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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 .
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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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    (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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    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

    (A) Representative plots and frequencies of splenic XCR1 + cDC1s, XCR1 − CD172a − merocytic DCs (mero), CLEC12A − cDC2A, and CLEC12A + cDC2B of total cDCs (Lin − MHCII + CD11c + CD26 + ) or of total cDC2s (CD172a + ) in female control (top) and Kdm5c ΔItgax (bottom) mice. (B) Representative plots, proportions, and counts of splenic Ly6C + pDCs and Ly6C − pDCs from female control and Kdm5c ΔItgax mice (parent gate: Lin(B220) + SiglecH + CD11c int CD11b − ). (C) BM chimeras were generated in CD45.1 + host mice by reconstituting their BM with a 1:1 mixture of CD45.1 + control and CD45.2 + Kdm5c ΔItgax BM or CD45.2 + Kdm5c ΔItgax BM alone. Proportions of splenic DC subsets are derived from CD45.1 + control and CD45.2 + Kdm5c ΔItgax cells 7 weeks post injection. (D) Proportions of splenic cDCs of mice administered α-IgG2b or α-PDCA1 to deplete pDCs. (E) Frequencies of splenic cDCs from control and Ifnar1 −/− mice. Each symbol represents an individual mouse. Data were pooled from 2–3 experiments of 9–11 mice per group. (A, B, D, and E) Statistical significance was determined by unpaired t test or (C) one-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. All error bars represent mean and SEM. See also .

    Journal: Cell reports

    Article Title: Transcriptional programming mediated by the histone demethylase KDM5C regulates dendritic cell population heterogeneity and function

    doi: 10.1016/j.celrep.2024.114506

    Figure Lengend Snippet: (A) Representative plots and frequencies of splenic XCR1 + cDC1s, XCR1 − CD172a − merocytic DCs (mero), CLEC12A − cDC2A, and CLEC12A + cDC2B of total cDCs (Lin − MHCII + CD11c + CD26 + ) or of total cDC2s (CD172a + ) in female control (top) and Kdm5c ΔItgax (bottom) mice. (B) Representative plots, proportions, and counts of splenic Ly6C + pDCs and Ly6C − pDCs from female control and Kdm5c ΔItgax mice (parent gate: Lin(B220) + SiglecH + CD11c int CD11b − ). (C) BM chimeras were generated in CD45.1 + host mice by reconstituting their BM with a 1:1 mixture of CD45.1 + control and CD45.2 + Kdm5c ΔItgax BM or CD45.2 + Kdm5c ΔItgax BM alone. Proportions of splenic DC subsets are derived from CD45.1 + control and CD45.2 + Kdm5c ΔItgax cells 7 weeks post injection. (D) Proportions of splenic cDCs of mice administered α-IgG2b or α-PDCA1 to deplete pDCs. (E) Frequencies of splenic cDCs from control and Ifnar1 −/− mice. Each symbol represents an individual mouse. Data were pooled from 2–3 experiments of 9–11 mice per group. (A, B, D, and E) Statistical significance was determined by unpaired t test or (C) one-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. All error bars represent mean and SEM. See also .

    Article Snippet: Anti-mouse CD11b APC/Cy7 (clone M1/70) , eBioscience , 47-0112-82; RRID:AB_1603193.

    Techniques: Control, Generated, Derivative Assay, Injection

    KEY RESOURCES TABLE

    Journal: Cell reports

    Article Title: Transcriptional programming mediated by the histone demethylase KDM5C regulates dendritic cell population heterogeneity and function

    doi: 10.1016/j.celrep.2024.114506

    Figure Lengend Snippet: KEY RESOURCES TABLE

    Article Snippet: Anti-mouse CD11b APC/Cy7 (clone M1/70) , eBioscience , 47-0112-82; RRID:AB_1603193.

    Techniques: Control, Blocking Assay, Virus, Recombinant, Protease Inhibitor, Lysis, Enzyme-linked Immunosorbent Assay, Staining, Cell Isolation, DNA Library Preparation, Purification, RNA HS Assay, Mutagenesis, Software