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PE CYANINE7 ANTI MOUSE CD4 GK1 5
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Anti Mouse CD4 Flow Cytometry Monoclonal Clone GK15 PE/Cyanine7 from Innovative Research is a flow cytometry antibody, buffered in PBS with 0.05% Proclin300, 1% BSA. This flow cytometry antibody has been specifically designed to work
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Image Search Results
Journal: Advanced Science
Article Title: CXCL13 Expression Promotes CAR T Cell Antitumor Activity and Potentiates Response to PD‐1 Blockade
doi: 10.1002/advs.202508095
Figure Lengend Snippet: CXCL13 is highly expressed in T cells from responders to ICB therapy. a). UMAP plot displaying 237231 CD3 + T cells across 8 cancer types: BCC (basal cell carcinoma, n = 11 patients; n = 22 samples), SCC (squamous cell carcinoma, n = 3 patients; n = 8 samples), BLCA (bladder cancer, n = 6 patients; n = 6 samples), TNBC (triple‐negative breast cancer, n = 8 patients; n = 14 samples), RCC (Renal cell carcinoma, n = 7 patients; n = 7 samples), HNSCC (head and neck cancer, n = 4 patients; n = 8 samples), NSCLC (non‐small‐cell lung cancer, n = 36 patients; n = 47 samples), and PRAD (prostate cancer, n = 10 patients; n = 12 samples), categorized into 13 distinct cell types. b). Comparison of differential genes in CD3 + , CD8 + , and CD4 + T cells in the response and non‐response groups. c,d). UMAP plots (c) and dot plots (d) showing the expression of CXCL13 in CD3 + , CD8 + , and CD4 + T cells of pre‐treatment non‐response, pre‐treatment response, post‐treatment non‐response, and post‐treatment response groups. e). CXCL13 expression levels in responders and non‐responders across multiple tumor cohorts treated with ICB: HNSC, melanoma cohort 1 (anti‐PD‐1 and anti‐CTLA‐4), melanoma cohort 2 (anti‐PD‐1), STAD (stomach adenocarcinoma), and BLCA. f). Comparison of CXCL13 expression in pre‐treatment and post‐treatment groups from melanoma cohort 1 and melanoma cohort 2 treated with ICB. g). Kaplan‐Meier survival curves stratified by high and low CXCL13 expression in ICB‐treated patients from BLCA, melanoma cohort 1, and melanoma cohort 2. h). Heatmap showing the correlation of CXCL13 expression with various cell types across tumor types in the TCGA dataset. Cell‐type deconvolution was performed using TIMER2.0, with significant correlations ( p < 0.05) marked by solid indicators.
Article Snippet: The following antibodies were used for staining: anti‐mouse CD45.1, BV450 (E‐AB‐F1184UQ), Elabscience, Cat # AF19855; anti‐mouse CD45.1, PE (A20), Biolegend, Cat # 110 708; anti‐mouse CD3ε, PE/Cyanine7 (145‐2C11), Biolegend, Cat # 100 320; anti‐mouse PD‐1, PE/Cyanine7 (RMP1‐30), Biolegend, Cat # 109 110;
Techniques: Comparison, Expressing
![CXCL13 CAR T cells display enhanced antitumor characteristics. a). GSEA analysis of the mitochondrial membrane potential gene set in bulk RNA‐seq comparing CXCL13 CAR T cells with control CAR T cells. b–d). Flow cytometry analysis of mitochondrial membrane potential (TMRM) in control CAR T and CXCL13 CAR T cells. Representative TMRM peak plots are shown for GFP + (b) and GFP − (c) T cells cultured in vitro on day 10 and for cells isolated from the spleen (d). TMRM: Tetramethylrhodamine, methyl ester. Mean ± SEM, n = 3 (b, c); n = 5 (control CAR T), n = 4 (CXCL13 CAR T) (d). e). Intracellular ATP levels in control CAR T cells and CXCL13 CAR T cells. Mean ± SEM, n = 4. f,g). GSEA analysis of positive regulation of T cell migration gene set in CXCL13 CAR T cells versus control CAR T cells using bulk RNA‐seq data (f) and CXCL13 + cells versus CXCL13 − cells using scRNA‐seq data (g). h). Schematic overview of the transwell migration assay. i,j). The migration ability of CAR T cells was assessed by the transwell assay, showing the proportion (i) and number (j) of cells that migrated through the membrane. Mean ± SEM, n = 4. k–m). C57BL/6 mice injected s.c. with 5 × 10 5 B16‐CD19 cells were treated with 2×10⁶ CAR T cells on day 5 post‐tumor establishment. The number of CAR T cells was detected after 7 days of adoptive transfer in the spleen (k), draining lymph nodes (l), and tumor sites (m). Mean ± SEM, n = 3. n). Percentage of CD4 + T cells among CD3 + T cells from patients with GPC3‐positive solid tumors treated with CAR T cells (non‐responders [NR], n = 6; responders [R], n = 15). Mean ± SEM. o,p). Flow cytometry plots (o) and line graphs (p) showing the percentage of CD4⁺ CAR T cells in vitro from day 4 to day 10. Mean ± SEM, n = 4. q–s). Proportions of CD4 + and CD8 + CAR T cells in blood (q), spleen (r), and draining lymph nodes (s). Mean ± SEM, blood ( n = 6), spleen ( n = 6 for control CAR T; n = 4 for CXCL13 CAR T), draining lymph nodes ( n = 6 for control CAR T; n = 4 for CXCL13 CAR T). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; two‐tailed unpaired t‐test (b–e,i–n,p–s).](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_2523/pmc12412523/pmc12412523__ADVS-12-e08095-g005.jpg.jpg)
Journal: Advanced Science
Article Title: CXCL13 Expression Promotes CAR T Cell Antitumor Activity and Potentiates Response to PD‐1 Blockade
doi: 10.1002/advs.202508095
Figure Lengend Snippet: CXCL13 CAR T cells display enhanced antitumor characteristics. a). GSEA analysis of the mitochondrial membrane potential gene set in bulk RNA‐seq comparing CXCL13 CAR T cells with control CAR T cells. b–d). Flow cytometry analysis of mitochondrial membrane potential (TMRM) in control CAR T and CXCL13 CAR T cells. Representative TMRM peak plots are shown for GFP + (b) and GFP − (c) T cells cultured in vitro on day 10 and for cells isolated from the spleen (d). TMRM: Tetramethylrhodamine, methyl ester. Mean ± SEM, n = 3 (b, c); n = 5 (control CAR T), n = 4 (CXCL13 CAR T) (d). e). Intracellular ATP levels in control CAR T cells and CXCL13 CAR T cells. Mean ± SEM, n = 4. f,g). GSEA analysis of positive regulation of T cell migration gene set in CXCL13 CAR T cells versus control CAR T cells using bulk RNA‐seq data (f) and CXCL13 + cells versus CXCL13 − cells using scRNA‐seq data (g). h). Schematic overview of the transwell migration assay. i,j). The migration ability of CAR T cells was assessed by the transwell assay, showing the proportion (i) and number (j) of cells that migrated through the membrane. Mean ± SEM, n = 4. k–m). C57BL/6 mice injected s.c. with 5 × 10 5 B16‐CD19 cells were treated with 2×10⁶ CAR T cells on day 5 post‐tumor establishment. The number of CAR T cells was detected after 7 days of adoptive transfer in the spleen (k), draining lymph nodes (l), and tumor sites (m). Mean ± SEM, n = 3. n). Percentage of CD4 + T cells among CD3 + T cells from patients with GPC3‐positive solid tumors treated with CAR T cells (non‐responders [NR], n = 6; responders [R], n = 15). Mean ± SEM. o,p). Flow cytometry plots (o) and line graphs (p) showing the percentage of CD4⁺ CAR T cells in vitro from day 4 to day 10. Mean ± SEM, n = 4. q–s). Proportions of CD4 + and CD8 + CAR T cells in blood (q), spleen (r), and draining lymph nodes (s). Mean ± SEM, blood ( n = 6), spleen ( n = 6 for control CAR T; n = 4 for CXCL13 CAR T), draining lymph nodes ( n = 6 for control CAR T; n = 4 for CXCL13 CAR T). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; two‐tailed unpaired t‐test (b–e,i–n,p–s).
Article Snippet: The following antibodies were used for staining: anti‐mouse CD45.1, BV450 (E‐AB‐F1184UQ), Elabscience, Cat # AF19855; anti‐mouse CD45.1, PE (A20), Biolegend, Cat # 110 708; anti‐mouse CD3ε, PE/Cyanine7 (145‐2C11), Biolegend, Cat # 100 320; anti‐mouse PD‐1, PE/Cyanine7 (RMP1‐30), Biolegend, Cat # 109 110;
Techniques: Membrane, RNA Sequencing, Control, Flow Cytometry, Cell Culture, In Vitro, Isolation, Migration, Transwell Migration Assay, Transwell Assay, Injection, Adoptive Transfer Assay, Two Tailed Test