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anti cd3  (Bio X Cell)


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    Structured Review

    Bio X Cell anti cd3
    Figure 5 Deficiency of GSDME blunts the immune response triggered by PAPR inhibitor in vivo. (A–L) Immunocompetent C57BL/6 mice were transplanted with wild type (WT) or Gsdme-deficient ID8 cells and challenged with niraparib for about 4 weeks. Tumors were harvested and subjected to bulk T-cell receptor (TCR) sequencing and evaluation of immune status. The frequency of T-cell clonotypes in the top 25% of TCR repertoires was shown using pie charts ((A) n=4) and quantified (B). The clonal expansion was evaluated using clonality (C). The TCR diversity was calculated by normalized Shannon diversity entropy (D). The proportion of dendritic cell differentiation (CD11c+MHCIIHigh) and maturation (CD11c+MHCIIHighCD86High) in tumors (E), lymph nodes (F), and spleens (G) was determined by flow cytometry. The proportion of <t>CD3+</t> T cells and NK cells among CD45+ immune cells in tumors was determined by flow cytometry (H). The production of IFN-γ in tumor-infiltrated CD4/8+ T and NK cells was examined by flow cytometry (I). The expression of granzyme B in tumor-infiltrated CD8+ T and NK cells was evaluated by mean fluorescence intensity (J). Representative images of GSDME, CD4, CD8, and GZMB IHC staining in tumor sections (K) and numbers of indicated immune cells in a ×20 field of a microscope (L). Scale bars: 200 µm. WT or Gsdme-deficient ID8 cells were intrabursally transplanted into C57BL/6 mice and received niraparib and/or anti-PD-1 treatment. Representative bioluminescent images of mice bearing WT and Gsdme-KO ID8 tumors at the endpoint (M). The tumor weight was quantified in each mouse treated with niraparib and/or anti-PD-1 antibodies ((N) n=7). Mean values±SEM. *P<0.05, **p<0.01, and ***p<0.001 by Student’s t-test in (B–J, L, and N).
    Anti Cd3, supplied by Bio X Cell, used in various techniques. Bioz Stars score: 96/100, based on 274 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cd3/pm39366751-329-8-10?v=Bio+X+Cell
    Average 96 stars, based on 274 article reviews
    anti cd3 - by Bioz Stars, 2026-08
    96/100 stars

    Images

    1) Product Images from "PARP inhibitors enhance antitumor immune responses by triggering pyroptosis via TNF-caspase 8-GSDMD/E axis in ovarian cancer."

    Article Title: PARP inhibitors enhance antitumor immune responses by triggering pyroptosis via TNF-caspase 8-GSDMD/E axis in ovarian cancer.

    Journal: Journal for immunotherapy of cancer

    doi: 10.1136/jitc-2024-009032

    Figure 5 Deficiency of GSDME blunts the immune response triggered by PAPR inhibitor in vivo. (A–L) Immunocompetent C57BL/6 mice were transplanted with wild type (WT) or Gsdme-deficient ID8 cells and challenged with niraparib for about 4 weeks. Tumors were harvested and subjected to bulk T-cell receptor (TCR) sequencing and evaluation of immune status. The frequency of T-cell clonotypes in the top 25% of TCR repertoires was shown using pie charts ((A) n=4) and quantified (B). The clonal expansion was evaluated using clonality (C). The TCR diversity was calculated by normalized Shannon diversity entropy (D). The proportion of dendritic cell differentiation (CD11c+MHCIIHigh) and maturation (CD11c+MHCIIHighCD86High) in tumors (E), lymph nodes (F), and spleens (G) was determined by flow cytometry. The proportion of CD3+ T cells and NK cells among CD45+ immune cells in tumors was determined by flow cytometry (H). The production of IFN-γ in tumor-infiltrated CD4/8+ T and NK cells was examined by flow cytometry (I). The expression of granzyme B in tumor-infiltrated CD8+ T and NK cells was evaluated by mean fluorescence intensity (J). Representative images of GSDME, CD4, CD8, and GZMB IHC staining in tumor sections (K) and numbers of indicated immune cells in a ×20 field of a microscope (L). Scale bars: 200 µm. WT or Gsdme-deficient ID8 cells were intrabursally transplanted into C57BL/6 mice and received niraparib and/or anti-PD-1 treatment. Representative bioluminescent images of mice bearing WT and Gsdme-KO ID8 tumors at the endpoint (M). The tumor weight was quantified in each mouse treated with niraparib and/or anti-PD-1 antibodies ((N) n=7). Mean values±SEM. *P<0.05, **p<0.01, and ***p<0.001 by Student’s t-test in (B–J, L, and N).
    Figure Legend Snippet: Figure 5 Deficiency of GSDME blunts the immune response triggered by PAPR inhibitor in vivo. (A–L) Immunocompetent C57BL/6 mice were transplanted with wild type (WT) or Gsdme-deficient ID8 cells and challenged with niraparib for about 4 weeks. Tumors were harvested and subjected to bulk T-cell receptor (TCR) sequencing and evaluation of immune status. The frequency of T-cell clonotypes in the top 25% of TCR repertoires was shown using pie charts ((A) n=4) and quantified (B). The clonal expansion was evaluated using clonality (C). The TCR diversity was calculated by normalized Shannon diversity entropy (D). The proportion of dendritic cell differentiation (CD11c+MHCIIHigh) and maturation (CD11c+MHCIIHighCD86High) in tumors (E), lymph nodes (F), and spleens (G) was determined by flow cytometry. The proportion of CD3+ T cells and NK cells among CD45+ immune cells in tumors was determined by flow cytometry (H). The production of IFN-γ in tumor-infiltrated CD4/8+ T and NK cells was examined by flow cytometry (I). The expression of granzyme B in tumor-infiltrated CD8+ T and NK cells was evaluated by mean fluorescence intensity (J). Representative images of GSDME, CD4, CD8, and GZMB IHC staining in tumor sections (K) and numbers of indicated immune cells in a ×20 field of a microscope (L). Scale bars: 200 µm. WT or Gsdme-deficient ID8 cells were intrabursally transplanted into C57BL/6 mice and received niraparib and/or anti-PD-1 treatment. Representative bioluminescent images of mice bearing WT and Gsdme-KO ID8 tumors at the endpoint (M). The tumor weight was quantified in each mouse treated with niraparib and/or anti-PD-1 antibodies ((N) n=7). Mean values±SEM. *P<0.05, **p<0.01, and ***p<0.001 by Student’s t-test in (B–J, L, and N).

    Techniques Used: In Vivo, Sequencing, Cell Differentiation, Flow Cytometry, Expressing, Fluorescence, Immunohistochemistry, Microscopy



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    Nano flow cytometry measures of MV phenotype in males and females. (a) <t>CD3+</t> lymphocyte‐derived MVs. (b) CD14+ monocyte‐derived MVs. (c) CD16+ neutrophil‐derived MVs. (d) CD45+ leukocyte‐derived MVs. (e) CD31+ endothelial cell‐derived MVs. (f) CD62E+ endothelial activation‐derived MVs. (g) CD41+ platelet‐derived MVs. (h) MVs expressing Annexin A5. Individual data points are presented as MV counts/μL. Clear circles represent females and dark filled circles represent males. Statistical comparisons between sexes were performed using linear models adjusted for age and BMI. Data are presented as untransformed values for visualization following outlier removal using a 3*SD criterion. Statistical analyses were performed on log‐transformed data where appropriate.
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    Miltenyi Biotec anti cd3 antibody
    Nano flow cytometry measures of MV phenotype in males and females. (a) <t>CD3+</t> lymphocyte‐derived MVs. (b) CD14+ monocyte‐derived MVs. (c) CD16+ neutrophil‐derived MVs. (d) CD45+ leukocyte‐derived MVs. (e) CD31+ endothelial cell‐derived MVs. (f) CD62E+ endothelial activation‐derived MVs. (g) CD41+ platelet‐derived MVs. (h) MVs expressing Annexin A5. Individual data points are presented as MV counts/μL. Clear circles represent females and dark filled circles represent males. Statistical comparisons between sexes were performed using linear models adjusted for age and BMI. Data are presented as untransformed values for visualization following outlier removal using a 3*SD criterion. Statistical analyses were performed on log‐transformed data where appropriate.
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    Image Search Results


    Nano flow cytometry measures of MV phenotype in males and females. (a) CD3+ lymphocyte‐derived MVs. (b) CD14+ monocyte‐derived MVs. (c) CD16+ neutrophil‐derived MVs. (d) CD45+ leukocyte‐derived MVs. (e) CD31+ endothelial cell‐derived MVs. (f) CD62E+ endothelial activation‐derived MVs. (g) CD41+ platelet‐derived MVs. (h) MVs expressing Annexin A5. Individual data points are presented as MV counts/μL. Clear circles represent females and dark filled circles represent males. Statistical comparisons between sexes were performed using linear models adjusted for age and BMI. Data are presented as untransformed values for visualization following outlier removal using a 3*SD criterion. Statistical analyses were performed on log‐transformed data where appropriate.

    Journal: Physiological Reports

    Article Title: Sex differences in circulating platelet‐derived CD41 + extracellular vesicles in healthy adults

    doi: 10.14814/phy2.70932

    Figure Lengend Snippet: Nano flow cytometry measures of MV phenotype in males and females. (a) CD3+ lymphocyte‐derived MVs. (b) CD14+ monocyte‐derived MVs. (c) CD16+ neutrophil‐derived MVs. (d) CD45+ leukocyte‐derived MVs. (e) CD31+ endothelial cell‐derived MVs. (f) CD62E+ endothelial activation‐derived MVs. (g) CD41+ platelet‐derived MVs. (h) MVs expressing Annexin A5. Individual data points are presented as MV counts/μL. Clear circles represent females and dark filled circles represent males. Statistical comparisons between sexes were performed using linear models adjusted for age and BMI. Data are presented as untransformed values for visualization following outlier removal using a 3*SD criterion. Statistical analyses were performed on log‐transformed data where appropriate.

    Article Snippet: Panel 2 received 2 μL each of CD3 PE (130‐114‐519, Miltenyi Biotec), CD14 PerCP‐Vio700 (130‐110‐523), CD16 PE‐Vio615 (130‐119‐995), CD31 FITC (130‐110‐668), CD41 APC (130‐123‐301), and 10 μL of CD62E PE (130‐104‐643).

    Techniques: Flow Cytometry, Derivative Assay, Activation Assay, Expressing, Transformation Assay