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anti human mouse cd11b apc cy7  (Cytek Biosciences)


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    Structured Review

    Cytek Biosciences anti human mouse cd11b apc cy7
    (A) Overview of single dose paradigm where tumors are harvested 48 h after a single dose of aPD1 or isotype control in order to capture the initial effects of treatment. (B) UMAP plot depicting an overview of heterogeneity in single-cell transcriptomes derived from responder and non-responder strain tumors and highlighting the T/NK cell cluster. (C) Subclustering of the T/NK cell cluster reveals transcriptionally distinct cell subsets showing enrichment of subclusters 3 and 13 in responding tumors. (D) Fraction of exhausted CTLs (cluster 3) as portion of all cells in responder and non-responder strain groups, Wilcoxon test, *** p < 0.001, * p < 0.05, respectively. (E) Fraction of IFN-γ + CTLs (cluster 13) as portion of all cells in responder and non-responder strain groups, Wilcoxon test, ** p < 0.01; n.s., not significant, respectively. (F) Expression of an 18-gene signature reflecting IFN-γ + stimulation applied to all cells in each cluster (left) or macrophage subcluster (right), with dot size proportional to the relative number of cells of each type, dot color relative to the median IFN-γ + stimulation score, and bars depicting the difference in summed pathway score between responder and non-responder cells within each (sub)cluster. (G) Fraction of IFN-γ-stimulated macrophage clusters (clusters 2, 5, and 26) as a portion of all cells in responder and non-responder strain groups, Wilcoxon test, **** p < 0.0001, * p < 0.05, respectively. (H) Visium spatial transcriptomics images showing expression of CD45 ( Ptprc ) (top row) and Cxcl9 (bottom row) in spatially resolved spots of tumors harvested from responder (CC75F1) and non-responder (CC80F1) mouse tumors. Hematoxylin and eosin stains showed no evidence of necrosis in these tumor sections. (I) Percentage of Ptprc + spatial transcriptomics spots co-expressing either macrophage lineage markers ( Adgre1, Cd68, <t>Itgam</t> , and Cxcl9 ) or dendritic cell markers (Batf3 and/or Zbtb46) along with CTL markers ( Thy1, Cd8a , and Gzmb ) across all tissue regions in responder vs. non-responder strain tumors. **** p < 0.0001, permutation test (see ). See also .
    Anti Human Mouse Cd11b Apc Cy7, supplied by Cytek Biosciences, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response"

    Article Title: Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response

    Journal: Cell reports

    doi: 10.1016/j.celrep.2025.115698

    (A) Overview of single dose paradigm where tumors are harvested 48 h after a single dose of aPD1 or isotype control in order to capture the initial effects of treatment. (B) UMAP plot depicting an overview of heterogeneity in single-cell transcriptomes derived from responder and non-responder strain tumors and highlighting the T/NK cell cluster. (C) Subclustering of the T/NK cell cluster reveals transcriptionally distinct cell subsets showing enrichment of subclusters 3 and 13 in responding tumors. (D) Fraction of exhausted CTLs (cluster 3) as portion of all cells in responder and non-responder strain groups, Wilcoxon test, *** p < 0.001, * p < 0.05, respectively. (E) Fraction of IFN-γ + CTLs (cluster 13) as portion of all cells in responder and non-responder strain groups, Wilcoxon test, ** p < 0.01; n.s., not significant, respectively. (F) Expression of an 18-gene signature reflecting IFN-γ + stimulation applied to all cells in each cluster (left) or macrophage subcluster (right), with dot size proportional to the relative number of cells of each type, dot color relative to the median IFN-γ + stimulation score, and bars depicting the difference in summed pathway score between responder and non-responder cells within each (sub)cluster. (G) Fraction of IFN-γ-stimulated macrophage clusters (clusters 2, 5, and 26) as a portion of all cells in responder and non-responder strain groups, Wilcoxon test, **** p < 0.0001, * p < 0.05, respectively. (H) Visium spatial transcriptomics images showing expression of CD45 ( Ptprc ) (top row) and Cxcl9 (bottom row) in spatially resolved spots of tumors harvested from responder (CC75F1) and non-responder (CC80F1) mouse tumors. Hematoxylin and eosin stains showed no evidence of necrosis in these tumor sections. (I) Percentage of Ptprc + spatial transcriptomics spots co-expressing either macrophage lineage markers ( Adgre1, Cd68, Itgam , and Cxcl9 ) or dendritic cell markers (Batf3 and/or Zbtb46) along with CTL markers ( Thy1, Cd8a , and Gzmb ) across all tissue regions in responder vs. non-responder strain tumors. **** p < 0.0001, permutation test (see ). See also .
    Figure Legend Snippet: (A) Overview of single dose paradigm where tumors are harvested 48 h after a single dose of aPD1 or isotype control in order to capture the initial effects of treatment. (B) UMAP plot depicting an overview of heterogeneity in single-cell transcriptomes derived from responder and non-responder strain tumors and highlighting the T/NK cell cluster. (C) Subclustering of the T/NK cell cluster reveals transcriptionally distinct cell subsets showing enrichment of subclusters 3 and 13 in responding tumors. (D) Fraction of exhausted CTLs (cluster 3) as portion of all cells in responder and non-responder strain groups, Wilcoxon test, *** p < 0.001, * p < 0.05, respectively. (E) Fraction of IFN-γ + CTLs (cluster 13) as portion of all cells in responder and non-responder strain groups, Wilcoxon test, ** p < 0.01; n.s., not significant, respectively. (F) Expression of an 18-gene signature reflecting IFN-γ + stimulation applied to all cells in each cluster (left) or macrophage subcluster (right), with dot size proportional to the relative number of cells of each type, dot color relative to the median IFN-γ + stimulation score, and bars depicting the difference in summed pathway score between responder and non-responder cells within each (sub)cluster. (G) Fraction of IFN-γ-stimulated macrophage clusters (clusters 2, 5, and 26) as a portion of all cells in responder and non-responder strain groups, Wilcoxon test, **** p < 0.0001, * p < 0.05, respectively. (H) Visium spatial transcriptomics images showing expression of CD45 ( Ptprc ) (top row) and Cxcl9 (bottom row) in spatially resolved spots of tumors harvested from responder (CC75F1) and non-responder (CC80F1) mouse tumors. Hematoxylin and eosin stains showed no evidence of necrosis in these tumor sections. (I) Percentage of Ptprc + spatial transcriptomics spots co-expressing either macrophage lineage markers ( Adgre1, Cd68, Itgam , and Cxcl9 ) or dendritic cell markers (Batf3 and/or Zbtb46) along with CTL markers ( Thy1, Cd8a , and Gzmb ) across all tissue regions in responder vs. non-responder strain tumors. **** p < 0.0001, permutation test (see ). See also .

    Techniques Used: Control, Derivative Assay, Expressing



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    Cytek Biosciences anti human mouse cd11b apc cy7
    (A) Overview of single dose paradigm where tumors are harvested 48 h after a single dose of aPD1 or isotype control in order to capture the initial effects of treatment. (B) UMAP plot depicting an overview of heterogeneity in single-cell transcriptomes derived from responder and non-responder strain tumors and highlighting the T/NK cell cluster. (C) Subclustering of the T/NK cell cluster reveals transcriptionally distinct cell subsets showing enrichment of subclusters 3 and 13 in responding tumors. (D) Fraction of exhausted CTLs (cluster 3) as portion of all cells in responder and non-responder strain groups, Wilcoxon test, *** p < 0.001, * p < 0.05, respectively. (E) Fraction of IFN-γ + CTLs (cluster 13) as portion of all cells in responder and non-responder strain groups, Wilcoxon test, ** p < 0.01; n.s., not significant, respectively. (F) Expression of an 18-gene signature reflecting IFN-γ + stimulation applied to all cells in each cluster (left) or macrophage subcluster (right), with dot size proportional to the relative number of cells of each type, dot color relative to the median IFN-γ + stimulation score, and bars depicting the difference in summed pathway score between responder and non-responder cells within each (sub)cluster. (G) Fraction of IFN-γ-stimulated macrophage clusters (clusters 2, 5, and 26) as a portion of all cells in responder and non-responder strain groups, Wilcoxon test, **** p < 0.0001, * p < 0.05, respectively. (H) Visium spatial transcriptomics images showing expression of CD45 ( Ptprc ) (top row) and Cxcl9 (bottom row) in spatially resolved spots of tumors harvested from responder (CC75F1) and non-responder (CC80F1) mouse tumors. Hematoxylin and eosin stains showed no evidence of necrosis in these tumor sections. (I) Percentage of Ptprc + spatial transcriptomics spots co-expressing either macrophage lineage markers ( Adgre1, Cd68, <t>Itgam</t> , and Cxcl9 ) or dendritic cell markers (Batf3 and/or Zbtb46) along with CTL markers ( Thy1, Cd8a , and Gzmb ) across all tissue regions in responder vs. non-responder strain tumors. **** p < 0.0001, permutation test (see ). See also .
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    (A) Overview of single dose paradigm where tumors are harvested 48 h after a single dose of aPD1 or isotype control in order to capture the initial effects of treatment. (B) UMAP plot depicting an overview of heterogeneity in single-cell transcriptomes derived from responder and non-responder strain tumors and highlighting the T/NK cell cluster. (C) Subclustering of the T/NK cell cluster reveals transcriptionally distinct cell subsets showing enrichment of subclusters 3 and 13 in responding tumors. (D) Fraction of exhausted CTLs (cluster 3) as portion of all cells in responder and non-responder strain groups, Wilcoxon test, *** p < 0.001, * p < 0.05, respectively. (E) Fraction of IFN-γ + CTLs (cluster 13) as portion of all cells in responder and non-responder strain groups, Wilcoxon test, ** p < 0.01; n.s., not significant, respectively. (F) Expression of an 18-gene signature reflecting IFN-γ + stimulation applied to all cells in each cluster (left) or macrophage subcluster (right), with dot size proportional to the relative number of cells of each type, dot color relative to the median IFN-γ + stimulation score, and bars depicting the difference in summed pathway score between responder and non-responder cells within each (sub)cluster. (G) Fraction of IFN-γ-stimulated macrophage clusters (clusters 2, 5, and 26) as a portion of all cells in responder and non-responder strain groups, Wilcoxon test, **** p < 0.0001, * p < 0.05, respectively. (H) Visium spatial transcriptomics images showing expression of CD45 ( Ptprc ) (top row) and Cxcl9 (bottom row) in spatially resolved spots of tumors harvested from responder (CC75F1) and non-responder (CC80F1) mouse tumors. Hematoxylin and eosin stains showed no evidence of necrosis in these tumor sections. (I) Percentage of Ptprc + spatial transcriptomics spots co-expressing either macrophage lineage markers ( Adgre1, Cd68, <t>Itgam</t> , and Cxcl9 ) or dendritic cell markers (Batf3 and/or Zbtb46) along with CTL markers ( Thy1, Cd8a , and Gzmb ) across all tissue regions in responder vs. non-responder strain tumors. **** p < 0.0001, permutation test (see ). See also .
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    (A) Overview of single dose paradigm where tumors are harvested 48 h after a single dose of aPD1 or isotype control in order to capture the initial effects of treatment. (B) UMAP plot depicting an overview of heterogeneity in single-cell transcriptomes derived from responder and non-responder strain tumors and highlighting the T/NK cell cluster. (C) Subclustering of the T/NK cell cluster reveals transcriptionally distinct cell subsets showing enrichment of subclusters 3 and 13 in responding tumors. (D) Fraction of exhausted CTLs (cluster 3) as portion of all cells in responder and non-responder strain groups, Wilcoxon test, *** p < 0.001, * p < 0.05, respectively. (E) Fraction of IFN-γ + CTLs (cluster 13) as portion of all cells in responder and non-responder strain groups, Wilcoxon test, ** p < 0.01; n.s., not significant, respectively. (F) Expression of an 18-gene signature reflecting IFN-γ + stimulation applied to all cells in each cluster (left) or macrophage subcluster (right), with dot size proportional to the relative number of cells of each type, dot color relative to the median IFN-γ + stimulation score, and bars depicting the difference in summed pathway score between responder and non-responder cells within each (sub)cluster. (G) Fraction of IFN-γ-stimulated macrophage clusters (clusters 2, 5, and 26) as a portion of all cells in responder and non-responder strain groups, Wilcoxon test, **** p < 0.0001, * p < 0.05, respectively. (H) Visium spatial transcriptomics images showing expression of CD45 ( Ptprc ) (top row) and Cxcl9 (bottom row) in spatially resolved spots of tumors harvested from responder (CC75F1) and non-responder (CC80F1) mouse tumors. Hematoxylin and eosin stains showed no evidence of necrosis in these tumor sections. (I) Percentage of Ptprc + spatial transcriptomics spots co-expressing either macrophage lineage markers ( Adgre1, Cd68, <t>Itgam</t> , and Cxcl9 ) or dendritic cell markers (Batf3 and/or Zbtb46) along with CTL markers ( Thy1, Cd8a , and Gzmb ) across all tissue regions in responder vs. non-responder strain tumors. **** p < 0.0001, permutation test (see ). See also .
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    PBMCs were isolated and cultured for 24 hours with green fluorescent protein (GFP)+ microparticles, and then washed, stained, and analyzed by flow cytometry. A , Cells that internalize or bind to GFP+ microparticles (right) exhibit green fluorescence compared to cells not treated with microparticles (left). B , Cells were gated on GFP and then subgated on <t>CD11b,</t> followed by CD3 and CD19 to identify specific cell types. C , PBMCs from three representative donors demonstrate that the majority of the GFP positive cells are positive for CD11b (white boxes). D , Ten times more microparticles were added to PBMCs (High MP∶target) to identify the any other subpopulation to internalize microparticles. One representative donor PBMC demonstrates that CD3+ cells (grey boxes) were the second cell type to internalize microparticles according to percentage (left) and numbers (right) of GFP-positive PBMCs.
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    Image Search Results


    (A) Overview of single dose paradigm where tumors are harvested 48 h after a single dose of aPD1 or isotype control in order to capture the initial effects of treatment. (B) UMAP plot depicting an overview of heterogeneity in single-cell transcriptomes derived from responder and non-responder strain tumors and highlighting the T/NK cell cluster. (C) Subclustering of the T/NK cell cluster reveals transcriptionally distinct cell subsets showing enrichment of subclusters 3 and 13 in responding tumors. (D) Fraction of exhausted CTLs (cluster 3) as portion of all cells in responder and non-responder strain groups, Wilcoxon test, *** p < 0.001, * p < 0.05, respectively. (E) Fraction of IFN-γ + CTLs (cluster 13) as portion of all cells in responder and non-responder strain groups, Wilcoxon test, ** p < 0.01; n.s., not significant, respectively. (F) Expression of an 18-gene signature reflecting IFN-γ + stimulation applied to all cells in each cluster (left) or macrophage subcluster (right), with dot size proportional to the relative number of cells of each type, dot color relative to the median IFN-γ + stimulation score, and bars depicting the difference in summed pathway score between responder and non-responder cells within each (sub)cluster. (G) Fraction of IFN-γ-stimulated macrophage clusters (clusters 2, 5, and 26) as a portion of all cells in responder and non-responder strain groups, Wilcoxon test, **** p < 0.0001, * p < 0.05, respectively. (H) Visium spatial transcriptomics images showing expression of CD45 ( Ptprc ) (top row) and Cxcl9 (bottom row) in spatially resolved spots of tumors harvested from responder (CC75F1) and non-responder (CC80F1) mouse tumors. Hematoxylin and eosin stains showed no evidence of necrosis in these tumor sections. (I) Percentage of Ptprc + spatial transcriptomics spots co-expressing either macrophage lineage markers ( Adgre1, Cd68, Itgam , and Cxcl9 ) or dendritic cell markers (Batf3 and/or Zbtb46) along with CTL markers ( Thy1, Cd8a , and Gzmb ) across all tissue regions in responder vs. non-responder strain tumors. **** p < 0.0001, permutation test (see ). See also .

    Journal: Cell reports

    Article Title: Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response

    doi: 10.1016/j.celrep.2025.115698

    Figure Lengend Snippet: (A) Overview of single dose paradigm where tumors are harvested 48 h after a single dose of aPD1 or isotype control in order to capture the initial effects of treatment. (B) UMAP plot depicting an overview of heterogeneity in single-cell transcriptomes derived from responder and non-responder strain tumors and highlighting the T/NK cell cluster. (C) Subclustering of the T/NK cell cluster reveals transcriptionally distinct cell subsets showing enrichment of subclusters 3 and 13 in responding tumors. (D) Fraction of exhausted CTLs (cluster 3) as portion of all cells in responder and non-responder strain groups, Wilcoxon test, *** p < 0.001, * p < 0.05, respectively. (E) Fraction of IFN-γ + CTLs (cluster 13) as portion of all cells in responder and non-responder strain groups, Wilcoxon test, ** p < 0.01; n.s., not significant, respectively. (F) Expression of an 18-gene signature reflecting IFN-γ + stimulation applied to all cells in each cluster (left) or macrophage subcluster (right), with dot size proportional to the relative number of cells of each type, dot color relative to the median IFN-γ + stimulation score, and bars depicting the difference in summed pathway score between responder and non-responder cells within each (sub)cluster. (G) Fraction of IFN-γ-stimulated macrophage clusters (clusters 2, 5, and 26) as a portion of all cells in responder and non-responder strain groups, Wilcoxon test, **** p < 0.0001, * p < 0.05, respectively. (H) Visium spatial transcriptomics images showing expression of CD45 ( Ptprc ) (top row) and Cxcl9 (bottom row) in spatially resolved spots of tumors harvested from responder (CC75F1) and non-responder (CC80F1) mouse tumors. Hematoxylin and eosin stains showed no evidence of necrosis in these tumor sections. (I) Percentage of Ptprc + spatial transcriptomics spots co-expressing either macrophage lineage markers ( Adgre1, Cd68, Itgam , and Cxcl9 ) or dendritic cell markers (Batf3 and/or Zbtb46) along with CTL markers ( Thy1, Cd8a , and Gzmb ) across all tissue regions in responder vs. non-responder strain tumors. **** p < 0.0001, permutation test (see ). See also .

    Article Snippet: Anti-Human/Mouse CD11b APC-Cy7 (clone M1/70) , Tonbo Biosciences , CAT#25-0112; RRID:AB_2621625.

    Techniques: Control, Derivative Assay, Expressing

    Journal: iScience

    Article Title: Engraftment of adult hematopoietic stem and progenitor cells in a novel model of humanized mice

    doi: 10.1016/j.isci.2024.109238

    Figure Lengend Snippet:

    Article Snippet: Mouse CD11b-APC/Cy7 (M1/70) , TONBO , 25-0112-U100; RRID: AB_3094465.

    Techniques: Recombinant, Staining, Red Blood Cell Lysis, Enzyme-linked Immunosorbent Assay, Software

    PBMCs were isolated and cultured for 24 hours with green fluorescent protein (GFP)+ microparticles, and then washed, stained, and analyzed by flow cytometry. A , Cells that internalize or bind to GFP+ microparticles (right) exhibit green fluorescence compared to cells not treated with microparticles (left). B , Cells were gated on GFP and then subgated on CD11b, followed by CD3 and CD19 to identify specific cell types. C , PBMCs from three representative donors demonstrate that the majority of the GFP positive cells are positive for CD11b (white boxes). D , Ten times more microparticles were added to PBMCs (High MP∶target) to identify the any other subpopulation to internalize microparticles. One representative donor PBMC demonstrates that CD3+ cells (grey boxes) were the second cell type to internalize microparticles according to percentage (left) and numbers (right) of GFP-positive PBMCs.

    Journal: PLoS ONE

    Article Title: Microparticles Engineered to Highly Express Peroxisome Proliferator-Activated Receptor-γ Decreased Inflammatory Mediator Production and Increased Adhesion of Recipient Monocytes

    doi: 10.1371/journal.pone.0113189

    Figure Lengend Snippet: PBMCs were isolated and cultured for 24 hours with green fluorescent protein (GFP)+ microparticles, and then washed, stained, and analyzed by flow cytometry. A , Cells that internalize or bind to GFP+ microparticles (right) exhibit green fluorescence compared to cells not treated with microparticles (left). B , Cells were gated on GFP and then subgated on CD11b, followed by CD3 and CD19 to identify specific cell types. C , PBMCs from three representative donors demonstrate that the majority of the GFP positive cells are positive for CD11b (white boxes). D , Ten times more microparticles were added to PBMCs (High MP∶target) to identify the any other subpopulation to internalize microparticles. One representative donor PBMC demonstrates that CD3+ cells (grey boxes) were the second cell type to internalize microparticles according to percentage (left) and numbers (right) of GFP-positive PBMCs.

    Article Snippet: Antibodies used in flow cytometry analysis were: biotin mouse anti-human CD49e (555616, BD Biosciences) with streptavidin-APC (SA1005, Caltag, Buckingham, MK18 1TF), alexa fluor 647 mouse anti-fibronectin (563098, BD Biosciences), alexa fluor 700 mouse anti-human CD19 (557921, BD Biosciences), APC-Cy7 mouse anti-human CD11b (560914 BD Biosciences), PE mouse anti-human CD3 (9515-09, Southern Biotechnology, Birmingham, AL), APC mouse anti-human CD36 (561822, BD Biosciences).

    Techniques: Isolation, Cell Culture, Staining, Flow Cytometry, Fluorescence