad recommends the use of Leucoperm (Product Code BUF09) for this purpose.2This product may require antigen retrieval using heat treatment prior to staining of paraffin sections. Either sodium citrate buffer or Tris/EDTA buffer may be used for this purpose. See Martin-Manso for details. Staining has also been achieved without antigen retrieval, see Lu for details.3 Non-reducing conditions recommended. 1 Membrane permeabilisation is required for this application. Bio-Rad recommends the use of Leucoperm (Product Code BUF09) for this purpose.The Fc region of monoclonal antibodies may bind non-specifically to cells expressing low affinity Fc receptors. This may be reduced by using SeroBlock FcR (Product Code BUF041). 1 Membrane permeabilisation is required for this application. Bio-Rad recommends the use of Leucoperm (Product Code BUF09) for this purpose.The Fc region of monoclonal antibodies may bind non-specifically to cells expressing low affinity Fc receptors. This may be reduced by using SeroBlock FcR (Product Code BUF041). 1 Membrane permeabilisation is required for this application. Bio-Rad recommends the use of Leucoperm (Product Code BUF09) for this purpose.The Fc region of monoclonal antibodies may bind non-specifically to cells expressing low affinity Fc receptors. This may be reduced by using SeroBlock FcR (Product Code BUF041) Where this product has not been tested for use in a particular technique this does not necessarily exclude its use in such procedures. Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own system using appropriate negative/positive controls. Where this product has not been tested for use in a particular technique this does not necessarily exclude its use in such procedures. Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own system using appropriate negative/positive controls. Where this product has not been tested for use in a particular technique this does not necessarily exclude its use in such procedures. Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own system using appropriate negative/positive controls. Where this product has not been tested for use in a particular technique this does not necessarily exclude its use in such procedures. Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own system using appropriate negative/positive controls. Where this antibody has not been tested for use in a particular technique this does not necessarily exclude its use in such procedures. Suggested working dilutions are given as a guide only. It is recommended that the user titrates the antibody for use in their own system using appropriate negative/positive controls. Where this product has not been tested for use in a particular technique this does not necessarily exclude its use in such procedures. Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own system using appropriate negative/positive controls. Where this product has not been tested for use in a particular technique this does not necessarily exclude its use in such procedures. Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own system using appropriate negative/positive controls. Where this product has not been tested for use in a particular technique this does not necessarily exclude its use in such procedures. Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own system using appropriate negative/positive controls. Where this product has not been tested for use in a particular technique this does not necessarily exclude its use in such procedures. Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own system using appropriate negative/positive controls. Flow Cytometry Use 10ul of the suggested working dilution to label 106 cells in 100ul. Recommended protocols are available Here Flow Cytometry Use 10ul of the suggested working dilution to label 106 cells in 100ul. Recommended protocols are available Here Flow Cytometry Use 10ul of the suggested working dilution to label 106 cells in 100ul. Recommended protocols are available Here Flow Cytometry Use 10ul of the suggested working dilution to label 106 cells in 100ul. Recommended protocols are available Here Flow Cytometry Use 10ul of the suggested working dilution to label 1x106 cells in 100ul. Flow Cytometry Use 10ul of the suggested working dilution to label 106 cells in 100ul. Recommended protocols are available Here Flow Cytometry Use 10ul of the suggested working dilution to label 106 cells in 100ul. Recommended protocols are available Here Flow Cytometry Use 10ul of the suggested working dilution to label 106 cells in 100ul. Recommended protocols are available Here Flow Cytometry Use 10ul of the suggested working dilution to label 106 cells in 100ul. Recommended protocols are available Here Smith, M. and Koch, G. (1987) Differential expression of murine macrophage surface glycoprotein antigens in intracellular membranes. J Cell Sci. 87:113-9. Ramprasad, M.P. et al. (1996) Cell surface expression of mouse macrosialin and human CD68 and their role as macrophage receptors for oxidized low density lipoprotein. Proc Natl Acad Sci U S A. 93 (25): 14833-8. Rabinowitz, S.S. & Gordon, S. (1991) Macrosialin, a macrophage-restricted membrane sialoprotein differentially glycosylated in response to inflammatory stimuli. J Exp Med. 174 (4): 827-36. da Silva, R.P. & Gordon, S. (1999) Phagocytosis stimulates alternative glycosylation of macrosialin (mouse CD68), a macrophage-specific endosomal protein. Biochem J. 338 ( Pt 3): 687-94. Schleicher, U. et al. (2005) Minute numbers of contaminant CD8+ T cells or CD11b+CD11c+ NK cells are the source of IFN-{gamma} in IL-12/IL-18-stimulated mouse macrophage populations. Blood 105: 1319-1328. Choi, E.J. et al. (2014) Novel brain arteriovenous malformation mouse models for type 1 hereditary hemorrhagic telangiectasia. PLoS One. 9(2): e88511. Kassim, S. et al. (2010) Gene therapy in a humanized mouse model of familial hypercholesterolemia leads to marked regression of atherosclerosis. PloS ONE 5: e13424. Rahaman, S.O. et al. (2011) Vav family Rho guanine nucleotide exchange factors regulate CD36-mediated macrophage foam cell formation. J Biol Chem. 286: 7010-7. Frossard, J.L. et al. (2011) Role of CCL-2, CCR-2 and CCR-4 in cerulein-induced acute pancreatitis and pancreatitis-associated lung injury. J Clin Pathol. 64: 387-93 West, E.L. et al. (2010) Long-term survival of photoreceptors transplanted into the adult murine neural retina requires immune modulation. Stem Cells. 28: 1997-2007. Lopez, M.E. et al. (2011) Anatomically defined neuron-based rescue of neurodegenerative niemann-pick type C disorder. J Neurosci. 31: 4367-78. Leung, V.W. et al. (2009) Decay-accelerating factor suppresses complement C3 activation and retards atherosclerosis in low-density lipoprotein receptor-deficient mice. Am J Pathol. 175: 1757-67. Devey, L. et al. (2009) Tissue-resident macrophages protect the liver from ischemia reperfusion injury via a heme oxygenase-1-dependent mechanism. Mol Ther. 17: 65-72. Lu, W. et al. (2010) Photoacoustic imaging of living mouse brain vasculature using hollow gold nanospheres. Biomaterials. 31: 2617-26. de Beer, M.C. et al. (2003) Lack of a direct role for macrosialin in oxidized LDL metabolism. J Lipid Res. 44: 674-85. Daldrup-Link, H.E. et al. (2011) MR Imaging of Tumor Associated Macrophages with Clinically-Applicable Iron Oxide Nanoparticles. Clin Cancer Res. 17: 5695-704. Macauley, S.L. et al. (2011) The Role of Attenuated Astrocyte Activation in Infantile Neuronal Ceroid Lipofuscinosis J. Neurosci 31: 15575-85. Martin-Manso, G. et al. (2008) Thrombospondin 1 promotes tumor macrophage recruitment and enhances tumor cell cytotoxicity of differentiated U937 cells. Cancer Res. 68: 7090-9. Lazarini, F. et al. (2012) Early Activation of Microglia Triggers Long-Lasting Impairment of Adult Neurogenesis in the Olfactory Bulb J Neurosci 32: 3652-64 Hemmi, H. et al. (2009) A new triggering receptor expressed on myeloid cells (Trem) family member, Trem-like 4, binds to dead cells and is a DNAX activation protein 12-linked marker for subsets of mouse macrophages and dendritic cells. J Immunol. 182: 1278-86. Akbarshahi, H. et al. (2012) Enrichment of Murine CD68(+)CCR2(+) and CD68(+)CD206(+) Lung Macrophages in Acute Pancreatitis-Associated Acute Lung Injury. PLoS One. 7: e42654. Xiang, X. et al. (2016) TREM2 deficiency reduces the efficacy of immunotherapeutic amyloid clearance. EMBO Mol Med. 8 (9): 992-1004. Masaki, T. et al. (2003) Heterogeneity of antigen expression explains controversy over glomerular macrophage accumulation in mouse glomerulonephritis. Nephrol. Dial. Transplant 18:178-81. Dormishian, M. et al. (2013) Prokineticin receptor-1 is a new regulator of endothelial insulin uptake and capillary formation to control insulin sensitivity and cardiovascular and kidney functions. J Am Heart Assoc. 2 (5): e000411. von Bargen, K. et al. (2014) Cervical Lymph Nodes as a Selective Niche for Brucella during Oral Infections. PLoS One. 10 (4): e0121790. Hamour, S. et al. (2015) Local IL-17 Production Exerts a Protective Role in Murine Experimental Glomerulonephritis. PLoS One. 10 (8): e0136238. Wang L et al. (2016) Bone Fracture Pre-Ischemic Stroke Exacerbates Ischemic Cerebral Injury in Mice. PLoS One. 11 (4): e0153835. Nguyen, T.V. et al. (2016) Multiplex immunoassay characterization and species comparison of inflammation in acute and non-acute ischemic infarcts in human and mouse brain tissue. Acta Neuropathol Commun. 4 (1): 100. Pena-Philippides, J.C. et al. (2016) In vivo inhibition of miR-155 significantly alters post-stroke inflammatory response. J Neuroinflammation. 13 (1): 287. Paiva, A. A. et al. (2017) Apolipoprotein CIII Overexpression-Induced Hypertriglyceridemia Increases Nonalcoholic Fatty Liver Disease in Association with Inflammation and Cell Death. Oxidative Med Cellular Longev. 2017: 1-18. 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(2018) Indoleamine 2 3-dioxygenase knockout limits angiotensin II-induced aneurysm in low density lipoprotein receptor-deficient mice fed with high fat diet. PLoS One. 13 (3): e0193737. Hill, N.R. et al. (2018) RIPK3-deficient mice were not protected from nephrotoxic nephritis. BMC Nephrol. 19 (1): 61. Fumagalli, S. et al. (2019) The phagocytic state of brain myeloid cells after ischemia revealed by superresolution structured illumination microscopy. J Neuroinflammation. 16 (1): 9. Gratuze, M. et al.. (2020) Impact of TREM2R47H variant on tau pathology-induced gliosis and neurodegeneration J Clin Invest130(9):4954-68. Garrett, M.C. et al. (2020) Injectable diblock copolypeptide hydrogel provides platform to deliver effective concentrations of paclitaxel to an intracranial xenograft model of glioblastoma. PLoS One. 15 (7): e0219632. Rahman, K. et al. (2017) Inflammatory Ly6Chi monocytes and their conversion to M2 macrophages drive atherosclerosis regression. 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(2020) YAP/TAZ deficiency reprograms macrophage phenotype and improves infarct healing and cardiac function after myocardial infarction. PLoS Biol. 18 (12): e3000941. Zaghloul, N. et al. (2020) Prophylactic inhibition of NF- B expression in microglia leads to attenuation of hypoxic ischemic injury of the immature brain. J Neuroinflammation. 17 (1): 365. Huang, J. et al. (2020) Bone Fracture Enhanced Blood-Brain Barrier Breakdown in the Hippocampus and White Matter Damage of Stroke Mice. Int J Mol Sci. 21 (22)Nov 11 [Epub ahead of print]. Lowe, P.P. et al. (2020) Chronic alcohol-induced neuroinflammation involves CCR2/5-dependent peripheral macrophage infiltration and microglia alterations. J Neuroinflammation. 17 (1): 296. Stroobants, S. et al. (2020) Aged Tmem106b knockout mice display gait deficits in coincidence with Purkinje cell loss and only limited signs of non-motor dysfunction. Brain Pathol. : e12903. Alberti, S. et al. (2020) The antiplatelet agent revacept prevents the increase of systemic thromboxane A2 biosynthesis and neointima hyperplasia. Sci Rep. 10 (1): 21420. H rdtner, C. et al. (2020) Inhibition of macrophage proliferation dominates plaque regression in response to cholesterol lowering. Basic Res Cardiol. 115 (6): 78. Ribeiro, P.C. et al. (2020) Therapeutic potential of human induced pluripotent stem cells and renal progenitor cells in experimental chronic kidney disease. Stem Cell Res Ther. 11 (1): 530. Miró, L. et al. (2020) Dietary Supplementation with Spray-Dried Porcine Plasma Attenuates Colon Inflammation in a Genetic Mouse Model of Inflammatory Bowel Disease. Int J Mol Sci. 21(18): 6760. Zhou, F. et al. (2020) -Carotene conversion to vitamin A delays atherosclerosis progression by decreasing hepatic lipid secretion in mice. J Lipid Res. 61 (11): 1491-1503. Nelvagal, H.R. et al. (2020) Comparative proteomic profiling reveals mechanisms for early spinal cord vulnerability in CLN1 disease. Sci Rep. 10 (1): 15157. Grubi i , V. et al. (2020) Enteric Glia Modulate Macrophage Phenotype and Visceral Sensitivity following Inflammation. Cell Rep. 32 (10): 108100. Riedl, K.A. et al. (2020) Wall shear stress analysis using 17.6 Tesla MRI: A longitudinal study in ApoE-/- mice with histological analysis. PLoS One. 15 (8): e0238112. Rojanathammanee, L. et al. (2013) Pomegranate polyphenols and extract inhibit nuclear factor of activated T-cell activity and microglial activation in vitro and in a transgenic mouse model of Alzheimer disease. J Nutr. 143 (5): 597-605. Shahraz, A. et al. (2021) Phagocytosis-related NADPH oxidase 2 subunit gp91phox contributes to neurodegeneration after repeated systemic challenge with lipopolysaccharides. Glia. 69 (1): 137-50. Shi, Q. et al. 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(2021) TREM-1 orchestrates angiotensin II-induced monocyte trafficking and promotes experimental abdominal aortic aneurysm. J Clin Invest. 131 (2): e142468. Apodaca, L.A. et al. (2021) Human neural stem cell-derived extracellular vesicles mitigate hallmarks of Alzheimer\'s disease. Alzheimers Res Ther. 13 (1): 57. Colombo, A. et al. (2021) Loss of NPC1 enhances phagocytic uptake and impairs lipid trafficking in microglia. Nat Commun. 12 (1): 1158. Galle-Treger, L. et al. (2020) Targeted invalidation of SR-B1 in macrophages reduces macrophage apoptosis and accelerates atherosclerosis. Cardiovasc Res. 116 (3): 554-565. Sun, Y. et al. (2008) Temporal gene expression profiling reveals CEBPD as a candidate regulator of brain disease in prosaposin deficient mice. BMC Neurosci. 9: 76. Miteva, K. et al. (2020) Cardiotrophin-1 Deficiency Abrogates Atherosclerosis Progression. Sci Rep. 10 (1): 5791. El Gaamouch, F. et al. 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Leipner, J. et al. (2021) Myeloid cell-specific Irf5 deficiency stabilizes atherosclerotic plaques in Apoe-/- mice. Mol Metab.May 12 : 101250 [Epub ahead of print]. Shariq, M. et al. (2021) Adult neural stem cells have latent inflammatory potential that is kept suppressed by Tcf4 to facilitate adult neurogenesis. Sci Adv. 7 (21)May 21 [Epub ahead of print]. Mart nez-Beamonte, R. et al. (2021) Dietary Avian Proteins Are Comparable to Soybean Proteins on the Atherosclerosis Development and Fatty Liver Disease in Apoe-Deficient Mice Nutrients. 13 (6): 1838. Colombo, A.V. et al. (2021) Microbiota-derived short chain fatty acids modulate microglia and promote A plaque deposition. Elife. 10:e59826. Ilyas, G. et al. (2019) Decreased Macrophage Autophagy Promotes Liver Injury and Inflammation from Alcohol. Alcohol Clin Exp Res. 43 (7): 1403-13. Riester, K. et al. (2020) In vivo. characterization of functional states of cortical microglia during peripheral inflammation. Brain Behav Immun. 87: 243-55. Yuan, C. et al. (2018) Human Aldose Reductase Expression Prevents Atherosclerosis Regression in Diabetic Mice. Diabetes. 67 (9): 1880-91. Johnson, T.B. et al. (2019) Changes in motor behavior, neuropathology, and gut microbiota of a Batten disease mouse model following administration of acidified drinking water. Sci Rep. 9 (1): 14962. Kaji, N. et al. (2018) Disruption of the pacemaker activity of interstitial cells of Cajal via nitric oxide contributes to postoperative ileus. Neurogastroenterol Motil. Mar 15 [Epub ahead of print]. Soto, I. et al. (2016) Meox2 haploinsufficiency increases neuronal cell loss in a mouse model of Alzheimer\'s disease. Neurobiol Aging. 42: 50-60. Wagner, M. et al. (2019) Clinical improvement and enhanced collateral vessel growth after xenogenic monocyte transplantation. Am J Transl Res. 11 (7): 4063-76. Zhang, Y. et al. (2019) Angiotensin II deteriorates advanced atherosclerosis by promoting MerTK cleavage and impairing efferocytosis through the AT1R/ROS/p38 MAPK/ADAM17 pathway. Am J Physiol Cell Physiol. 317 (4): C776-C787. Guo, S.D. et al. (2019) Nasal delivery of Fasudil-modified immune cells exhibits therapeutic potential in experimental autoimmune encephalomyelitis. CNS Neurosci Ther. 25 (6): 783-95. Welc, S.S. et al. (2019) Targeting a therapeutic LIF transgene to muscle via the immune system ameliorates muscular dystrophy. Nat Commun. 10 (1): 2788. Start by selecting the application you are interested in, with the option to select an instrument from the drop down menu or create a customized instrument Select the fluorophores or fluorescent proteins you want to include in your panel to check compatibility All you need to know about immune cells, lineage, marker expression and the marker protein itself. Providing a direct link to antibodies available to your chosen marker. Immunofluorescence staining of a mouse lymph node cryosection with Rat anti Mouse CD68 antibody, clone FA11 (MCA1957), green in A and Rat anti Mouse CD8 antibody, clone YTS105.18 (MCA1108), red in B. C is the merged image with nuclei counterstained blue using DAPI. Low power Immunofluorescence staining of a mouse lymph node cryosection with Rat anti Mouse CD68 antibody, clone FA11 (MCA1957), green in A and Rat anti Mouse CD8 antibody, clone YTS105.18 (MCA1108), red in B. C is the merged image with nuclei counterstained blue using DAPI. Medium power Immunofluorescence staining of a mouse lymph node cryosection with Rat anti Mouse CD68 antibody, clone FA11 (MCA1957), green in A and Rat anti Mouse CD8 antibody, clone YTS105.18 (MCA1108), red in B. C is the merged image with nuclei counterstained blue using DAPI. High power Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957GA) used for the identification of microglia in mouse brain by immunofluorescence.Image caption:CB2 receptors are expressed in microglial cells and do not accumulate in A plaques of APPswe/PS1 E9 mice. A representative confocal image of staining for CB2 receptors (green, H60 antibody) in the cortex of 12 mo-old transgenic mice. (B) An overlap of red (CD68) and blue (DAPI) channels for the image shown in A. Note a characteristic gathering of activated microglia around an amyloid plaque (marked by an asterisk). (C) An overlap of channels shown in A-B. Note that areas with high CB2 intensities overlap with CD68-positive areas. White rectangle shows an example of areas used for quantifications presented in E-F. Scale bar is 15 m. (D) Quantification of CB2 densities (integrated intensities/area) in CD68-positive and –negative areas. 26 areas like that shown in A-C were used for the quantification (n = 2 transgenic mice). Asterisk indicates a significant difference between CD68+ and CD68- areas (one-way ANOVA, p 0.0001). (E) A scatterplot of CB2 and DAPI intensities as a function of distance from the center of an A plaque with radius 10 μm. Note low CB2 signal in the core of the plaque. CB2 and DAPI intensities were normalized ( ) to a maximum signal on each channel. An example of an area used for calculations is shown by a white rectangle in C. (F) Quantification of CB2 signal at different distances from a plaque center. 4–6 slices of z stacks from five plaques (range of radiuses 7–15 m) were used in one-way ANOVA. Asterisks indicate a significant increase (p 0.0001, post-hoc test) in CB2 intensities as compared to the core of plaques (radius ≤ 7 m).From: Savonenko AV, Melnikova T, Wang Y, Ravert H, Gao Y, Koppel J, et al. (2015)Cannabinoid CB2 Receptors in a Mouse Model of A Amyloidosis: Immunohistochemical Analysis and Suitability as a PET Biomarker of Neuroinflammation.PLoS ONE 10(6): e0129618.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 used for the identification of microglia in mouse brain by immunofluorescence.Image caption:Comparison of CB2 immunoreactivity in neurons, activated microglia and astrocytes. (A) Representative confocal images from the cortex of 12 mo-old non-transgenic (NTG) and APPswe/PS1 E9 transgenic (AD) mice stained with a CB2 receptor antibody (H60sc; left columns; green) and markers for neurons (NeuN, far red), activated microglia (CD68, red), and astrocytes (GFAP, far red). Brain slides were counterstained with DAPI shown with a grey pseudo color. Note substantial micro- and astro-gliosis in the cortex of the AD mouse brain. In the NTG mice, CD68+ and/or GFAP+ areas were rare (indicated in the upper right panel by an arrowhead and arrow, respectively). (B) Quantification of densities (+-SEM) for CB2 receptor immunoreactivity (integrated intensities/area) in areas positive for NeuN, CD68, and GFAP markers. Densities were averaged over 22 (AD) and 14 (NTG) images of the cortex as shown in A (n = 2 mice per genotype). Single and double asterisks indicate a significant difference between NTG and AD groups as a result of LSD post-hoc test with p levels 0.01 and 0.0001, respectively. Arcs indicate non-significant (NS) differences. Single and double pound signs (p levels 0.05 and 0.001) indicate markers that correspond to the highest CB2 density in the NTG (blue sign) or AD (red sign) groups (LSD post-hoc test). Solid black line at the level of 4,930 shows average densities for the background. (C) An example of NeuN (blue), CD68 (red), and GFAP (green) masks from the AD image shown in A. NeuN masks were drawn by hand as shown in Fig 2C; masks for CD68 and GFAP were created by a threshold function. Black area represents background. Scale is 15 m.From: Savonenko AV, Melnikova T, Wang Y, Ravert H, Gao Y, Koppel J, et al. (2015)Cannabinoid CB2 Receptors in a Mouse Model of A Amyloidosis: Immunohistochemical Analysis and Suitability as a PET Biomarker of Neuroinflammation.PLoS ONE 10(6): e0129618.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 (MCA1957) used for the detection of macrophages in mouse brain by immunohistochemistry on cryostat sections.Image caption:Primed innate immune response in the brain following a systemic bacterial infection. Phenotypic changes after intracerebral injection of 100 pg of LPS in naïve mice (A, B, E, F, I, J, M, N) or mice pretreated with SL3261 (C, D, G, H, K, L, O, P). Representative images of immune marker expression (CD11c (A-D), CD68 (E-H), MHCII (I-L) in the injected hemisphere (B, D, F, H, J, L, N, P) or contralateral site are shown. Panels M-P show a double immunofluorescent stain for MHCII (green) and laminin (red). n=5 animals per group, black scale bar=50 m, white scale bar=75 m.From: P ntener U, Booth SG, Perry VH, Teeling JL.Long-term impact of systemic bacterial infection on the cerebral vasculature and microglia.J Neuroinflammation. 2012 Jun 27;9:146.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 (MCA1957) used for the detection of macrophages in mouse by flow cytometry.Image caption:F4/80 and either CD11b or CD68 expression of whole liver MNCs. Liver MNCs were obtained from CD, HFD, HCD and HFCD mice and expression of F4/80 either with CD11b or CD68 were examined. The numbers were the means SE from four mice in each group. F4/80 positive gate was determined by using the isotype control Ab.From: Nakashima H, Ogawa Y, Shono S, Kinoshita M, Nakashima M, et al. (2013)Activation of CD11b+ Kupffer Cells/Macrophages as a Common Cause for Exacerbation of TNF/Fas-Ligand-Dependent Hepatitis in Hypercholesterolemic Mice.PLoS ONE 8(1): e49339.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 (MCA1957) used for the detection of macrophages in mouse by flow cytometry.Image caption:The expression of CD68 and CD11b by liver F4/80+ Kupffer cells. Liver MNCs were obtained from CD, HFD, HCD and HFCD mice, and Kupffer cells gated by F4/80 were analyzed for their expression levels of CD68 and CD11b. CD68 positive gate was determined by using the isotype control Ab. The numbers are the means SE from six to eight mice in each group. *P 0.05 vs. CD and HFD.From: Nakashima H, Ogawa Y, Shono S, Kinoshita M, Nakashima M, et al. (2013)Activation of CD11b+ Kupffer Cells/Macrophages as a Common Cause for Exacerbation of TNF/Fas-Ligand-Dependent Hepatitis in Hypercholesterolemic Mice.PLoS ONE 8(1): e49339.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 (MCA1957GA) used for the detection of macrophages in mouse aortic root tissue by immunohistochemistry on cryostat sections.Image caption:Immunohistochemical analysis of mouse atherosclerotic lesions. Representative aortic root sections immunostained for the foam cell marker CD68 (A), VCAM-1 (B), or Masson trichrome blue stain for collagen content (C). Original magnification, 40×. Note abundant immunostaining for foam cell marker, CD68 (brown), VCAM-1 adhesion molecules (also brown), and presence of collagen αblue) within lesion in baseline and AAV.TBG.nLacZ injected Ldlr-/-Apobec1-/-animals.From: Kassim SH, Li H, Vandenberghe LH, Hinderer C, Bell P, et al. (2010)Gene Therapy in a Humanized Mouse Model of Familial Hypercholesterolemia Leads to Marked Regression of Atherosclerosis.PLoS ONE 5(10): e13424. This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 (MCA1957) used for the detection of macrophages in mouse by flow cytometry.Image caption:Phenotype of pancreatic macrophages. (A) Identification of macrophage subsets in pancreas of CX3CR1GFP/+ C56BL/6 mice. Pancreatic single cell suspensions were gated on FSC-A vs FSC-W and CD45+. Histograms show receptor expression profile of CX3CR1hiLYVE-1− (green line) and CX3CR1loLYVE-1+ (red line) macrophages. (B) Sorted CX3CR1loLYVE-1+ and CX3CR1hiLYVE-1− macrophages spun onto glass slides and stained with Wright s stain. 1000× magnification. (C) mRNA expression profile of chemokine receptors, chemokines and VEGFs in pancreatic macrophage subsets. mRNA levels examined by qRT-PCR in duplicate or triplicate. 6–7 mice/group, data representative of 2–4 separate experiments.From: Yin N, Zhang N, Lal G, Xu J, Yan M, et al. (2011)Lymphangiogenesis Is Required for Pancreatic Islet Inflammation and Diabetes.PLoS ONE 6(11): e28023.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 (MCA1957GA) used for the detection of macrophages in mouse pancreas by immunofluorescence.Image caption:Interaction of LEC and pancreatic macrophages. (A) CX3CR1hi macrophages, LYVE-1+ macrophages, CD11b−-lymphocytes and LEC were sorted from pancreatic single cell suspensions of CX3CR1GFP/+ mice. Co-cultured CX3CR1hi macrophages-CFSE, LYVE-1+ macrophages-eFlour670, or lymphocytes-CFSE with/without LEC on Matrigel for 5 days. Scale bars: 60 m. 100× magnification. (B) Immunofluorescent staining of CD68 and LYVE-1 in pancreas from C57BL/6 mice. Scale bars: 160 m. 50× magnification. (C) Sorted CX3CR1hi macrophages labeled with CFSE and co-cultured with LEC (left upper panel) or without LEC (left lower panel) for 5 days, and stained for CD11b (red) and LYVE-1 (yellow). Scale bars: 10 m. 630× magnification. Right panel, quantitative analysis, total cells from 5 fields (1344×1024 pixels) were counted. All data representative of 2 to 4 separate experiments.From: Yin N, Zhang N, Lal G, Xu J, Yan M, et al. (2011)Lymphangiogenesis Is Required for Pancreatic Islet Inflammation and Diabetes.PLoS ONE 6(11): e28023.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 (MCA1957) used for the detection of macrophages in mouse pancreas by immunofluorescence.Image caption:Macrophages infiltrate into inflamed islets. MLDS treated BALB/c mice received sunitinib, or anti-VEGFR3 mAb starting from the first STZ injection 3 days. (A) Immunofluorescent analysis of CD68+LYVE-1+ (yellow arrows) and CD68+LYVE-1− (red arrows) macrophage subsets migrating near islets. 200× magnification. Scale bars: 30 m. (B) Quantitative analysis of CD68+LYVE-1+ and CD68+LYVE-1− cells surrounding islets. Each symbol represents one islet. 43–52 islets/group, 4–5 slides/mice, 3 mice/group. *** P 0.001. Mean ± SD.From: Yin N, Zhang N, Lal G, Xu J, Yan M, et al. (2011)Lymphangiogenesis Is Required for Pancreatic Islet Inflammation and Diabetes.PLoS ONE 6(11): e28023.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 used for the detection of macrophages in mouse brain by immunohistochemistry on formain fixed, paraffin embedded tissue.Image caption:Iminosugar-based GCS inhibitors decrease the number of brain CD68 positive cells. (A) CD68 immunolabeling of brain stem from 28, 56, 84 and 112 day old Sandhoff mice, untreated or treated with either Genz-529468 or NB-DNJ. Dark brown cells are positive for CD68; scale bar = 50 m. (B) Quantification of CD68+ cell counts in the brain stem, cerebellum, hippocampus and thalamus of 112 day old drug-treated Sandhoff mice (n = 4–5 mice per group). Cell counts are presented relative to those in untreated Sandhoff mice. Statistics are between untreated and treated Sandhoff mice, and were determined using the Graphpad Prism software t test; * = p 0.05. Error bars indicate SEM.From: Ashe KM, Bangari D, Li L, Cabrera-Salazar MA, Bercury SD, et al. (2011)Iminosugar-Based Inhibitors of Glucosylceramide Synthase Increase Brain Glycosphingolipids and Survival in a Mouse Model of Sandhoff Disease.PLoS One. 2011;6(6):e21758.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 used for the detection of macrophages in mouse atherosclerotic plaques by immunofluorescence.Image caption:Impact of SOCS-1 deficiency on atherosclerotic plaque composition A. Atherosclerotic plaques from Socs-1−/− triple-KO (Socs-1−/−) mice showed an increased CD68 (red);iNOS (green) double-positive cell content. B. CD68 (red); CD206 (green) double-positive cells were hardly detected. C. Atherosclerotic plaques from Socs-1−/−triple-KO (Socs-1−/−) mice contained slightly more MOMA-2 (red); Ly-6C (green) double-positive cells after 4 weeks of HCD as well as D. a higher number of Ly-6G positive cells (scale bar A–C: 20 m, scale bar D:50 m). N = 5–7 animals per group.From: Grothusen C, Schuett H, Hillmer A, Lumpe S, Grote K, et al. (2012)Role of Suppressor of Cytokine Signaling-1 In Murine Atherosclerosis.PLoS ONE 7(12): e51608.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 used for the detection of macrophages in mouse vacscular tissue by immunofluorescence.Image caption:CD68 positive macrophages/monocytes cells can be seen within early developing neointima in some mice. Sections from the same two mice shown in Figure 6 were stained with antibodies to CD68 (white). Left panels show mTomato (red)/mEGFP (green) co-stained sections and in the right panels are the same sections visualized for mEGFP (green) and CD68 (white). CD68-positive cells can be seen within the neointima of vessels from the mouse shown in the upper panels but not in the vessels of the mouse shown in the lower panels. Nuclei were visualized by staining with DAPI (blue). All images are shown at the same magnification with the scale bar shown in the bottom left panel representing 50 m.From: Herring BP, Hoggatt AM, Burlak C, Offermanns S.Previously differentiated medial vascular smooth muscle cells contribute to neointima formation following vascular injury.Vasc Cell. 2014 Oct 1;6:21.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Mouse anti CD68 antibody, clone FA-11 (MCA1957) used for the detection of macrophages in mouse lung and liver by immunohistochemistry on formalin fixed, paraffin embedded tissues.Image caption:Histology in 9V/9V/GCStg and 9V/null/GCStg mice. (A) The lung and liver sections from 9-wk old 9V/9V (row 1), 9V/9V/GCStg (row 2), 9V/null (row 3) and 9V/null/GCStg (row 4) were processed for H&E and CD68 antibody staining as indicated. Large and pale storage cells were observed in H&E stained lung and liver sections (arrows). The macrophages were indicated by anti-CD68 immunostaining (brown). Images were captured by Zeiss microscope with Spot Advance software. Scale bar was 40 m for all images. (B) The distribution and density of macrophages in 9V/null/GCStg lung and liver immunostained by anti-CD68 antibody (brown). Scale bar was 40 m for both images. (C) CD68 positive cells (CD68+) in 9V/9V/GCStg and 9V/null/GCStg lungs had significantly more CD68 stained macrophages than 9V/9V and 9V/null at 9 wks of age, respectively. The data present number of cells per image of total 5−15 images/mouse, 3 mice per genotype. Results with error bars are mean S.E. The p values were from Student's t-test.From: Barnes S, Xu Y-H, Zhang W, Liou B, Setchell KDR, et al. (2014)Ubiquitous Transgene Expression of the Glucosylceramide-Synthesizing Enzyme Accelerates Glucosylceramide Accumulation and Storage Cells in a Gaucher Disease Mouse Model.PLoS ONE 9(12): e116023.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA!957GA) used for the detection of infiltrating macrophages in mouse kidney by immunohistochemistry on paraffin embedded material.Image caption:Reduction in cellular infiltration and inflammatory markers in UUO kidneys exposed to telmisartan or PXS64. Untreated UUO kidneys showed increased F4/80, CD68 and CD45 positively stained cells as compared to the sham operated control animals. PXS64 significantly reduced F4/80 and CD45 positive stained cells (Fig. 6C and E) with a trend to a reduction in CD68 cells, although this was not statistically significant (Fig. 6D). Telmisartan treated kidneys showed a reduction in F4/80 positive cells but no difference in CD45 or CD68 stained cells, suggesting a differential action of PXS64 and telmisartan in modifying cellular infiltration. Results are presented as mean showed (n = 8, *P 0.05 vs. UUO, ** P 0.01 vs. UUO). Magnification x 400.From: Zhang J, Wong MG, Wong M, Gross S, Chen J, et al. (2015)A Cationic-Independent Mannose 6-Phosphate Receptor Inhibitor (PXS64) Ameliorates Kidney Fibrosis by Inhibiting Activation of Transforming Growth Factor- 1.PLoS ONE 10(2): e0116888.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 used for the detection of macrophages in murine cervical lymph nodes by immunofluorescence.Image caption:Brucella and fluorescent microspheres in the CLN localize in cells positive for CD68 and low or negative for CD11c. (A) C57BL/6 mice were fed by oral gavage with 0.2 m yellow green fluorescent microspheres. After 3 days, they were sacrificed and CLN processed for immunofluorescence microscopy. (B) Cells with internal beads from experiments as shown in (A) were quantified as to their expression of CD11c and CD68. At least 100 bead-containing cells per experiment were counted. (C) Mice infected by the oral route with 109 B. melitensis per mouse were sacrificed at day 8, CLN prepared for immunofluorescence analysis as described above and (D) the number of infected cells positive for either marker was determined. All available cuts from the CLN of one mouse were analyzed. Data shown represents mean and standard deviation of three independent experiments. Bars: 10 m.From: von Bargen K, Gagnaire A, Arce-Gorvel V, de Bovis B, Baudimont F, Chasson L, et al. (2015)Cervical Lymph Nodes as a Selective Niche for Brucella during Oral Infections.PLoS ONE 10(4): e0121790.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used for the identification of macrophages in atherosclerotic lesions by immunofluorescence.Image caption:Macrophage and VSMC accumulation is reduced in uPAR-/-/LDLR-/-. (A) Representative Mac-3 immunostaining and (B) %-Mac-3-positive lesion per lesion area. (C) Representative anti-SMC immunostaining and (D) % anti-SMC-positive lesion per lesion area. (E) PCNA/CD68 double staining excludes differences in macrophage proliferation in the lesions. (F) Macrophage apoptosis was not responsible for the differences in macrophage content as evidenced by cleaved caspase 3 staining. Mean SEM, n = 8. *P 0.05, **P 0.01, ***P 0.001. A/C: Bar = 250 m, E/F Bar = 100 m SMA: alpha smooth-muscle-actin, PCNA: Proliferating-Cell-Nuclear-Antigen, cC3: cleaved caspase-3, DAPI: 4′,6-Diamidin-2-phenylindol.From:Larmann J, Jurk K, Janssen H, M ller M, Herzog C, Lorenz A, et al. (2015)Hepatic Overexpression of Soluble Urokinase Receptor (uPAR) Suppresses Diet-Induced Atherosclerosis in Low-Density Lipoprotein Receptor-Deficient (LDLR-/-) Mice.PLoS ONE 10(8): e0131854.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957GA) used for the identification of macrophages in atherosclerotic lesions by immunohistochemistry on cryosections.Image caption:Guide-wire injury induced intimal hyperplasia. Mice were subjected to guide wire injury of the internal carotid artery after hypercholesterolemia had been induced. (A) Representative Micrographs of carotid artery lesions in the injured and the contralateral artery. GWI induced concentric lesions did not differ in (B) size or (C) lipid content. (D) Macrophage recruitment did occur, but (E) differences between uPAR-deficient and uPAR-wild-type lesions were not observed in this model. Additionally, no differences between uPAR+/+ and uPAR-/- animals were observable with respect to (F-G) VSMC content of the lesions. No relevant lesion formation was observed in the contralateral sham vessels. (H) Proliferating cells in atherosclerotic lesions are mainly non-VSMC. The amount of proliferating VSMC appears similar for the two genotypes. A, D, F: Bar = 250 m, H: Bar: 50 m, mean SEM, n = 8. n.s.: not significant, SMA: alpha smooth-muscle-actin, DAPI: 4′,6-Diamidin-2-phenylindol, GWI: guide-wire injury, L: left, R: right, PCNA: Proliferating Cell Nuclear Antigen.From:Larmann J, Jurk K, Janssen H, M ller M, Herzog C, Lorenz A, et al. (2015)Hepatic Overexpression of Soluble Urokinase Receptor (uPAR) Suppresses Diet-Induced Atherosclerosis in Low-Density Lipoprotein Receptor-Deficient (LDLR-/-) Mice.PLoS ONE 10(8): e0131854.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957GA) used for the identification of macrophages in atherosclerotic lesions by immunofluorescence.Image caption:Hepatic overexpression of soluble full-length uPAR inhibits atherosclerotic lesion development and macrophage accumulation in LDLR-/- mice. A, Immunostaining for the c-myc-tag revealed expression of soluble uPAR in the livers of mice after hydrodynamic transfection. Bar = 100 m B. Oil red-O staining of aortic valve cryosections. Bar = 250 m C. Atherosclerotic lesion size was assessed as % total aortic sinus lumen area occupied. D, Representative CD68 immunostaining and E. % CD68-positive lesion area. F, Representative anti- SMC immunostaining and G. % anti- SMA-positive lesion area. Bar = 250 m, Mean SEM, n = 6/8. *Pet al. (2015)Hepatic Overexpression of Soluble Urokinase Receptor (uPAR) Suppresses Diet-Induced Atherosclerosis in Low-Density Lipoprotein Receptor-Deficient (LDLR-/-) Mice.PLoS ONE 10(8): e0131854.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Biotin conjugated Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957B) used for the assessment of CD68 expression on Kuppfer cells by flow cytometry. Image caption:The flow cytometric analysis of liver F4/80+CD11b+ cells and F4/80+CD68+ cells three days after Sham operated or PHx mice(A). The changes in the proportions of F4/80+CD11b+ cells in the remnant livers (B). The changes in the proportions of F4/80+CD68+ cells in the remnant livers (C). The percentages of F4/80+CD11b+ cells which are indicated by red dots and F4/80+CD68+ cells indicated by blue dots are the representative data from four to six mice (A). The percentages of each cellular population at the indicated time points are shown as the means SE (B, C). (*P .05 vs Sham).From: Nishiyama K, Nakashima H, Ikarashi M, Kinoshita M, Nakashima M, Aosasa S, et al. (2015)Mouse CD11b+Kupffer Cells Recruited from Bone Marrow Accelerate Liver Regeneration after Partial Hepatectomy.PLoS ONE 10(9): e0136774.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957)used for the identification of inflammatory macrophages at the site of tibial fracture by immunofluorescenceImage caption:Bone fracture increased CD68+ macrophages in the peri-infarct region. (A) Image illustrates infarct core (Core), infarct border (dotted line) and the peri-infarct region (P.I.). (B) Quantification of CD68+ cells. *: P = 0.004, compared to stroke-only group. (C) Representative images of anti-CD68 antibody-stained sections. BF + 6hS: mice that received tibia fracture 6 hours before pMCAO; BF+1dS: mice that received tibia fracture 24 hours before pMCAO. Scale bars: 50 m. N = 6. From: Wang L, Kang S, Zou D, Zhan L, Li Z, Zhu W, et al. (2016)Bone Fracture Pre-Ischemic Stroke Exacerbates Ischemic Cerebral Injury in Mice. PLoS ONE 11(4): e0153835.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA11 (MCA1957) used for the identification of macrophages and microglia in unfixed cryosections by immunofluorescence.Image caption:Engulfment of fibrillar A by BMDM and primary microglia AA schematic shows 10‐μm cryosections of unfixed brain from 6‐month‐old APP/PS1 mice, which show a high amyloid plaque burden (right panel with methoxy‐X04 staining), were incubated with antibody for 1 h, followed by adding BMDM or primary microglia on top of the sections. After 24 h incubation, sections were analyzed by immunostaining or immunoblotting.BmAb11 but not the isotype control (IC) co‐localized with methoxy‐X04. Scale bar: 10 m.C, DBMDM (C) or primary microglia (D) were cultured on cryosections pre‐incubated with mAb11 (1 g/ml). After 24 h, sections were processed for immunostaining using antibody against CD68 to identify myeloid cells and methoxy‐X04 staining to visualize A . Note that both cell types internalize A into intracellular vesicles (right panels show enlargement of insets). Scale bar: 10 m.From: Xiang X, Werner G, Bohrmann B, Liesz A, Mazaheri F, Capell A, Feederle R, Knuesel I, Kleinberger G, Haass C.TREM2 deficiency reduces the efficacy of immunotherapeutic amyloid clearance.EMBO Mol Med. 2016 Sep 1;8(9):992-1004.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA11 (MCA1957) used for the identification of macrophages in post stroke infarcts by immunohistochemistry on frozen tissue sections.Image caption:Immune cell composition in infarcts at the stage of liquefactive necrosis in humans and mice. a Representative images of CD3+ T-lymphocyte, CD20+ B-lymphocyte, and CD68+ macrophage/microglia infiltration in human infarcts at the stage of liquefactive necrosis. Scale bars, 10 m (human, CD3 and CD20 images) and 30 m (human, CD68 image). b Quantification of CD4+ and CD8+ T-lymphocyte, and CD20+ B-lymphocyte infiltration into the infarcts. c Representative images of CD3+ T-lymphocytes, B220+ B-lymphocytes, and CD68+ macrophages/microglia in the infarcts of C57BL/6 and BALB/c mice at 7 weeks post-stroke. Scale bar,100 m. d Higher magnification images of CD68+ macrophages/microglia in the infarct to reveal individual cells. Scale bar, 25 m. e Quantification of CD3+ T-lymphocyte infiltration, B220+ B-lymphocyte infiltration, and CD68 immunostaining in mouse infarcts. ****p Published customer image: Rat anti Mouse CD68 antibody, clone FA11 (MCA1957) used for the identification of macrophages in post stroke infarcts by immunohistochemistry on frozen tissue sections.Image caption:Impact of age on the chronic inflammatory response to stroke in C57BL/6 mice. a Comparison of the levels of 25 cytokines and chemokines in infarcts at the stage of liquefactive necrosis dissected from 3-month old and 18-month old C57BL/6 mice at 7 weeks post-stroke. Data are expressed as a fold-change relative to age matched sham control values. Data represent mean SEM. There is no significant difference in the overall cytokine and chemokine profile at the stage of liquefactive necrosis between 3-month old and 18-month old mice by two-way ANOVA. Cytokines and chemokines that are significantly different between the 3-month old and 18-month old mice corrected for multiple comparisons are denoted by an asterisk (*p 0.05 versus 3-month old mice). b Representative images of CD3+ T-lymphocytes, B220+ B-lymphocytes, and CD68+ macrophages/microglia in the infarcts of 3-month old and 18-month old C57BL/6 mice at 7 weeks post-stroke. Scale bar, 50 m. Red dotted lines indicate locations of the glial scar in each image. c Quantification of CD3+ T-lymphocyte and B220+ B-lymphocyte infiltration into the mouse infarcts.From: Nguyen TV, Frye JB, Zbesko JC, Stepanovic K, Hayes M, Urzua A, Serrano G, Beach TG, Doyle KP.Acta Neuropathol Commun. 2016 Sep 6;4(1):100.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Alexaflour 488 conjugated Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957A488) used for visualisation of CD68 expressing cells in brain lesions by immunofluorescence and purified Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to assess CD68 expression in similar lesions by western blotting.Image caption:Analysis of M/M phenotypic markers at different time points after dMCAO. a Coronal sections of the lesioned hemispheres of the inhibitor and control mice brains, at seven (two upper rows of panels) and 14 days (two lower rows) after dMCAO. The sections were triple-immunostained with anti-Iba-1 (red), anti-CD45 (blue), and anti-CD68 (green) antibodies. Representative merged and single-channel images depict part of the infarct core (I, outlined with white dotted lines) and peri-infarct area of stroke. High magnification images demonstrate distribution of Iba-1, CD45, and CD68 in the glial scar area (right panels). Imaging was performed using Zeiss LSM800 Airyscan confocal microscope, using single-scan and tile-scan image acquisitions. Bars: from left to right: 100 and 10 m. b Quantification of the corrected fluorescence intensity for CD45 and CD68 immunofluorescence staining in the inhibitor (black bars) and control groups (white bar), at 7 and 14 days after dMCAO. N = 5–6 mice per group/per time point, three brain sections per mouse. Error bars: SEM; Student s t test, *p 0.05; **p 0.01. c Representative Western blots and quantification analysis (graphs) of CD206, CD45, CD68, and Iba-1 expression in lysates prepared from the lesioned cortical tissue of the animals from the inhibitor (black bars) and control (white bars) groups, at 7 and 14 days after dMCAO. Graphs: optical density of each band was normalized to -actin (loading control). N = 5–6 mice per group/per time point. Error bars: SEM; Student s t test, *p 0.05From: Pena-Philippides JC, Caballero-Garrido E, Lordkipanidze T, Roitbak T.In vivo inhibition of miR-155 significantly alters post-stroke inflammatory response.J Neuroinflammation. 2016 Nov 9;13(1):287.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 used for the identification of infiltrating microglia in a murine model of Retinitis pigmentosa by immunofluorescence on vibrotome sections. Image caption:Transient expression of phagocytic molecules and exposure of the \"eat-me” signal phosphatidylserine (PS) in the outer nuclear layer during rod degenerationA–C Microglia infiltrating the ONL demonstrate upregulation of the phagocytic molecule, CD68. Top images in (A) show composites of CD68 (red), Iba1 (green), and DAPI (blue) staining; bottom images show the same field with CD68 staining only. At P18, non-infiltrating microglia expressed low or undetectable levels of CD68, a lysosome-associated membrane protein. At P21–23, microglia infiltrating the ONL strongly upregulated CD68 (arrowheads). At P30, CD68 immunopositivity in ONL microglia decreased and was mostly confined to amoeboid cells in the subretinal space. (B) Magnified view of inset in (A) demonstrates localization of CD68 to microglia phagosomes. (C) CD68 expression (area of immunopositivity as a fraction of the ONL) demonstrated a peaked at P22 and decreased by P30. Scale bar, 20 m.D–F Upregulation of MFG-E8, a secreted glycoprotein that serves as a bridging molecule for phagocytosis receptors, in the ONL. (D) MFG-E8 was low or absent in the ONL at P18, but emerged at P21–23, localizing to photoreceptor cell bodies in a column-like pattern (arrow) and as a punctate signal within infiltrating microglia (arrowhead), before decreasing throughout the ONL at P30. (E) A magnified orthogonal view of the inset from (D) demonstrating punctate MFG-E8 immunopositivity within ONL microglia. (F) Quantification of MFG-E8 expression demonstrated a prominent emergence at P22 and a subsequent decrement by P30. Scale bar, 20 m.G–K Increase in phosphatidylserine (PS) exposure in the ONL during photoreceptor degeneration. (G) At P18, PS immunopositivity is near absent in the ONL, but increased significantly in ONL somata at P21–23, before decreasing at P30. (H) Quantitation of PS exposure by image analysis (by fractional area of PS immunopositivity within the ONL (top), and the mean intensity of PS staining in the ONL (bottom)) demonstrated a transient increase at P22. (I) Co-immunolabeling of rods with rhodopsin at P22 demonstrates that PS exposure was present in a majority of rods (inset shows at high magnification the co-labeling of PS and rhodopsin in multiple rod somata). (J) Conversely, immunolabeling of cones with cone arrestin demonstrates the sparse co-localization of PS in cones (inset shows close juxtaposition but no colocalization of PS and arrestin labeling). (K) Scoring of rhodopsin+ rods and arrestin+ cones for PS co-labeling demonstrates that a large majority of rods, but only a small minority of cones, showed PS exposure (two-sided unpaired t-test, n = 3 animals at P22). Scale bars = 20 m.Data information: Quantitative analyses in (C, F, H, and K) involved three animals at each time point. Column heights and error bars indicate mean SEM.From: Zhao L, Zabel MK, Wang X, Ma W, Shah P, Fariss RN, Qian H, Parkhurst CN, Gan WB, Wong WT.Microglial phagocytosis of living photoreceptors contributes to inherited retinal degeneration.EMBO Mol Med. 2015 Jul 2;7(9):1179-97.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957GA) used for the identification of microglia engulfing rods in the retinal outer nuclear layer (ONL) in a murine model of retinitis pigmentoisa by immunofluorescence. Image caption:Infiltrating microglia phagocytose non-apoptotic photoreceptor rods during rod degenerationA–C Phagocytosis of rods by infiltrating microglia. (A) Representative example of a Iba1+ microglial process extending into the ONL with a phagosome at its terminal end. Each phagosome contained a photoreceptor nucleus (labeled with DAPI, arrow) that was identified as a rod photoreceptor by rhodopsin immunopositivity (superposition of Iba1+ phagosome with rhodopsin+ soma in orthogonal views). (B) Example of an amoeboid microglia in the ONL with multiple phagosomes containing both rhodopsin-positive (arrowhead) and rhodopsin-negative (arrow) nuclei. (C) Rhodopsin+ nuclei can be localized within CD68-positive phagosomes in infiltrating microglia, indicating phagocytic engulfment of rods. Scale bar, 10 m.From: Zhao L, Zabel MK, Wang X, Ma W, Shah P, Fariss RN, Qian H, Parkhurst CN, Gan WB, Wong WT.Microglial phagocytosis of living photoreceptors contributes to inherited retinal degeneration.EMBO Mol Med. 2015 Jul 2;7(9):1179-97.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA11 used for the demonstration of macrophages in murine muscle tissue by immunofluorescence on cryosections. Image caption:Osteopontin deletion in laminin α2 chain-deficient muscle temporarily influences macrophage numbers, but does not change the general character of macrophage-mediated immune response.(a) CD68 immunostaining of 2-week-old dy3K/dy3K and dy3K/OPN triceps muscle reveals increased infiltration of macrophages/monocytes in double knockout muscle. Representative areas of triceps and whole triceps are shown. (a ) Quantification of CD68-stained muscle area confirms significant escalation of macrophage numbers in 2-week-old double knockout mice compared to dy3K/dy3K single knockout mice (p = 0.0317, Mann Whitney) (b) Increase in macrophage numbers in younger double knockout mice is only transient. Three-week-old triceps muscle from both dy3K/dy3K and dy3K/OPN mice show the same appearance when stained against CD68 (top panel, green staining). M1 macrophages are present in both dy3K/dy3K and dy3K/OPN triceps, as demonstrated by immunostaining against iNOS (red, middle panel) and CD68 (merged staining, bottom panel). iNOS is expressed at low levels in vessels in wild-type and osteopontin-deficient muscle. (b ) Quantification of CD68 and iNOS labelling confirms no change of M1 macrophage-mediated immune response upon osteopontin deletion in 3-week-old mice (p = 0.2222 and p = 0.6905, respectively; Mann-Whitney). Five mice from each group were analysed in (a) and (b). Bars: 50 and 100 m.From: Gawlik KI, Holmberg J, Svensson M, Einerborg M, Oliveira BM, Deierborg T, Durbeej M. Potent pro-inflammatory and pro-fibrotic molecules, osteopontin and galectin-3, are not major disease modulators of laminin 2 chain-deficient muscular dystrophy.Sci Rep. 2017 Mar 10;7:44059.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957GA) used for the identifcation of macrophages in kidney sections by immunohistochemistry on cryosections. Image caption:Renal markers of inflammation at Week 32.CD68 representative images at 200x magnification, B. Area (%) of CD68 staining. Results are expressed as mean SEM, N = 4–6. *P 0.05, **P 0.01, ***P 0.001, ****P 0.0001 compared to CC.From: Glastras SJ, Chen H, Tsang M, Teh R, McGrath RT, Zaky A, et al. (2017)The renal consequences of maternal obesity in offspring are overwhelmed by postnatal high fat diet.PLoS ONE 12(2): e0172644.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957GA) used for the demonstration of macrophages in murine peritoneal tissue by immunohistochemistry.Image caption:BIX01294 inhibits monocyte/macrophage infiltration, TGF- 1, and H3K9me1 in mice with peritoneal fibrosis(A) Immunohistochemical staining shows typical CD68 expression in peritoneal tissue of control mice, MGO-injected mice, and MGO-injected mice treated with BIX01294 (original magnification, ×200). (B) Graph indicates the number of CD68-positive cells in the three groups of mice. (C) Immunohistochemical staining shows typical TGF- 1 expression in peritoneal tissue of control mice, MGO-injected mice, and MGO-injected mice treated with BIX01294 (original magnification, ×200). (D) Graph indicates the number of TGF- 1-positive cells in the three groups of mice. (E) Two-color immunohistochemical staining shows that most CD68 cells (brown) are immunoreactive for TGF- 1 (blue-gray) (arrows). (F) TGF- 1 protein levels in mouse PD effluent were quantified by ELISA. ( Data are expressed as the mean SE. Statistical analysis were performed by analysis of variance followed by Tukey s post-hoc test. *P 0.05, n = 5 mice per group.From: Maeda K, Doi S, Nakashima A, Nagai T, Irifuku T, Ueno T, et al. (2017)Inhibition of H3K9 methyltransferase G9a ameliorates methylglyoxal-induced peritoneal fibrosis.PLoS ONE 12(3): e0173706.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Moouse CD68 antibody, clone FA11 (MCA1957)Image caption:Astrogliosis and white matter volume loss in PVL model.Studies of microglial M1 and M2 phenotypes at P15 (10 days after HI) in HI group versus sham.Panel A: Immunostaining for all Microglia (Iba1) in green (top), CD 68 (marker of activated microglia only) in red (middle). Co-localization in yellow indicating amount of activated microglia. Scale Bar = 100 m. Panel B: Immunostaining for Arginase 1 (M2 microglial marker) in green (top); for Microglia (Iba1) in blue (middle); and Co-localization (bottom) indicating the percentage of M2 microglia. Co-localization showed scare M2 microglial phenotype cells in HI group. Scale Bar = 100 m. Panel C: Quantification of CD68/Iba1 per section Panel D: Arginase 1/Iba1 per section. There was significant increase of M1 microglia and a significant reduction of M2 microlgia in HI group. N = 5 animals/group & 4 sections/animal. Bars represent the Mean + SE. **** indicates P 0.0001.From: Zaghloul N, Patel H, Ahmed MN (2017)A model of Periventricular Leukomalacia (PVL) in neonate mice with histopathological and neurodevelopmental outcomes mimicking human PVL in neonates.PLoS ONE 12(4): e0175438.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody (MCA1957) used to indicate macrophages in mouse brain by immunofluorescence (panels A-C-see text below)Image caption:Microglia activation was not observed in the corpus callosum three days after the stimulation at 300 Hz, and also not in sham-treated animals.(A-C) Sham-treated animal: Coronal section of corpus callosum from a showing double channel immunofluorescent labeling with DAPI (A, blue), CD68 (B, red), and the overlay of two channels (C). Left column: Overview image taken with an open pinhole. The dashed and white squares indicate the region of electrode implantation and the region of interest used for counting of oligodendroglial cells, respectively. These regions are shown at a higher magnification in the middle- and right-column images. Note that cell counting area is far away from injury site. ctx = cortex, cc = corpus callosum, cc = hippocampus. Scale bars: 500 m. Middle column: Higher magnification of the area indicated on the left image with the dashed square. The image shows the site of cortical injury caused by electrode implantation. Single confocal plane. Scale bars: 100 m. Right column: Higher magnification of the area indicated on the left image with the white square. The image shows the region of corpus callosum with white dashed line denoting the region of interest where counting of oligodendroglial cells was performed. Single confocal plane. Scale bars: 100 m. (D-F) As in (A-C) but for 300 Hz stimulation. Note that in both sham-treated and stimulated animal CD68-expressing cells are visible only at the injury site, but not in corpus callosum. All images are representative examples. Samples from the group of mice received stimulation at 25 Hz (not shown) followed very similar pattern, i.e. CD68-expressing cells appeared at the injury site, but not in the corpus callosum.From: Citation: Nagy B, Hovhannisyan A, Barzan R, Chen T-J, Kukley M (2017)Different patterns of neuronal activity trigger distinct responses of oligodendrocyte precursor cells in the corpus callosum.PLoS Biol 15(8): e2001993.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody (MCA1957) used to indicate macrophages in mouse brain by immunofluorescence (panels A-C-see text below)Image caption:Microglia activation was not observed in the corpus callosum three days after the stimulation at 300 Hz, and also not in sham-treated animals.(A-C) Sham-treated animal: Coronal section of corpus callosum from a showing double channel immunofluorescent labeling with DAPI (A, blue), CD68 (B, red), and the overlay of two channels (C). Left column: Overview image taken with an open pinhole. The dashed and white squares indicate the region of electrode implantation and the region of interest used for counting of oligodendroglial cells, respectively. These regions are shown at a higher magnification in the middle- and right-column images. Note that cell counting area is far away from injury site. ctx = cortex, cc = corpus callosum, cc = hippocampus. Scale bars: 500 m. Middle column: Higher magnification of the area indicated on the left image with the dashed square. The image shows the site of cortical injury caused by electrode implantation. Single confocal plane. Scale bars: 100 m. Right column: Higher magnification of the area indicated on the left image with the white square. The image shows the region of corpus callosum with white dashed line denoting the region of interest where counting of oligodendroglial cells was performed. Single confocal plane. Scale bars: 100 m. (D-F) As in (A-C) but for 300 Hz stimulation. Note that in both sham-treated and stimulated animal CD68-expressing cells are visible only at the injury site, but not in corpus callosum. All images are representative examples. Samples from the group of mice received stimulation at 25 Hz (not shown) followed very similar pattern, i.e. CD68-expressing cells appeared at the injury site, but not in the corpus callosum.From: Citation: Nagy B, Hovhannisyan A, Barzan R, Chen T-J, Kukley M (2017)Different patterns of neuronal activity trigger distinct responses of oligodendrocyte precursor cells in the corpus callosum.PLoS Biol 15(8): e2001993.This is an open access article distributed under the terms of a Creative Commons AttributionLicense. Published customer image: Rat anti Mouse CD68 antibody, clone FA11 (MCA1957) used to identify macrophages in murine kidney sections by immunohistochemistry on cryostat sections.Image caption:Histology at day 8 after NTN induction. Representative histology from PAS stained sections from Experiment 2, of WT and RIPK3−/− kidney. a) WT b) RIPK3- /−. Immunoperoxidase staining for CD68 in WT and RIPK3−/− kidney showing glomerular macrophage infiltration following the induction of NTN. c) WT d) RIPK3−/−From: Hill NR, Cook HT, Pusey CD, Tarzi RM.RIPK3-deficient mice were not protected from nephrotoxic nephritis.BMC Nephrol. 2018 Mar 14;19(1):61.This is an open access article distributed under the terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11(MCA1957) used to identify lysozomes by immunofluorescence.Image caption:CD68-positive brain myeloid cells after permanent ischemia and simplified scheme of the phagocytic process. Confocal images of the ischemic hemisphere showing cells positive for the lysosomal marker CD68 (red) and for the myeloid cell membrane marker CD11b (green) in the ischemic area at 48 h (a) or 7 days (b) after pMCAo, the latter time showing increased density of CD68-positive cells (nuclei in blue, scale bar = 200 m). Steps leading to phagocytosis include cell targeting by eat-me-signals, recognition by the phagocytic cell, and vesicular trafficking within the phagocyting cell. There, primary lysosomes get close to cell membrane and fuse with phagosomes. The mature lysosomes complete digestion with lysozimes, leaving residual bodies within the cytoplasm or getting back to Golgi. From: Fumagalli S, Fiordaliso F, Perego C, Corbelli A, Mariani A, De Paola M, De Simoni MG.The phagocytic state of brain myeloid cells after ischemia revealed by superresolution structured illumination microscopy.J Neuroinflammation. 2019: 16(1):9.This image is from an open access article distributed under the terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11(MCA1957) used to identify lysozomes by immunofluorescence.Image caption:Confocal microscopy vs. SIM and CD68 SIM dataset validation by image diagnosis. Planar xy view with xz (below) and yz (right) projections of CD11b (green) and CD68 (red) showing merged signal (yellow) by confocal microscopy (a), or signal proximity with no colocalization by SIM (a′). Image overimposition details the different resolutions achieved by confocal microscopy vs. SIM (a′′). Three-dimensional view of the same cell by confocal (b) and SIM (b′). The arrow in (b) show a lysosome (CD68) entirely surrounded by cell membrane (CD11b) in confocal microscopy. SIM yields enough resolution to visualize lysosome proximity to cell mebrane with no fusion (b′, arrow). Scale bars = 2 m. Plot profiles over the lines in a and a′ confirm that SIM, but not confocal microscopy, allows to visualize close, non-overlapping CD11b and CD68 signals. From: Fumagalli S, Fiordaliso F, Perego C, Corbelli A, Mariani A, De Paola M, De Simoni MG.The phagocytic state of brain myeloid cells after ischemia revealed by superresolution structured illumination microscopy.J Neuroinflammation. 2019: 16(1):9.This image is from an open access article distributed under the terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957)used for the identification of microglia in mouse brain by immunofluorescence.Image caption:Localization of CB2 receptors in microglial cells and engulfment synapses. (A) A confocal image of CB2 (green) and CD68 staining (red) centered at the core of an A plaque (marked by an asterisk). Note a region of high intensity for CB2 and CD68 staining around the plaque implying that CB2 receptors are localized in microglial processes surrounding the plaque. Scale 15 m. (B) A magnification of a microglia cell body (red) and its process (red) forming an engulfment synapse on a dense core amyloid plaque (marked by an asterisk, DAPI). Note CB2 receptor staining along the edge of CD68-positive staining and at the engulfment synapse. White boxes indicate areas used for quantifications in C-D. (C-D) Quantification of CB2, CD68, and DAPI signals from the image of a microglia cell body (C) and engulfment synapse (D). The quantification was done using a Plot profile analysis tool (Fiji). Signals were averaged along short axes of boxes shown in B and normalized to a max value (100%) for each channel. Units of X axis are pixels, scale: 11.1 pixels/ m. (E) 3D reconstruction of the engulfment synapse shown in B, D. A z stack of 0.31 m slices (n = 29) was processed by using a background subtraction function and normalization for each of the channels. Surfaces for the plaque (DAPI), microglia process (CD68), and CB2 signal were created by arbitrary thresholding at an upper third of intensity distributions. Note high intensities of CB2 signals are located between CD68 and DAPI surfaces. Insert shows orientation of a 3D window as related to a position of the brain slide.From: Savonenko AV, Melnikova T, Wang Y, Ravert H, Gao Y, Koppel J, et al. (2015)Cannabinoid CB2 Receptors in a Mouse Model of A Amyloidosis: Immunohistochemical Analysis and Suitability as a PET Biomarker of Neuroinflammation.PLoS ONE 10(6): e0129618.This is an open access article distributed under the terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957GA) used for the detection of macrophages in murine kidney using immunohistochemistry on PLP fixed cryosections.Image caption:Representative histological sections from the 3 bone marrow transplant groups with NTN. (A) PAS-stained sections of renal histology. The WT to IL-17-/- group have severe glomerular thrombosis with profound tubular dilatation and casts, significantly more than the other groups. (B) and (C) Immunofluorescence for glomerular deposition of sheep and mouse IgG respectively. There was no difference between the groups. (D) and (E) Representative glomerular staining for CD68 and CD4 respectively. Magnification x400.From: Hamour S, Gan P-Y, Pepper R, Florez Barros F, Wang H-H, O Sullivan K, et al. (2015)Local IL-17 Production Exerts a Protective Role in Murine Experimental Glomerulonephritis.PLoS ONE 10(8): e0136238. This is an open access article distributed under the terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA11 (MCA1957) used for the identification of macrophages in mouse liver by immunohistochemistry on formalin fixed, paraffin tissue sections. Image caption:Expression of F4/80 and CD68 in liver tissue assessed by immunostaining using anti-F4/80 or anti-CD68 antibody.From: Citation: Ibusuki R, Uto H, Oda K, Ohshige A, Tabu K, Mawatari S, et al. (2017)Human neutrophil peptide-1 promotes alcohol-induced hepatic fibrosis and hepatocyte apoptosis.PLoS ONE 12(4): e0174913.This is an open access article distributed under the terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA11 (MCA1957GA) used for the identification of macrophages in vascular smooth muscle by immunohistochemistry on formalin fixed, paraffin embedded tissue sections.Image caption:A-D Representative images and quantifications of macrophages (CD68 staining) (A) T lymphocytes (CD3 staining) (B), apoptotic area as assessed by TUNEL assay (C) and -actin (D) in Ldlr-/- infused either PBS (n = 5), AngII (n = 5) and Ldlr-/-Ido1-/- mice infused with AngII (n = 5) for 7 days. Mean values SEM are shown. *P 0.05, **P 0.001.From: Metghalchi S, Vandestienne M, Haddad Y, Esposito B, Dairou J, Tedgui A, et al. (2018)IDO deficiency prevents AngII-induced vascular smooth muscle cell apoptosis.PLoS ONE 13(3): e0193737.This is an open access article distributed under the terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used for the detection of macrophages in mouse brain by immunofluorescence.Image caption:DCH-paclitaxel exhibits good biocompatibility in healthy CNS in contrast to paclitaxel in Cremophor EL vehicle. A-D. Images of caudate putamen at 1 week after injection into healthy, uninjured tissue of Cremophor EL vehicle (A), Cremophor EL + paclitaxel (B), DCH only (C), or DCH + paclitaxel (D), showing single channel and merged multichannel immunofluorescence for multiple markers of inflammation and gliosis, CD 68, IBA-1 and GFAP. Scale bar, 200 m for all images, D = DCH depot.From: Garrett MC, O’Shea TM, Wollenberg AL, Bernstein AM, Hung D, Staarman B, et al. (2020)Injectable diblock copolypeptide hydrogel provides platform to deliver effective concentrations of paclitaxel to an intracranial xenograft model of glioblastoma.PLoS ONE 15(7): e0219632.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to label macrophages in mouse aortic samples by immunofluorescence.Image caption:Nba2.Yaa mutation in Apoe−/−mice does not affect atherosclerosis lesion size. Representative pictures CD68, iNos and Arginase (Arg) staining in the roots of Apoe−/− or Apoe−/−Nba2.Yaa mice on HCD.From: Santiago-Raber ML, Montecucco F, Vuilleumier N, Miteva K, Baptista D, Carbone F, Pagano S, Roth A, Burger F, Mach F, Brandt KJ.Atherosclerotic plaque vulnerability is increased in mouse model of lupus.Sci Rep. 2020 Oct 27;10(1):18324.doi: 10.1038/s41598-020-74579-8.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used for labeling macrophages in mouseImage caption:Targeted silencing of miR-33 does not influence macrophage and smooth muscle cell content in atherosclerotic lesions. Low density lipoprotein receptor knockout (Ldlr-/-) mice were placed on a western diet (WD) for 3 months, and then switched to a chow diet andreceived anti-miR-33 peptide nucleic acid delivery vector (anti-miR33pHLIP) or scrambled control (SrcpHLIP) at a dose of 1 mg/kg body weight every week for a total of 5 injections. Representative immunofluorescence staining of macrophage (CD68 positive) and smooth muscle cell ( -smooth muscle actin) in cross sections of the aortic root from Ldlr-/- mice injected with anti-miR33pHLIP or SrcpHLIP vectors.From: Xinbo Zhang, Noemi Rotllan, Alberto Canfr n-Duque et al.Targeted suppression of microRNA-33 in lesional macrophages using pH low-insertion peptides (pHLIP) improves atherosclerotic plaque regression, 29 October 2020, PREPRINT (Version 1) available at Research Square10.21203/rs.3.rs-92252/v1This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used for the demonstration of macrophages in murine lungs by immunohistochemistry on formalin fixed, paraffin embedded tissue sections.Image caption:Immunolocalization of macrophages in lung tissue sections from female mice sham surgery (Sham) or ovariectomized (OVX) inoculated with the ATCC 25923 strain of S. aureusem> or saline (Sham Control or OVX Control). (B) Representative photomicrographs of immunolocalization of macrophages (original magnification ×400).From: Souza CLSE, Oliveira HBM, Santos J nior MN, Silva MO, Coqueiro IL, Silva ÍBSD, Campos GB, Silva RAAD, Soares TJ, Oliveira MV, Timenetsky J, Marques LM.Ovarian hormones influence immune response to Staphylococcus aureus infection.Braz J Infect Dis. 2020 Nov 10:S1413-8670(20)30156-2.doi: 10.1016/j.bjid.2020.10.004.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse antibody, clone FA-11 (MCA1957) used for the demonstration of macrophages in murine aortic arches by immunohistochemistry on vibratome sections. Image caption:Histological analyses of atherosclerotic lesions in the aortic valve of 26-week-old low-density lipoprotein receptor knockout (Ldlr-/-) mice. Mice were fed a Western diet with adequate (0.3%; P0.3) or high (1.5%; P1.5) phosphorus levels coupled with adequate (1000 IU; D1000) or low (50 IU; D50) vitamin D levels over a 17-week period. Shown are (c) the percentage of macrophages in the aortic valve lesions and representative images of aortic valve sections that were stained by immunohistochemical staining with CD68 antibodies and haematoxylin.From: Grundmann SM, Schutkowski A, Berger C, Baur AC, K nig B, Stangl GI.High-phosphorus diets reduce aortic lesions and cardiomyocyte size and modify lipid metabolism in Ldl receptor knockout mice.Sci Rep. 2020 Nov 27;10(1):20748.doi: 10.1038/s41598-020-77509-w.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used for the demonstration of macrophages in murine brain by immunofluorescenceImage caption:NF- B modulates microglial activation to an inflammatory, neurotoxic phenotype. a Immunostaining for all microglia (Iba1) in green (top) and CD 68 (marker of activated microglia M1 only) in red (middle). Co-localization in yellow indicating amount of activated microglia at postnatal day 15. * indicates lateral ventricle. From: Zaghloul N, Kurepa D, Bader MY, Nagy N, Ahmed MN.Prophylactic inhibition of NF- B expression in microglia leads to attenuation of hypoxic ischemic injury of the immature brain.J Neuroinflammation. 2020 Dec 1;17(1):365.doi: 10.1186/s12974-020-02031-9.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to stain CD68 expressing cells in murine hippocampus by immunofluorescence on cryosections.Image caption:BF increased the amount of CD68+ cells in the ipsilateral hippocampal CA1 region. (A). Representative microscopic images of CD68+ antibody (red) stained sections. The nuclei were stained with DAPI (Blue). Scale bar: 500 m. (B). Quantification of the number of CD68+ cells. The groups represented by different colors are indicated on the X-axis. N = 6. con: contralateral to stroke injury. ips: ipsilateral to stroke injury. BFS: BF 6 h before stroke.From: Huang J, Lyu H, Huo K, Do Prado LB, Tang C, Wang Z, Li Q, Wong J, Su H.Bone Fracture Enhanced Blood-Brain Barrier Breakdown in the Hippocampus and White Matter Damage of Stroke Mice.Int J Mol Sci. 2020 Nov 11;21(22):8481.doi: 10.3390/ijms21228481.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to identify microglia in mouse brain tissue by immunofluorescence on formalin fixed cryosections. Image caption:Alcohol downregulates the microglial expression of CD68.a). Representative images of the hippocampal sections stained for Iba1 (green), CD68 (red), and DAPI (blue) from pair-fed (PF) and alcohol-fed (EtOH) mice, acquired at × 63 magnification. From: Lowe PP, Morel C, Ambade A, Iracheta-Vellve A, Kwiatkowski E, Satishchandran A, Furi I, Cho Y, Gyongyosi B, Catalano D, Lefebvre E, Fischer L, Seyedkazemi S, Schafer DP, Szabo G.Chronic alcohol-induced neuroinflammation involves CCR2/5-dependent peripheral macrophage infiltration and microglia alterations.J Neuroinflammation. 2020 Oct 9;17(1):296.doi: 10.1186/s12974-020-01972-5. This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to identify macrophages in murine femoral arteries by immunohistochemistry on formalin fixed, paraffin embedded tissue sections.Image caption:Effects of Revacept administration to mice on CD68 expression in femoral artery sections. Immunohistochemistry of femoral artery sections to assess CD68 at 28 days after surgery in mice treated with Revacept or Fc.From: Alberti S, Zhang Q, D\'Agostino I, Bruno A, Tacconelli S, Contursi A, Guarnieri S, Dovizio M, Falcone L, Ballerini P, Münch G, Yu Y, Patrignani P.The antiplatelet agent revacept prevents the increase of systemic thromboxane A2 biosynthesis and neointima hyperplasia.Sci Rep. 2020 Dec 8;10(1):21420.doi: 10.1038/s41598-020-77934-x.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to stain macrophages in murine aortic root by immunohistochemistry on cryostat sections. Image caption:Serum cholesterol lowering leads to phenotypic plaque regression in APOE*3-Leiden.CETP mice.a. Representative images of aortic root sections stained with Oil-red O (ORO), anti-CD68 (for macrophages, M ) on the left. On the right, lesion area was measured on 8 aortic root sections at 50 m intervals starting from valve initiation. Plaque composition was analyzed by quantifying the percent ORO+ and CD68+ and areas within lesions. Data are presented as mean SEM percent change over values in the baseline group to visualize relative changes during plaque progression and regression. *, , p 0.05 denote statistically significant differences between the Ctrl and Base ( ), Statin (*) and Free ( ) groups, respectively, baseline n = 6, other 3 groups n = 8 per group, one-way ANOVA.From: H rdtner C, et al. Inhibition of macrophage proliferation dominates plaque regression in response to cholesterol lowering.Basic Res Cardiol. 2020 Dec 9;115(6):78.doi: 10.1007/s00395-020-00838-4.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to label macrophages in murine renal tissue by immunohistochemistry on formalin fixed, paraffin embedded sections.Image caption:Immunohistochemistry and quantitative analysis for anti-CD68 and anti- -SMA. Anti-CD68 for the a CKD group, b RPC group, and c hiPSC group, magnification of × 40. d Anti-CD68 quantitative analysis for all the three groups. Anti- -SMA for the e CKD group, f RPC group, and g hiPSC group, magnification of × 40. h Anti- -SMA quantitative analysis for all the three groups. *p value 0.05 vs. CKD.From: Ribeiro PC, Lojudice FH, Fernandes-Charpiot IMM, Baptista MASF, de Almeida Araújo S, Mendes GEF, Sogayar MC, Abbud-Filho M, Caldas HC.Therapeutic potential of human induced pluripotent stem cells and renal progenitor cells in experimental chronic kidney disease.Stem Cell Res Ther. 2020 Dec 9;11(1):530.doi: 10.1186/s13287-020-02060-4.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to stain microglia in mouse brain by immunohistochemistry on free floating sections.Image caption:Threshold imaging analysis of sections stained for microglia (CD68) show a significant increase in both the dorsal and ventral horns of the lumbo-sacral cord at early (3MO) and late (7MO) disease states in Ppt1−/− cords compared to WT. From: Nelvagal HR, Hurtado ML, Eaton SL, Kline RA, Lamont DJ, Sands MS, Wishart TM, Cooper JD.Comparative proteomic profiling reveals mechanisms for early spinal cord vulnerability in CLN1 disease.Sci Rep. 2020 Sep 16;10(1):15157.doi: 10.1038/s41598-020-72075-7.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody (MCA1957) used to identify macrophages in mouse atherosclerotic plaques by immunofluorescence on cryostat sections.Image caption:CD68 staining in ApoE-/- mice after 12 weeks with Western Diet.(A) without plaque formation in the aortic arch, (B) with big plaque formation with macrophages inside in the thoracic part of the aorta.From: Riedl KA, Kampf T, Herold V, Behr VC, Bauer WR (2020)Wall shear stress analysis using 17.6 Tesla MRI: A longitudinal study in ApoE-/- mice with histological analysis.PLoS ONE 15(8): e0238112.doi: 10.1371/journal.pone.0238112This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to identify microglia in mouse brain free floating sections by immunohistochemistry.Image caption:Microglial activation, revealed by CD68 immunoreactivity (C), is increased all brain regions for Cln3Q352X mice of both sexes, except for the S1BF of female Cln3Q352X mice. Two-way ANOVA, Fisher’s LSD post-hoc. Mean SEM, *p 0.05; **p 0.01; ****p 0.0001. WT images are representative of female mice. Mutant images are representative for male mice (SubC, CD68) and female mice (GFAP). Scale bar = 100 m.From: Langin L, Johnson TB, Kov cs AD, Pearce DA, Weimer JM.A tailored Cln3Q352X mouse model for testing therapeutic interventions in CLN3 Batten disease.Sci Rep. 2020 Jun 29;10(1):10591.doi: 10.1038/s41598-020-67478-5.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used for the detection of activated micropahe cells in mouse brain sections by immunofluorescence.Image caption:Maximum intensity projections of confocal stacks, showing a representative image of activated myeloid cells around plaques (distance 10 m) and less activated myeloid cells distant from the plaque; scale bar = 25 m. (j) Quantification of the percentage of CD68 + activated myeloid cells close and distant from plaques; n = 3 animals, 4-6 fields of view per animal; 2-way ANOVA with Bonferroni post-hoc test; df = 57; interaction; ***p 0.001.From: Drost N, Houtman J, Cseresny s Z, Niesner R, Rinnenthal JL, Miller KR, Prokop S, Heppner FL.The Amyloid-beta rich CNS environment alters myeloid cell functionality independent of their origin.Sci Rep. 2020 Apr 28;10(1):7152.doi: 10.1038/s41598-020-63989-3.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to illustrate microglia in mouse brain by immunofluorescence.Image caption:Switch in microglial proteomic signatures and increased phagocytosis occur already in pre-symptomatic Npc1−/− mice and precede neuronal loss.Immunostaining of cerebellum of P7 WT and Npc1−/− mice from three independent experiments (n = 3) using antibodies against neuronal markers (green) Calbindin (Purkinje cells, cerebellum), NeuN (cortex) and lysosomal microglial marker CD68 (red) reveal no neurodegeneration in Npc1−/− mice (10×, upper panels). In contrast, CD68 immunoreactivity showed activated Npc1−/− microglia with amoeboid morphology already at this early pathological stage (100×, lower panels). Hoechst was used for nuclear staining (blue). Scale bars: 250 m (10×, left panels) and 25 m (100×, right panels). From: Colombo A, Dinkel L, M ller SA, Sebastian Monasor L, Schifferer M, Cantuti-Castelvetri L, König J, Vidatic L, Bremova-Ertl T, Lieberman AP, Hecimovic S, Simons M, Lichtenthaler SF, Strupp M, Schneider SA, Tahirovic S.Loss of NPC1 enhances phagocytic uptake and impairs lipid trafficking in microglia.Nat Commun. 2021 Feb 24;12(1):1158.doi: 10.1038/s41467-021-21428-5.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to illustrate microglia in mouse brain by immunofluorescence.Image caption:Switch in microglial proteomic signatures and increased phagocytosis occur already in pre-symptomatic Npc1−/− mice and precede neuronal loss.Immunostaining of cortex of P7 WT and Npc1−/− mice from three independent experiments (n = 3) using antibodies against neuronal markers (green) Calbindin (Purkinje cells, cerebellum), NeuN (cortex) and lysosomal microglial marker CD68 (red) reveal no neurodegeneration in Npc1−/− mice (10×, upper panels). In contrast, CD68 immunoreactivity showed activated Npc1−/− microglia with amoeboid morphology already at this early pathological stage (100×, lower panels). Hoechst was used for nuclear staining (blue). Scale bars: 250 m (10×, left panels) and 25 m (100×, right panels). From: Colombo A, Dinkel L, M ller SA, Sebastian Monasor L, Schifferer M, Cantuti-Castelvetri L, K nig J, Vidatic L, Bremova-Ertl T, Lieberman AP, Hecimovic S, Simons M, Lichtenthaler SF, Strupp M, Schneider SA, Tahirovic S.Loss of NPC1 enhances phagocytic uptake and impairs lipid trafficking in microglia.Nat Commun. 2021 Feb 24;12(1):1158.doi: 10.1038/s41467-021-21428-5.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to illustrate microglial expression of CD68 in mouse brain by western blotting.Image caption:Switch in microglial proteomic signatures and increased phagocytosis occur already in pre-symptomatic Npc1−/− mice and precede neuronal loss.Representative immunoblots of acutely isolated microglia from WT mice and Npc1−/− littermates showing increased level of late endosomal/lysosomal markers (NPC2, LAMP1, CTSB, CTSD, CD68, and CD63). Calnexin was used as a loading control.From: Colombo A, Dinkel L, M ller SA, Sebastian Monasor L, Schifferer M, Cantuti-Castelvetri L, K nig J, Vidatic L, Bremova-Ertl T, Lieberman AP, Hecimovic S, Simons M, Lichtenthaler SF, Strupp M, Schneider SA, Tahirovic S.Loss of NPC1 enhances phagocytic uptake and impairs lipid trafficking in microglia.Nat Commun. 2021 Feb 24;12(1):1158.doi: 10.1038/s41467-021-21428-5.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to illustrate microglial expression of CD68 in mouse brain by western blotting.Image caption:Cell autonomous function of NPC1 in microglia.Western blot analysis and corresponding quantification of 8-weeks old Npc1flox/cre+ (Cre+) mice with specific depletion of NPC1 in microglia and their littermate controls Npc1flox/cre− (Cre−). Representative immunoblots showing specific NPC1 depletion in microglia enriched (MG enriched) compared to microglia depleted (MG depleted) fraction of Cre+ microglia. Increased levels of late endosomal/lysosomal markers (LAMP1, CD68, and CD63) could only be detected in MG enriched fraction of Cre+ microglia. GAPDH was used as a loading control.From: Colombo A, Dinkel L, M ller SA, Sebastian Monasor L, Schifferer M, Cantuti-Castelvetri L, K nig J, Vidatic L, Bremova-Ertl T, Lieberman AP, Hecimovic S, Simons M, Lichtenthaler SF, Strupp M, Schneider SA, Tahirovic S.Loss of NPC1 enhances phagocytic uptake and impairs lipid trafficking in microglia.Nat Commun. 2021 Feb 24;12(1):1158.doi: 10.1038/s41467-021-21428-5.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to illustrate microglial expression of CD68 in mouse brain by western blotting.Image caption:Npc1−/− microglia display impairment in myelin turnover.In vitro myelin phagocytosis assay. Cultured primary microglia isolated from P7 mice from three independent experiments (n = 3) were incubated with fluorescently labeled myelin (green) and analyzed. Microglial lysosomes were stained with anti-CD68 antibody (red). Hoechst was used for nuclear staining (blue). At 48 h fluorescently labeled lipid vesicles were observed in WT microglia, indicating myelin turnover. In contrast, Npc1−/− microglia accumulated myelin within the CD68 positive compartments and no fluorescently labeled lipid vesicles were detected. Scale bars: 25 m.From: Colombo A, Dinkel L, M ller SA, Sebastian Monasor L, Schifferer M, Cantuti-Castelvetri L, K nig J, Vidatic L, Bremova-Ertl T, Lieberman AP, Hecimovic S, Simons M, Lichtenthaler SF, Strupp M, Schneider SA, Tahirovic S.Loss of NPC1 enhances phagocytic uptake and impairs lipid trafficking in microglia.Nat Commun. 2021 Feb 24;12(1):1158.doi: 10.1038/s41467-021-21428-5.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Published customer image: Rat anti Mouse CD68 antibody, clone FA-11 (MCA1957) used to demonstrate macrophages in murine spinal chord tissue by immunofluorescence.Image caption:Fasudil‐modified mononuclear cells (MNCs) inhibit inflammation and improve myelination in spinal cords. Chronic experimental autoimmune encephalomyelitis was induced in C57BL/6 mice with MOG35‐55. Fasudil‐modified MNCs were administrated by bilateral intranasal instillation with 3 × 106 cells/unilateral nasal cavity on day 3 postimmunization (p.i.) and 11 p.i. Phosphate buffered solution (PBS)‐treated MNCs were set up as control in a similar manner. On day 28 p.i., spinal cords were used for immunohistochemistry staining. From: Guo SD, Liu CY, Yu JW, Chai Z, Wang Q, Mi XT, Song GB, Li YH, Yang PW, Feng L, Xiao BG, Ma CG.Nasal delivery of Fasudil-modified immune cells exhibits therapeutic potential in experimental autoimmune encephalomyelitis.Infiltration of CD4+ T cells and CD68+ macrophage. Results are shown as mean SEM of five mice in each group. Differences are analyzed using Student s t‐test. **P 0.01; ***P 0.001CNS Neurosci Ther. 2019 Jun;25(6):783-95.doi: 10.1111/cns.13111.This image is from an open access article distributed under terms of a Creative Commons Attribution License. Create mode – the default mode when you create a requisition and PunchOut to Bio-Rad. 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