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antibodies against cd163 (Bio-Rad)

Name: antibodies against cd163
Brand: Bio-Rad
Rating: 94 (229 reviews)

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Bio-Rad antibodies against cd163
$Effect of ADAPT-3D on finicky antigens and compatibility with deep immunolabeling. A ) Maximum intensity projections of tight junctions (arachnoid barrier: occludin in red and claudin-11 in green, endothelial-cell specific: claudin-5 in grey) found in leptomeninges from a wildtype mouse imaged by confocal microscopy. B ) Extended display showing en face and x-z projections of mouse ileum that was immunolabeled with alpha smooth muscle actin (yellow), lymphatic vasculature (LYVE-1, magenta), myeloid cells (S100A9, cyan), and nuclei (DAPI, grey) followed by imaging with confocal microscopy. C ) Extended display showing en face and x-z projections of ileum from a 16-week-old mouse that expresses TNF ΔARE , a model of ileitis. D ) Extended display showing en face, z-side, and 3D projections of fixed human ileum applied with decolorization, delipidation, immunolabeling with <t>CD163</t> (green), IBA1 (red), and nuclei (DAPI, grey) followed by refractive index matching.$
Antibodies Against Cd163, supplied by Bio-Rad, used in various techniques. Bioz Stars score: 94/100, based on 229 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/antibodies against cd163/product/Bio-Rad
Average 94 stars, based on 229 article reviews

antibodies against cd163 - by Bioz Stars, 2026-03

94/100 stars

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1) Product Images from "ADAPT-3D:accelerated deep adaptable processing of tissue for 3-dimensional fluorescence tissue imaging for research and clinical settings"

Article Title: ADAPT-3D:accelerated deep adaptable processing of tissue for 3-dimensional fluorescence tissue imaging for research and clinical settings

Journal: Scientific Reports

doi: 10.1038/s41598-025-16766-z

$Effect of ADAPT-3D on finicky antigens and compatibility with deep immunolabeling. A ) Maximum intensity projections of tight junctions (arachnoid barrier: occludin in red and claudin-11 in green, endothelial-cell specific: claudin-5 in grey) found in leptomeninges from a wildtype mouse imaged by confocal microscopy. B ) Extended display showing en face and x-z projections of mouse ileum that was immunolabeled with alpha smooth muscle actin (yellow), lymphatic vasculature (LYVE-1, magenta), myeloid cells (S100A9, cyan), and nuclei (DAPI, grey) followed by imaging with confocal microscopy. C ) Extended display showing en face and x-z projections of ileum from a 16-week-old mouse that expresses TNF ΔARE , a model of ileitis. D ) Extended display showing en face, z-side, and 3D projections of fixed human ileum applied with decolorization, delipidation, immunolabeling with CD163 (green), IBA1 (red), and nuclei (DAPI, grey) followed by refractive index matching.$
Figure Legend Snippet: Effect of ADAPT-3D on finicky antigens and compatibility with deep immunolabeling. A ) Maximum intensity projections of tight junctions (arachnoid barrier: occludin in red and claudin-11 in green, endothelial-cell specific: claudin-5 in grey) found in leptomeninges from a wildtype mouse imaged by confocal microscopy. B ) Extended display showing en face and x-z projections of mouse ileum that was immunolabeled with alpha smooth muscle actin (yellow), lymphatic vasculature (LYVE-1, magenta), myeloid cells (S100A9, cyan), and nuclei (DAPI, grey) followed by imaging with confocal microscopy. C ) Extended display showing en face and x-z projections of ileum from a 16-week-old mouse that expresses TNF ΔARE , a model of ileitis. D ) Extended display showing en face, z-side, and 3D projections of fixed human ileum applied with decolorization, delipidation, immunolabeling with CD163 (green), IBA1 (red), and nuclei (DAPI, grey) followed by refractive index matching.

Techniques Used: Immunolabeling, Confocal Microscopy, Imaging, Refractive Index

Image Search Results

Journal: Scientific Reports

Article Title: ADAPT-3D:accelerated deep adaptable processing of tissue for 3-dimensional fluorescence tissue imaging for research and clinical settings

doi: 10.1038/s41598-025-16766-z

Figure Lengend Snippet: Effect of ADAPT-3D on finicky antigens and compatibility with deep immunolabeling. A ) Maximum intensity projections of tight junctions (arachnoid barrier: occludin in red and claudin-11 in green, endothelial-cell specific: claudin-5 in grey) found in leptomeninges from a wildtype mouse imaged by confocal microscopy. B ) Extended display showing en face and x-z projections of mouse ileum that was immunolabeled with alpha smooth muscle actin (yellow), lymphatic vasculature (LYVE-1, magenta), myeloid cells (S100A9, cyan), and nuclei (DAPI, grey) followed by imaging with confocal microscopy. C ) Extended display showing en face and x-z projections of ileum from a 16-week-old mouse that expresses TNF ΔARE , a model of ileitis. D ) Extended display showing en face, z-side, and 3D projections of fixed human ileum applied with decolorization, delipidation, immunolabeling with CD163 (green), IBA1 (red), and nuclei (DAPI, grey) followed by refractive index matching.

Article Snippet: 1 cm 3 samples were rinsed in 1X PBS-H for 2 h, incubated in ADAPT:DC for 2 days, ADAPT:PDL for 1 day, followed by ADAPT:BS containing antibodies against CD163 (Clone EDHu-1, Bio-Rad, 1:100), IBA1 (Fujifilm Wako, 019-19741, 1:100), and DAPI (Sigma-Aldrich, D9542, 1:200) for 2 days.

Techniques: Immunolabeling, Confocal Microscopy, Imaging, Refractive Index

Journal: Cellular and Molecular Life Sciences

Article Title: Macrophage re-programming by JAK inhibitors relies on MAFB

doi: 10.1007/s00018-024-05196-1

Figure Lengend Snippet: Upadacitinib promotes monocyte-derived macrophages with an anti-inflammatory gene expression and functional profile A Schematic representation of the experiments. Monocytes were exposed to 10–100 nM Upadacitinib daily during macrophage differentiation process with GM-CSF and the RNA levels were determined at day 7 on GM-MØ, 10Upa-GM-MØ and 100Upa-GM-MØ. Right, immunoblot analysis of pSTAT5, STAT5, pERK, ERK and pp38 by monocytes treated for 1 h to 100 nM Upadacitinib (Upa) and exposed to GM-CSF for the indicated time points. B Number of annotated genes whose expression is regulated in GM-MØ after 7d of Upadacitinib treatment (adj p < 0.05). C Volcano plot of RNAseq results showing the 100 nM Upadacitinib-induced gene expression changes in GM-MØ. D PCA analysis of GM-MØ, 10Upa-GM-MØ and 100Upa-GM-MØ.Three independent donors are identified as I, II and III. E GSEA on the ranked comparison of the GM-MØ versus 10Upa-GM-MØ and GM-MØ versus 100Upa-GM-MØ transcriptomes, using the genes significantly modulated by GM-CSF (GM-MØ-specific markers) and M-CSF (M-MØ-specific markers) as data set. Normalized Enrichment Score (NES) and False Discovery Rate (FDRq) are indicated. F Relative expression of the indicated genes as determined by RNA-sequencing on GM-MØ, 10Upa-GM-MØ and 100Upa-GM-MØ. Mean ± SEM of 4 independent donors are shown, with the indication of the P adj . G Production of activin A, IL-10 and LGMN by GM-MØ, 10Upa-GM-MØ and 100Upa-GM-MØ. Mean ± SEM of 8 independent donors are shown (* p < 0.05, ** p < 0.01, one-way ANOVA with Tukey´s post hoc test; F = 92.63 for Activin A, F = 17.85 for IL-10, F = 33.39 for LGMN). H Immunoblot analysis of CD163 and FOLR2 (down) by GM-MØ, 10Upa-GM-MØ, 100Upa-GM-MØ and monocytes differentiated with M-CSF (M-MØ). In panels A-G, vinculin or GAPDH protein levels were determined as protein loading controls and a representative experiment of two independent donors is shown. I Phagocytic activity in GM-MØ, 100Upa-GM-MØ and M-MØ . Mean ± SEM of 5 independent donors are shown (* p < 0.05, one-way ANOVA with Tukey’s post hoc test, F = 13.74). J Production of TNFα, IL-6 and IL-10 by GM-MØ and 100Upa-GM-MØ challenged with LPS for 24 h, as determined by ELISA. Mean ± SEM of 7–8 independent donors are shown (* p < 0.05, ** p < 0.01, paired t-test)

Article Snippet: Protein detection was carried out using rabbit antibodies against pp38 and pERK (clones D3F9 and D13.14.4E, Cell Signaling, 1/1000), MAFB (HPA005653, Santa Cruz, 1/1000), pGSK3β (clone D85E12, Cell Signaling, 1/1000) and mouse monoclonal antibody against human CD163 (clone EDHu-1, Bio-Rad, 1/1000), pSTAT5 (clone 8-5-2, Millipore, 1/1000), FOLR2 (FRβ, kindly provided by Dr. Takami Matsuyama [ ], dilution 1/800).

Techniques: Derivative Assay, Gene Expression, Functional Assay, Western Blot, Expressing, Comparison, RNA Sequencing, Activity Assay, Enzyme-linked Immunosorbent Assay

JAKi increases the expression of MAFB transcription factor in macrophages A Discriminant regulon expression analysis (DoRothEA) of 100Upa-GM-MØ compared with GM-MØ. Top 25 transcription factors are shown. B GSEA of genes downregulated by siRNA MAFB and by siRNA MAF on macrophages (GSE155719) on the ranked comparison of the transcriptomes of 100Upa-GM-MØ and GM-MØ transcriptomes. NES and FDRq value are indicated. C Relative expression of MAFB and MAF as determined by RNA-sequencing on GM-MØ, 10Upa-GM-MØ and 100Upa-GM-MØ. Mean ± SEM of 4 independent donors are shown, with the indication of the P adj . D Immunoblot analysis of MAFB and pGSK3S9 by GM-MØ, 10Upa-GM-MØ, 100Upa-GM-MØ and M-MØ. E Immunoblot analysis of MAFB and CD163 along the monocyte to macrophage differentiation in the presence of 100 nM Upadacitinib (Upa). In panels (D-E), GAPDH protein levels were determined as protein loading control and a representative experiment of two ( E ) and four ( D ) independent donors is shown. F Schematic representation of the experiments: short term-Upadacitinib treatment to mature macropahges (GM-MØ). Immunoblot analysis of MAFB and pGSK3S9 ( G ) and production of activin A ( H ) by GM-MØ exposed to 10–100 nM Upadacitinib for the last 48 h. GAPDH protein levels were determined as protein loading control. In ( G ) a representative experiment of three independent donors is shown. In ( H ) mean ± SEM of 5 independent donors are shown (* p < 0.05, F = 12.28). I Immunoblot analysis of MAFB in two independent preparations of differentiating GM-MØ (day 2) generated from monocytes exposed to DMSO (−), Upadacitinib (Upa, 100 nM), STAT5 phosphorylation specific inhibitor (ST5i, 50 µM) or MEK1/2 inhibitor (UO, 2,5 µM). Right, quantification of MAFB expression. J Immunoblot analysis of MAFB in two independent preparations of differentiating GM-MØ (day 2) generated from monocytes transfected with either siCNT or MAFB-specific siRNA (siMAFB) and exposed to DMSO (−) or 100 nM Upadacitinib (+). Right, quantification of MAFB expression. In panels I-J, mean ± SEM of the relative MAFB protein levels in the macrophage subtypes from four independent donors are shown (* p < 0.05, ** p < 0.01). K Relative mRNA expression of the indicated MAFB-dependent genes in siCNT GM-MØ, siMAFB GM-MØ, siCNT Upa-GM-MØ and siMAFB Upa-GM-MØ (day 2). Mean ± SEM of four independent experiments are shown (* p < 0.05; ** p < 0.01; *** p < 0.001, F = 3.7 for IL10 , F = 6.8 for CMKLR1 , F = 4.4 for LGMN , F = 56.89 for CD163 , F = 9.24 for FOLR2 , F = 8.34 for MS4A6A )

Journal: Cellular and Molecular Life Sciences

Article Title: Macrophage re-programming by JAK inhibitors relies on MAFB

doi: 10.1007/s00018-024-05196-1

Figure Lengend Snippet: JAKi increases the expression of MAFB transcription factor in macrophages A Discriminant regulon expression analysis (DoRothEA) of 100Upa-GM-MØ compared with GM-MØ. Top 25 transcription factors are shown. B GSEA of genes downregulated by siRNA MAFB and by siRNA MAF on macrophages (GSE155719) on the ranked comparison of the transcriptomes of 100Upa-GM-MØ and GM-MØ transcriptomes. NES and FDRq value are indicated. C Relative expression of MAFB and MAF as determined by RNA-sequencing on GM-MØ, 10Upa-GM-MØ and 100Upa-GM-MØ. Mean ± SEM of 4 independent donors are shown, with the indication of the P adj . D Immunoblot analysis of MAFB and pGSK3S9 by GM-MØ, 10Upa-GM-MØ, 100Upa-GM-MØ and M-MØ. E Immunoblot analysis of MAFB and CD163 along the monocyte to macrophage differentiation in the presence of 100 nM Upadacitinib (Upa). In panels (D-E), GAPDH protein levels were determined as protein loading control and a representative experiment of two ( E ) and four ( D ) independent donors is shown. F Schematic representation of the experiments: short term-Upadacitinib treatment to mature macropahges (GM-MØ). Immunoblot analysis of MAFB and pGSK3S9 ( G ) and production of activin A ( H ) by GM-MØ exposed to 10–100 nM Upadacitinib for the last 48 h. GAPDH protein levels were determined as protein loading control. In ( G ) a representative experiment of three independent donors is shown. In ( H ) mean ± SEM of 5 independent donors are shown (* p < 0.05, F = 12.28). I Immunoblot analysis of MAFB in two independent preparations of differentiating GM-MØ (day 2) generated from monocytes exposed to DMSO (−), Upadacitinib (Upa, 100 nM), STAT5 phosphorylation specific inhibitor (ST5i, 50 µM) or MEK1/2 inhibitor (UO, 2,5 µM). Right, quantification of MAFB expression. J Immunoblot analysis of MAFB in two independent preparations of differentiating GM-MØ (day 2) generated from monocytes transfected with either siCNT or MAFB-specific siRNA (siMAFB) and exposed to DMSO (−) or 100 nM Upadacitinib (+). Right, quantification of MAFB expression. In panels I-J, mean ± SEM of the relative MAFB protein levels in the macrophage subtypes from four independent donors are shown (* p < 0.05, ** p < 0.01). K Relative mRNA expression of the indicated MAFB-dependent genes in siCNT GM-MØ, siMAFB GM-MØ, siCNT Upa-GM-MØ and siMAFB Upa-GM-MØ (day 2). Mean ± SEM of four independent experiments are shown (* p < 0.05; ** p < 0.01; *** p < 0.001, F = 3.7 for IL10 , F = 6.8 for CMKLR1 , F = 4.4 for LGMN , F = 56.89 for CD163 , F = 9.24 for FOLR2 , F = 8.34 for MS4A6A )

Techniques: Expressing, Comparison, RNA Sequencing, Western Blot, Control, Generated, Phospho-proteomics, Transfection

Macrophage re-programming by other JAK inhibitors A Monocytes were exposed to 10 nM Baricitinib daily during macrophage differentiation process with GM-CSF and the RNA levels were determined at day 7 on GM-MØ and 10Bari-GM-MØ. GSEA on the ranked comparison of the GM-MØ versus 10Bari-GM-MØ transcriptomes, using the genes preferentially expressed by GM-CSF (GM-MØ-specific) and M-CSF (M-MØ-specific) (GSE188278) and RA-specific clusters of synovial tissue macrophages (E-MTAB-8322) as data set. NES and FDRq value are indicated (FDRq < 0.01, dark filled circle; FDRq > 0.250, empty circle). B Production of activin A, IL-10 and LGMN by GM-MØ and 10Bari-GM-MØ. Mean ± SEM of 8–9 independent donors are shown (* p < 0.05, ** p < 0.01, one-way ANOVA with Tukey´s post hoc test). C – D Immunoblot analysis of FOLR2 ( C ) MAFB, CD163 and pGSK3S9 ( D ) by GM-MØ, 10Bari-GM-MØ, 100Bari-GM-MØ and monocytes differentiated with M-CSF (M-MØ). Vinculin and GAPDH protein levels were determined as protein loading control. A representative experiment of two ( C ) and four ( D ) independent donors is shown. E Schematic representation of the experiments: short-term Baricitinib treatment to GM-MØ. Immunoblot analysis of MAFB and pGSK3S9 ( F ) and production of activin A ( G ) by GM-MØ exposed to 10–100 nM Baricitinib for the last 48 h. GAPDH protein levels were determined as protein loading control. In ( F ) a representative experiment of three independent donors is shown. In ( G ) mean ± SEM of 5 independent donors are shown (* p < 0.05, F = 7.26). H Immunoblot analysis of MAFB and CD163 in GM-MØ (day 2) generated from monocytes exposed to DMSO (−) or 100 nM Tofacitinib (Tofa), Baricitinib (Bari), Upadacitinib (Upa), Peficitinib (Pefi), Filgotinib (Filgo) or Deucravacitinib (Deucra). A representative experiment of two independent donors is shown

Journal: Cellular and Molecular Life Sciences

Article Title: Macrophage re-programming by JAK inhibitors relies on MAFB

doi: 10.1007/s00018-024-05196-1

Figure Lengend Snippet: Macrophage re-programming by other JAK inhibitors A Monocytes were exposed to 10 nM Baricitinib daily during macrophage differentiation process with GM-CSF and the RNA levels were determined at day 7 on GM-MØ and 10Bari-GM-MØ. GSEA on the ranked comparison of the GM-MØ versus 10Bari-GM-MØ transcriptomes, using the genes preferentially expressed by GM-CSF (GM-MØ-specific) and M-CSF (M-MØ-specific) (GSE188278) and RA-specific clusters of synovial tissue macrophages (E-MTAB-8322) as data set. NES and FDRq value are indicated (FDRq < 0.01, dark filled circle; FDRq > 0.250, empty circle). B Production of activin A, IL-10 and LGMN by GM-MØ and 10Bari-GM-MØ. Mean ± SEM of 8–9 independent donors are shown (* p < 0.05, ** p < 0.01, one-way ANOVA with Tukey´s post hoc test). C – D Immunoblot analysis of FOLR2 ( C ) MAFB, CD163 and pGSK3S9 ( D ) by GM-MØ, 10Bari-GM-MØ, 100Bari-GM-MØ and monocytes differentiated with M-CSF (M-MØ). Vinculin and GAPDH protein levels were determined as protein loading control. A representative experiment of two ( C ) and four ( D ) independent donors is shown. E Schematic representation of the experiments: short-term Baricitinib treatment to GM-MØ. Immunoblot analysis of MAFB and pGSK3S9 ( F ) and production of activin A ( G ) by GM-MØ exposed to 10–100 nM Baricitinib for the last 48 h. GAPDH protein levels were determined as protein loading control. In ( F ) a representative experiment of three independent donors is shown. In ( G ) mean ± SEM of 5 independent donors are shown (* p < 0.05, F = 7.26). H Immunoblot analysis of MAFB and CD163 in GM-MØ (day 2) generated from monocytes exposed to DMSO (−) or 100 nM Tofacitinib (Tofa), Baricitinib (Bari), Upadacitinib (Upa), Peficitinib (Pefi), Filgotinib (Filgo) or Deucravacitinib (Deucra). A representative experiment of two independent donors is shown

Techniques: Comparison, Western Blot, Control, Generated

Immunofluorescence staining of inflammatory cells in pediatric kidneys. A CD68 + macrophages. B CD163 + cells. C Merge of CD68 + and CD163 + cells representing M2c-like macrophages. D CD68 + macrophages. E CD 206 + cells. F Merge CD68 + and CD206 + cells, representing M2a-like macrophages. G Renal T lymphocytes (CD3 + cells). H Renal B lymphocytes (CD20 + cells). I B and T Lymphocyte overlap (CD3 + and CD20 + cells. Scale bar represents 50 µm

Journal: Arthritis Research & Therapy

Article Title: Macrophage subpopulations in pediatric patients with lupus nephritis and other inflammatory diseases affecting the kidney

doi: 10.1186/s13075-024-03281-1

Figure Lengend Snippet: Immunofluorescence staining of inflammatory cells in pediatric kidneys. A CD68 + macrophages. B CD163 + cells. C Merge of CD68 + and CD163 + cells representing M2c-like macrophages. D CD68 + macrophages. E CD 206 + cells. F Merge CD68 + and CD206 + cells, representing M2a-like macrophages. G Renal T lymphocytes (CD3 + cells). H Renal B lymphocytes (CD20 + cells). I B and T Lymphocyte overlap (CD3 + and CD20 + cells. Scale bar represents 50 µm

Article Snippet: After blocking with normal goat serum and 1% blotto sections were incubated overnight at 4 °C using the following antibodies diluted in 1% BSA in 50 mM Tris(hydroxymethyl) aminomethan pH 7.6: iNOS, a rabbit polyclonal antibody against human iNOS (Abcam plc, Cambridge, UK); CD68, a mouse monoclonal IgG3 antibody against human CD68 (Dako Deutschland GmbH, Hamburg, Germany); CD163, a mouse monoclonal IgG1 antibody against human CD163 (Novocastra, Leica Biosystems Newcastle Ltd; Newcastle, UK); CD206, a mouse monoclonal IgG1 antibody against human CD206 (Abnova, Jhongli City, Taiwan); CD3, a monoclonal rat antibody against human CD3 (Bio-Rad AbD Serotec GmbH, Puchheim, Germany); CD20, a monoclonal mouse IgG2a antibody against human CD20 and MPO, a polyclonal rabbit antibody against myeloperoxidase (Abcam plc, Cambridge, UK).

Techniques: Immunofluorescence, Staining

Distribution of macrophage subsets in different ISN/RPS classes. A CD68 + macrophages in pediatric LN patient groups representing the total macrophages. B CD68 + CD206 − cells (M1-like macrophages) in pediatric LN patients. C CD68 + CD163 − cells (M1-like macrophages). D CD68 + as total macrophages in adult LN patients with a significant difference between groups II, V, and IV. E CD68 + CD206 − cells (M1-like macrophages) with a significant difference between groups IV and V. F CD 68 + CD163 − cells ((M1-like macrophages) ( E and F in adult LN patients). G – I Showing results for pediatric LN patients, G CD68 + CD206 + cells (M2a-like macrophages), H CD68 + CD163 + cells (M2c-like macrophages), I Ration of CD68 + CD206 − vs CD68 + CD206 + cells (M1-like macrophages and M2a-like macrophages) with a significant difference between groups II and IV. J – L representing adult LN results. J CD68 + CD206 + cells (M2a-like macrophages), K CD68 + CD163 + cells (M2c-like macrophages), with a significant difference between groups II, V, and IV. L Ration of CD68 + CD206 − vs CD68 + CD206 + cells (M1-like macrophages and M2a-like macrophages). (* p < 0.05; ** p < 0.01)

Journal: Arthritis Research & Therapy

Article Title: Macrophage subpopulations in pediatric patients with lupus nephritis and other inflammatory diseases affecting the kidney

doi: 10.1186/s13075-024-03281-1

Figure Lengend Snippet: Distribution of macrophage subsets in different ISN/RPS classes. A CD68 + macrophages in pediatric LN patient groups representing the total macrophages. B CD68 + CD206 − cells (M1-like macrophages) in pediatric LN patients. C CD68 + CD163 − cells (M1-like macrophages). D CD68 + as total macrophages in adult LN patients with a significant difference between groups II, V, and IV. E CD68 + CD206 − cells (M1-like macrophages) with a significant difference between groups IV and V. F CD 68 + CD163 − cells ((M1-like macrophages) ( E and F in adult LN patients). G – I Showing results for pediatric LN patients, G CD68 + CD206 + cells (M2a-like macrophages), H CD68 + CD163 + cells (M2c-like macrophages), I Ration of CD68 + CD206 − vs CD68 + CD206 + cells (M1-like macrophages and M2a-like macrophages) with a significant difference between groups II and IV. J – L representing adult LN results. J CD68 + CD206 + cells (M2a-like macrophages), K CD68 + CD163 + cells (M2c-like macrophages), with a significant difference between groups II, V, and IV. L Ration of CD68 + CD206 − vs CD68 + CD206 + cells (M1-like macrophages and M2a-like macrophages). (* p < 0.05; ** p < 0.01)

Techniques:

Distribution of macrophage-subtypes in pediatric LN ISN/RPN class IV in glomeruli with and without (w/o) crescents. A Representative multiple immunofluorescence staining for CD68 + and CD163 + cells using biopsies from patients with ISN/RPN class IV. B Multiple immunofluorescence staining for CD68 + , CD206 + CD20 + , and CD3 + cells using the same glomerulus imaged in ( A ) in another section. C Pie chart showing the distribution of different inflammatory cells in glomeruli from pediatric LN biopsies with ISN/RPN class IV. D MPO + cells /glomerular cross-section (GCS). E CD3 + T-cells / GCS. F Glomerular CD20 + B-cells. G Glomerular total CD68 + macrophages per GCS (first antibody panel). H Glomerular CD68 + CD206 − M1-like macrophages/ GCS. I Glomerular CD68 + CD206 + M2a-like macrophages. J Ratio of glomerular CD68 + CD206 − /CD68 + CD206 + macrophages. K glomerular total CD68 + macrophages per GCS (second antibody panel). H Glomerular CD68 + CD163 − M1-like macrophages/ GCS. I Glomerular CD68 + CD163 + M2c-like macrophages. J Ratio of glomerular CD68 + CD163 − /CD68 + CD163 + macrophages. (* p < 0,05). Scale bar represents 50 µm

Journal: Arthritis Research & Therapy

Article Title: Macrophage subpopulations in pediatric patients with lupus nephritis and other inflammatory diseases affecting the kidney

doi: 10.1186/s13075-024-03281-1

Figure Lengend Snippet: Distribution of macrophage-subtypes in pediatric LN ISN/RPN class IV in glomeruli with and without (w/o) crescents. A Representative multiple immunofluorescence staining for CD68 + and CD163 + cells using biopsies from patients with ISN/RPN class IV. B Multiple immunofluorescence staining for CD68 + , CD206 + CD20 + , and CD3 + cells using the same glomerulus imaged in ( A ) in another section. C Pie chart showing the distribution of different inflammatory cells in glomeruli from pediatric LN biopsies with ISN/RPN class IV. D MPO + cells /glomerular cross-section (GCS). E CD3 + T-cells / GCS. F Glomerular CD20 + B-cells. G Glomerular total CD68 + macrophages per GCS (first antibody panel). H Glomerular CD68 + CD206 − M1-like macrophages/ GCS. I Glomerular CD68 + CD206 + M2a-like macrophages. J Ratio of glomerular CD68 + CD206 − /CD68 + CD206 + macrophages. K glomerular total CD68 + macrophages per GCS (second antibody panel). H Glomerular CD68 + CD163 − M1-like macrophages/ GCS. I Glomerular CD68 + CD163 + M2c-like macrophages. J Ratio of glomerular CD68 + CD163 − /CD68 + CD163 + macrophages. (* p < 0,05). Scale bar represents 50 µm

Techniques: Immunofluorescence, Staining

Distribution of macrophage-subtypes in pediatric LN and a pediatric control group consisting of HUS, MPGN, PI-GN and PAUCI patients. A CD68 + total macrophages in the inflammatory kidney in pediatric patients with significantly higher in PAUCI patients compared to the LN and control group. B CD68 + CD206 − M1-like macrophages significantly higher in pediatric PAUCI patients compared to all other study groups. C CD68 + CD163 − M1-like macrophages significantly higher in PAUCI than in LN patients. D CD68 + CD206 + M2a-like macrophages, significantly higher in PAUCI than in LN patients. E CD68 + CD163 + M2c-like macrophages, significantly higher in HUS pediatric patients compared to MPGN, LN patients and our pediatric control group. F Ratio of CD68 + CD206 − and CD68 + CD206 + (M1-like and M2a-like macrophages) in pediatric patients. (* p < 0.05; ** p < 0.01)

Journal: Arthritis Research & Therapy

Article Title: Macrophage subpopulations in pediatric patients with lupus nephritis and other inflammatory diseases affecting the kidney

doi: 10.1186/s13075-024-03281-1

Figure Lengend Snippet: Distribution of macrophage-subtypes in pediatric LN and a pediatric control group consisting of HUS, MPGN, PI-GN and PAUCI patients. A CD68 + total macrophages in the inflammatory kidney in pediatric patients with significantly higher in PAUCI patients compared to the LN and control group. B CD68 + CD206 − M1-like macrophages significantly higher in pediatric PAUCI patients compared to all other study groups. C CD68 + CD163 − M1-like macrophages significantly higher in PAUCI than in LN patients. D CD68 + CD206 + M2a-like macrophages, significantly higher in PAUCI than in LN patients. E CD68 + CD163 + M2c-like macrophages, significantly higher in HUS pediatric patients compared to MPGN, LN patients and our pediatric control group. F Ratio of CD68 + CD206 − and CD68 + CD206 + (M1-like and M2a-like macrophages) in pediatric patients. (* p < 0.05; ** p < 0.01)

Techniques:

Clustering analysis of the abundance of inflammatory cells in different inflammatory kidney diseases in pediatric patients. Heatmap of the numbers of CD68 + CD163 + , CD68 + CD206 + , CD68 + CD163 − , CD68 + CD206 − , CD3 + , CD20 + , and MPO + cells in the analyzed patients (red: high number; blue: low number). The color-coded bar corresponding to the different rows (patients) indicates the diagnosis

Journal: Arthritis Research & Therapy

Article Title: Macrophage subpopulations in pediatric patients with lupus nephritis and other inflammatory diseases affecting the kidney

doi: 10.1186/s13075-024-03281-1

Figure Lengend Snippet: Clustering analysis of the abundance of inflammatory cells in different inflammatory kidney diseases in pediatric patients. Heatmap of the numbers of CD68 + CD163 + , CD68 + CD206 + , CD68 + CD163 − , CD68 + CD206 − , CD3 + , CD20 + , and MPO + cells in the analyzed patients (red: high number; blue: low number). The color-coded bar corresponding to the different rows (patients) indicates the diagnosis

Techniques:

Journal: Immunobiology

Article Title: CD163 overexpression using a macrophage-directed gene therapy approach improves wound healing in ex vivo and in vivo human skin models.

doi: 10.1016/j.imbio.2019.10.011

Figure Lengend Snippet: Primers used for qRT-PCR analyses.

Article Snippet: A mouse antibody against human CD163 (Serotec, Raleigh, NC, 1:150) was added and left in the preparation overnight at 4°C.

Techniques:

mRNA levels of CD163 in THP-1 macrophages and human primary macrophages transfected with a plasmid that encodes the CD163 gene (pCD163) or an Empty vector (pEmpty) following 48 hours of transfection. Representative microscopic images of nuclear staining using DAPI (blue) and CD163 protein (red) in THP-1 macrophages and human primary macrophages transfected with pEmpty or pCD163 for 48 hours (B). Quantification of the average of fluorescence of CD163 in THP-1 macrophages and human primary macrophages transfected with pEmpty or pCD163 for 48 hours (C). Scale bar = 100 μm. N= 3-6 per group. *p<0.05 pEmpty vs. pCD163 groups, by student’s t test.1.5-column fitting image.

Journal: Immunobiology

Article Title: CD163 overexpression using a macrophage-directed gene therapy approach improves wound healing in ex vivo and in vivo human skin models.

doi: 10.1016/j.imbio.2019.10.011

Figure Lengend Snippet: mRNA levels of CD163 in THP-1 macrophages and human primary macrophages transfected with a plasmid that encodes the CD163 gene (pCD163) or an Empty vector (pEmpty) following 48 hours of transfection. Representative microscopic images of nuclear staining using DAPI (blue) and CD163 protein (red) in THP-1 macrophages and human primary macrophages transfected with pEmpty or pCD163 for 48 hours (B). Quantification of the average of fluorescence of CD163 in THP-1 macrophages and human primary macrophages transfected with pEmpty or pCD163 for 48 hours (C). Scale bar = 100 μm. N= 3-6 per group. *p<0.05 pEmpty vs. pCD163 groups, by student’s t test.1.5-column fitting image.

Article Snippet: A mouse antibody against human CD163 (Serotec, Raleigh, NC, 1:150) was added and left in the preparation overnight at 4°C.

Techniques: Transfection, Plasmid Preparation, Staining, Fluorescence

A) Quantification of wound closure (%) in tissues without treatment (baseline, control on day 0) and in tissues in the presence of LPS-stimulated macrophages transfected with a plasmid that encodes the CD163 gene (pCD163) or an Empty vector (pEmpty) on days 1, 3 and 6 after macrophage addition. B) Representative microscopic images (5X) depicting epithelization on day 1 after the addition of macrophages transfected with pEmpty or pCD163. N= 3-4 per group. *P<0.05 pEmpty vs. M-pCD163 group, by student’s t-test. 1.5-column fitting image

Journal: Immunobiology

Article Title: CD163 overexpression using a macrophage-directed gene therapy approach improves wound healing in ex vivo and in vivo human skin models.

doi: 10.1016/j.imbio.2019.10.011

Figure Lengend Snippet: A) Quantification of wound closure (%) in tissues without treatment (baseline, control on day 0) and in tissues in the presence of LPS-stimulated macrophages transfected with a plasmid that encodes the CD163 gene (pCD163) or an Empty vector (pEmpty) on days 1, 3 and 6 after macrophage addition. B) Representative microscopic images (5X) depicting epithelization on day 1 after the addition of macrophages transfected with pEmpty or pCD163. N= 3-4 per group. *P<0.05 pEmpty vs. M-pCD163 group, by student’s t-test. 1.5-column fitting image

Article Snippet: A mouse antibody against human CD163 (Serotec, Raleigh, NC, 1:150) was added and left in the preparation overnight at 4°C.

Techniques: Transfection, Plasmid Preparation

A) Quantification of the wound closure (%) in tissues in the presence of LPS-stimulated macrophages transfected with a plasmid that encodes the CD163 gene (pCD163) or an Empty vector (pEmpty) on days 1 and 3 after macrophage addition. B) Representative microscopic images (5X) depicting epithelization on day 3 after the addition of macrophages transfected with pEmpty or pCD163. N= 3-4 per group. *P<0.05 M-pEmpty vs. M-pCD163 group, by student’s t-test. 1.5-column fitting image

Journal: Immunobiology

Article Title: CD163 overexpression using a macrophage-directed gene therapy approach improves wound healing in ex vivo and in vivo human skin models.

doi: 10.1016/j.imbio.2019.10.011

Figure Lengend Snippet: A) Quantification of the wound closure (%) in tissues in the presence of LPS-stimulated macrophages transfected with a plasmid that encodes the CD163 gene (pCD163) or an Empty vector (pEmpty) on days 1 and 3 after macrophage addition. B) Representative microscopic images (5X) depicting epithelization on day 3 after the addition of macrophages transfected with pEmpty or pCD163. N= 3-4 per group. *P<0.05 M-pEmpty vs. M-pCD163 group, by student’s t-test. 1.5-column fitting image

Article Snippet: A mouse antibody against human CD163 (Serotec, Raleigh, NC, 1:150) was added and left in the preparation overnight at 4°C.

Techniques: Transfection, Plasmid Preparation

Representative microscopic images (A, B) and quantification of epithelium thickness across the tissue wound (C) in the presence of LPS-stimulated human primary macrophages transfected with a plasmid that encodes the CD163 gene (pCD163) or an Empty vector (pEmpty) on day 3 after macrophage addition. The area under the curve (AUC) was calculated in every tissue and compared in both conditions (D). Scale bars = 50 μm (A, B) and 25 μm (Aa, Ab, Ba and Bb insets). The empty arrowhead indicates the absence of epithelium (Aa inset) and the solid black arrowheads and brackets (Ab, Ba and Bb insets) indicate the epithelium thickness in both conditions. N=6 per group. *P<0.05 M-pEmpty vs. M-pCD163 groups, by student’s t-test. 1.5-column fitting image

Journal: Immunobiology

Article Title: CD163 overexpression using a macrophage-directed gene therapy approach improves wound healing in ex vivo and in vivo human skin models.

doi: 10.1016/j.imbio.2019.10.011

Figure Lengend Snippet: Representative microscopic images (A, B) and quantification of epithelium thickness across the tissue wound (C) in the presence of LPS-stimulated human primary macrophages transfected with a plasmid that encodes the CD163 gene (pCD163) or an Empty vector (pEmpty) on day 3 after macrophage addition. The area under the curve (AUC) was calculated in every tissue and compared in both conditions (D). Scale bars = 50 μm (A, B) and 25 μm (Aa, Ab, Ba and Bb insets). The empty arrowhead indicates the absence of epithelium (Aa inset) and the solid black arrowheads and brackets (Ab, Ba and Bb insets) indicate the epithelium thickness in both conditions. N=6 per group. *P<0.05 M-pEmpty vs. M-pCD163 groups, by student’s t-test. 1.5-column fitting image

Article Snippet: A mouse antibody against human CD163 (Serotec, Raleigh, NC, 1:150) was added and left in the preparation overnight at 4°C.

Techniques: Transfection, Plasmid Preparation

Time course of the migration healing progression of K + F alone (control) or in the presence of LPS-stimulated human primary macrophages transfected with a plasmid that encodes the CD163 gene (M-pCD163) or an Empty vector (M-pEmpty) cultures at 0, 12, 15, 17 and 19 hours after the scratch (A). Comparison of wound healing (%) between K + F alone (control) or in the presence of M-pEmpty or M-pCD163 at 17 and 19 hours after the scratch (B). N = 10-16 per group. #p<0.05 Control vs. M-pEmpty or M-pCD163; *p<0.05 M-pEmpty vs. M-pCD163, by Two-way ANOVA and Bonferroni post-test. single-column fitting image

Journal: Immunobiology

Article Title: CD163 overexpression using a macrophage-directed gene therapy approach improves wound healing in ex vivo and in vivo human skin models.

doi: 10.1016/j.imbio.2019.10.011

Figure Lengend Snippet: Time course of the migration healing progression of K + F alone (control) or in the presence of LPS-stimulated human primary macrophages transfected with a plasmid that encodes the CD163 gene (M-pCD163) or an Empty vector (M-pEmpty) cultures at 0, 12, 15, 17 and 19 hours after the scratch (A). Comparison of wound healing (%) between K + F alone (control) or in the presence of M-pEmpty or M-pCD163 at 17 and 19 hours after the scratch (B). N = 10-16 per group. #p<0.05 Control vs. M-pEmpty or M-pCD163; *p<0.05 M-pEmpty vs. M-pCD163, by Two-way ANOVA and Bonferroni post-test. single-column fitting image

Article Snippet: A mouse antibody against human CD163 (Serotec, Raleigh, NC, 1:150) was added and left in the preparation overnight at 4°C.

Techniques: Migration, Transfection, Plasmid Preparation

Quantification for IL-6 (A), MCP-1 (B), TGF-α (C), and TGF-β (D) protein concentration in keratinocytes + fibroblasts in the presence of LPS-stimulated THP-1 macrophages transfected with a plasmid that encodes the CD163 gene (M-pCD163) or an Empty vector (M-pEmpty). N= 5-9/group. *P<0.05 M-pEmpty vs. M-pCD163 groups, by student’s t-test. 1.5-column fitting image

Journal: Immunobiology

Article Title: CD163 overexpression using a macrophage-directed gene therapy approach improves wound healing in ex vivo and in vivo human skin models.

doi: 10.1016/j.imbio.2019.10.011

Figure Lengend Snippet: Quantification for IL-6 (A), MCP-1 (B), TGF-α (C), and TGF-β (D) protein concentration in keratinocytes + fibroblasts in the presence of LPS-stimulated THP-1 macrophages transfected with a plasmid that encodes the CD163 gene (M-pCD163) or an Empty vector (M-pEmpty). N= 5-9/group. *P<0.05 M-pEmpty vs. M-pCD163 groups, by student’s t-test. 1.5-column fitting image

Article Snippet: A mouse antibody against human CD163 (Serotec, Raleigh, NC, 1:150) was added and left in the preparation overnight at 4°C.

Techniques: Protein Concentration, Transfection, Plasmid Preparation

THP-1 macrophages were stimulated with LPS and non-transfected (macrophage) or transfected with a plasmid that encodes the CD163 gene (M-pCD163) or an Empty vector (M-pEmpty). Following 66 hours of transfection (and 17 hours after the scratch), the levels of CD163 mRNA were determined in K +F alone (control) or co-cultured with THP-1 macrophages (A) by RT-PCR. The CD11b mRNA expression was not detected in K + F alone (control) (B). The CD163 and CD11b mRNA expressions were normalized to the respective levels of β-actin expression in each group. Then all values were normalized to 1 against K+F+M-pEmtpy group at 17 hours after the scratch. Representative microscopic images of nuclear staining using DAPI (blue) and CD163 protein (red) in K + F alone (control) or co-cultured with M-pCD163 or M-pEmpty (C). Quantification of the average of fluorescence of CD163 at 17 hours after the scratch (D). The quantification of average of intensity was normalized to 1 against K + F alone (control) group. N= 13-16 (A); 5-6 (B); 8-15 (D) per group. *p<0.05 K+F+M-pEmpty vs. K+F+M-pCD163 group, by One-way ANOVA and Bonferroni post-test. 1.5-column fitting image

Journal: Immunobiology

Article Title: CD163 overexpression using a macrophage-directed gene therapy approach improves wound healing in ex vivo and in vivo human skin models.

doi: 10.1016/j.imbio.2019.10.011

Figure Lengend Snippet: THP-1 macrophages were stimulated with LPS and non-transfected (macrophage) or transfected with a plasmid that encodes the CD163 gene (M-pCD163) or an Empty vector (M-pEmpty). Following 66 hours of transfection (and 17 hours after the scratch), the levels of CD163 mRNA were determined in K +F alone (control) or co-cultured with THP-1 macrophages (A) by RT-PCR. The CD11b mRNA expression was not detected in K + F alone (control) (B). The CD163 and CD11b mRNA expressions were normalized to the respective levels of β-actin expression in each group. Then all values were normalized to 1 against K+F+M-pEmtpy group at 17 hours after the scratch. Representative microscopic images of nuclear staining using DAPI (blue) and CD163 protein (red) in K + F alone (control) or co-cultured with M-pCD163 or M-pEmpty (C). Quantification of the average of fluorescence of CD163 at 17 hours after the scratch (D). The quantification of average of intensity was normalized to 1 against K + F alone (control) group. N= 13-16 (A); 5-6 (B); 8-15 (D) per group. *p<0.05 K+F+M-pEmpty vs. K+F+M-pCD163 group, by One-way ANOVA and Bonferroni post-test. 1.5-column fitting image

Article Snippet: A mouse antibody against human CD163 (Serotec, Raleigh, NC, 1:150) was added and left in the preparation overnight at 4°C.

Techniques: Transfection, Plasmid Preparation, Cell Culture, Reverse Transcription Polymerase Chain Reaction, Expressing, Staining, Fluorescence

Time course of the migration healing progression of K + F in the presence of LPS-stimulated macrophages transfected with a plasmid that encodes the CD163 gene (M-pCD163) or an Empty vector (M-pEmpty) untreated (alone) or treated with CD163 antibody (Ab) or its isotype control-mouse IgG1 (Iso) at 0, 12, 15 and 17 hours after the scratch (A). Representative microscopic images (pixels in red) of K+F+M-pCD163 group untreated (alone) or treated (Ab or Iso) at 17 hours after the scratch (B). Comparison of wound healing (%) in untreated (alone) or treated (Ab or Iso) groups at 17 hours after the scratch (C). The closure of the scratch gap (scratch width) was measured in pixels. N= 12 per group. *p<0.05 M-pCD163 alone vs. M-pEmpty alone or M-pCD163 Ab; #p<0.05 M-pCD163 Iso vs. M-pCD163 Ab, by Two-way ANOVA and Bonferroni post-test. 1.5-column fitting image

Journal: Immunobiology

Article Title: CD163 overexpression using a macrophage-directed gene therapy approach improves wound healing in ex vivo and in vivo human skin models.

doi: 10.1016/j.imbio.2019.10.011

Figure Lengend Snippet: Time course of the migration healing progression of K + F in the presence of LPS-stimulated macrophages transfected with a plasmid that encodes the CD163 gene (M-pCD163) or an Empty vector (M-pEmpty) untreated (alone) or treated with CD163 antibody (Ab) or its isotype control-mouse IgG1 (Iso) at 0, 12, 15 and 17 hours after the scratch (A). Representative microscopic images (pixels in red) of K+F+M-pCD163 group untreated (alone) or treated (Ab or Iso) at 17 hours after the scratch (B). Comparison of wound healing (%) in untreated (alone) or treated (Ab or Iso) groups at 17 hours after the scratch (C). The closure of the scratch gap (scratch width) was measured in pixels. N= 12 per group. *p<0.05 M-pCD163 alone vs. M-pEmpty alone or M-pCD163 Ab; #p<0.05 M-pCD163 Iso vs. M-pCD163 Ab, by Two-way ANOVA and Bonferroni post-test. 1.5-column fitting image

Article Snippet: A mouse antibody against human CD163 (Serotec, Raleigh, NC, 1:150) was added and left in the preparation overnight at 4°C.

Techniques: Migration, Transfection, Plasmid Preparation

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