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human cxcl16  (Boster Bio)


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    Boster Bio human cxcl16
    a Interaction specificity weights of ligand-receptor interactions between NC monocytes and DNαβ T cells in T-ALL group 2 patients (NATMI ). b Bubble heatmap showing expression of genes involved in the <t>CXCL16-CXCR6</t> axis in group 2 T-ALL patients at diagnosis. c mRNA expression of CXCL16 , ADAM10 and ADAM17 in peripheral blood NC monocytes for group 2 T-ALL patients at diagnosis ( n = 1603 cells), prophase ( n = 740 cells) and remission ( n = 103 cells) and healthy donors ( n = 168 cells). A Kruskal-Wallis test followed by Dunn’s post-hoc test with Holm correction was used for statistical testing and only significant comparisons are shown. d Barplot showing concentration of soluble CXCL16 in serum of primary peripheral blood samples grouped by percentage of NC monocytes of monocytes. Data are presented as mean values +/- SEM (0-30%: n = 3, 30-60%: n = 2, 60–100%: n = 2) including technical duplicates. A Kruskal-Wallis test followed by Dunn’s post-hoc test with Holm correction was used for statistical testing and only significant comparisons are shown. e Experimental approach for in vitro induction of CD8 low cells. CD8 + T cells were activated with anti-CD3/CD28 beads and cultured with 150 U/ml IL-2 alone or IL-2 with 100 ng/ml CXCL16 for 7 days. Upon harvest, CD8 high , CD8 mid and CD8 low CD3 + T cells were sorted and processed for low-input RNA-seq using the Smart-seq2 protocol . f , Heatmap of scaled normalized expression of low-input RNA-seq using the Smart-seq2 protocol of genes in the DNαβ T cell transcriptome score for in vitro induced CD8 high ( n = 3), CD8 mid ( n = 4) and CD8 low T cells at day7 in the absence ( n = 2) or presence ( n = 4) of CXCL16. g Heatmap of regulon activity (RScenic ) of top DNαβ T cell regulons shown in Fig. for sorted CD8 high , CD8 mid and CD8 low T cells from cultured CD8 + T cells harvested at day 7. h Boxplots showing regulon activity for in vitro induced CD8 low T cells at day 7 in the presence or absence of CXCL16 shown in ( g ) for each hierarchical cluster ( n = 3, n = 3 and n = 5 regulons in each cluster, respectively). A paired t-test was used for statistical analysis; n.s.: not significant.
    Human Cxcl16, supplied by Boster Bio, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Remodeling of the immune microenvironment is linked to adverse outcome in pediatric T cell acute lymphoblastic leukemia"

    Article Title: Remodeling of the immune microenvironment is linked to adverse outcome in pediatric T cell acute lymphoblastic leukemia

    Journal: Nature Communications

    doi: 10.1038/s41467-025-65134-y

    a Interaction specificity weights of ligand-receptor interactions between NC monocytes and DNαβ T cells in T-ALL group 2 patients (NATMI ). b Bubble heatmap showing expression of genes involved in the CXCL16-CXCR6 axis in group 2 T-ALL patients at diagnosis. c mRNA expression of CXCL16 , ADAM10 and ADAM17 in peripheral blood NC monocytes for group 2 T-ALL patients at diagnosis ( n = 1603 cells), prophase ( n = 740 cells) and remission ( n = 103 cells) and healthy donors ( n = 168 cells). A Kruskal-Wallis test followed by Dunn’s post-hoc test with Holm correction was used for statistical testing and only significant comparisons are shown. d Barplot showing concentration of soluble CXCL16 in serum of primary peripheral blood samples grouped by percentage of NC monocytes of monocytes. Data are presented as mean values +/- SEM (0-30%: n = 3, 30-60%: n = 2, 60–100%: n = 2) including technical duplicates. A Kruskal-Wallis test followed by Dunn’s post-hoc test with Holm correction was used for statistical testing and only significant comparisons are shown. e Experimental approach for in vitro induction of CD8 low cells. CD8 + T cells were activated with anti-CD3/CD28 beads and cultured with 150 U/ml IL-2 alone or IL-2 with 100 ng/ml CXCL16 for 7 days. Upon harvest, CD8 high , CD8 mid and CD8 low CD3 + T cells were sorted and processed for low-input RNA-seq using the Smart-seq2 protocol . f , Heatmap of scaled normalized expression of low-input RNA-seq using the Smart-seq2 protocol of genes in the DNαβ T cell transcriptome score for in vitro induced CD8 high ( n = 3), CD8 mid ( n = 4) and CD8 low T cells at day7 in the absence ( n = 2) or presence ( n = 4) of CXCL16. g Heatmap of regulon activity (RScenic ) of top DNαβ T cell regulons shown in Fig. for sorted CD8 high , CD8 mid and CD8 low T cells from cultured CD8 + T cells harvested at day 7. h Boxplots showing regulon activity for in vitro induced CD8 low T cells at day 7 in the presence or absence of CXCL16 shown in ( g ) for each hierarchical cluster ( n = 3, n = 3 and n = 5 regulons in each cluster, respectively). A paired t-test was used for statistical analysis; n.s.: not significant.
    Figure Legend Snippet: a Interaction specificity weights of ligand-receptor interactions between NC monocytes and DNαβ T cells in T-ALL group 2 patients (NATMI ). b Bubble heatmap showing expression of genes involved in the CXCL16-CXCR6 axis in group 2 T-ALL patients at diagnosis. c mRNA expression of CXCL16 , ADAM10 and ADAM17 in peripheral blood NC monocytes for group 2 T-ALL patients at diagnosis ( n = 1603 cells), prophase ( n = 740 cells) and remission ( n = 103 cells) and healthy donors ( n = 168 cells). A Kruskal-Wallis test followed by Dunn’s post-hoc test with Holm correction was used for statistical testing and only significant comparisons are shown. d Barplot showing concentration of soluble CXCL16 in serum of primary peripheral blood samples grouped by percentage of NC monocytes of monocytes. Data are presented as mean values +/- SEM (0-30%: n = 3, 30-60%: n = 2, 60–100%: n = 2) including technical duplicates. A Kruskal-Wallis test followed by Dunn’s post-hoc test with Holm correction was used for statistical testing and only significant comparisons are shown. e Experimental approach for in vitro induction of CD8 low cells. CD8 + T cells were activated with anti-CD3/CD28 beads and cultured with 150 U/ml IL-2 alone or IL-2 with 100 ng/ml CXCL16 for 7 days. Upon harvest, CD8 high , CD8 mid and CD8 low CD3 + T cells were sorted and processed for low-input RNA-seq using the Smart-seq2 protocol . f , Heatmap of scaled normalized expression of low-input RNA-seq using the Smart-seq2 protocol of genes in the DNαβ T cell transcriptome score for in vitro induced CD8 high ( n = 3), CD8 mid ( n = 4) and CD8 low T cells at day7 in the absence ( n = 2) or presence ( n = 4) of CXCL16. g Heatmap of regulon activity (RScenic ) of top DNαβ T cell regulons shown in Fig. for sorted CD8 high , CD8 mid and CD8 low T cells from cultured CD8 + T cells harvested at day 7. h Boxplots showing regulon activity for in vitro induced CD8 low T cells at day 7 in the presence or absence of CXCL16 shown in ( g ) for each hierarchical cluster ( n = 3, n = 3 and n = 5 regulons in each cluster, respectively). A paired t-test was used for statistical analysis; n.s.: not significant.

    Techniques Used: Expressing, Biomarker Discovery, Concentration Assay, In Vitro, Cell Culture, RNA Sequencing, Activity Assay



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    a Interaction specificity weights of ligand-receptor interactions between NC monocytes and DNαβ T cells in T-ALL group 2 patients (NATMI ). b Bubble heatmap showing expression of genes involved in the <t>CXCL16-CXCR6</t> axis in group 2 T-ALL patients at diagnosis. c mRNA expression of CXCL16 , ADAM10 and ADAM17 in peripheral blood NC monocytes for group 2 T-ALL patients at diagnosis ( n = 1603 cells), prophase ( n = 740 cells) and remission ( n = 103 cells) and healthy donors ( n = 168 cells). A Kruskal-Wallis test followed by Dunn’s post-hoc test with Holm correction was used for statistical testing and only significant comparisons are shown. d Barplot showing concentration of soluble CXCL16 in serum of primary peripheral blood samples grouped by percentage of NC monocytes of monocytes. Data are presented as mean values +/- SEM (0-30%: n = 3, 30-60%: n = 2, 60–100%: n = 2) including technical duplicates. A Kruskal-Wallis test followed by Dunn’s post-hoc test with Holm correction was used for statistical testing and only significant comparisons are shown. e Experimental approach for in vitro induction of CD8 low cells. CD8 + T cells were activated with anti-CD3/CD28 beads and cultured with 150 U/ml IL-2 alone or IL-2 with 100 ng/ml CXCL16 for 7 days. Upon harvest, CD8 high , CD8 mid and CD8 low CD3 + T cells were sorted and processed for low-input RNA-seq using the Smart-seq2 protocol . f , Heatmap of scaled normalized expression of low-input RNA-seq using the Smart-seq2 protocol of genes in the DNαβ T cell transcriptome score for in vitro induced CD8 high ( n = 3), CD8 mid ( n = 4) and CD8 low T cells at day7 in the absence ( n = 2) or presence ( n = 4) of CXCL16. g Heatmap of regulon activity (RScenic ) of top DNαβ T cell regulons shown in Fig. for sorted CD8 high , CD8 mid and CD8 low T cells from cultured CD8 + T cells harvested at day 7. h Boxplots showing regulon activity for in vitro induced CD8 low T cells at day 7 in the presence or absence of CXCL16 shown in ( g ) for each hierarchical cluster ( n = 3, n = 3 and n = 5 regulons in each cluster, respectively). A paired t-test was used for statistical analysis; n.s.: not significant.
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    a Interaction specificity weights of ligand-receptor interactions between NC monocytes and DNαβ T cells in T-ALL group 2 patients (NATMI ). b Bubble heatmap showing expression of genes involved in the <t>CXCL16-CXCR6</t> axis in group 2 T-ALL patients at diagnosis. c mRNA expression of CXCL16 , ADAM10 and ADAM17 in peripheral blood NC monocytes for group 2 T-ALL patients at diagnosis ( n = 1603 cells), prophase ( n = 740 cells) and remission ( n = 103 cells) and healthy donors ( n = 168 cells). A Kruskal-Wallis test followed by Dunn’s post-hoc test with Holm correction was used for statistical testing and only significant comparisons are shown. d Barplot showing concentration of soluble CXCL16 in serum of primary peripheral blood samples grouped by percentage of NC monocytes of monocytes. Data are presented as mean values +/- SEM (0-30%: n = 3, 30-60%: n = 2, 60–100%: n = 2) including technical duplicates. A Kruskal-Wallis test followed by Dunn’s post-hoc test with Holm correction was used for statistical testing and only significant comparisons are shown. e Experimental approach for in vitro induction of CD8 low cells. CD8 + T cells were activated with anti-CD3/CD28 beads and cultured with 150 U/ml IL-2 alone or IL-2 with 100 ng/ml CXCL16 for 7 days. Upon harvest, CD8 high , CD8 mid and CD8 low CD3 + T cells were sorted and processed for low-input RNA-seq using the Smart-seq2 protocol . f , Heatmap of scaled normalized expression of low-input RNA-seq using the Smart-seq2 protocol of genes in the DNαβ T cell transcriptome score for in vitro induced CD8 high ( n = 3), CD8 mid ( n = 4) and CD8 low T cells at day7 in the absence ( n = 2) or presence ( n = 4) of CXCL16. g Heatmap of regulon activity (RScenic ) of top DNαβ T cell regulons shown in Fig. for sorted CD8 high , CD8 mid and CD8 low T cells from cultured CD8 + T cells harvested at day 7. h Boxplots showing regulon activity for in vitro induced CD8 low T cells at day 7 in the presence or absence of CXCL16 shown in ( g ) for each hierarchical cluster ( n = 3, n = 3 and n = 5 regulons in each cluster, respectively). A paired t-test was used for statistical analysis; n.s.: not significant.
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    a Interaction specificity weights of ligand-receptor interactions between NC monocytes and DNαβ T cells in T-ALL group 2 patients (NATMI ). b Bubble heatmap showing expression of genes involved in the <t>CXCL16-CXCR6</t> axis in group 2 T-ALL patients at diagnosis. c mRNA expression of CXCL16 , ADAM10 and ADAM17 in peripheral blood NC monocytes for group 2 T-ALL patients at diagnosis ( n = 1603 cells), prophase ( n = 740 cells) and remission ( n = 103 cells) and healthy donors ( n = 168 cells). A Kruskal-Wallis test followed by Dunn’s post-hoc test with Holm correction was used for statistical testing and only significant comparisons are shown. d Barplot showing concentration of soluble CXCL16 in serum of primary peripheral blood samples grouped by percentage of NC monocytes of monocytes. Data are presented as mean values +/- SEM (0-30%: n = 3, 30-60%: n = 2, 60–100%: n = 2) including technical duplicates. A Kruskal-Wallis test followed by Dunn’s post-hoc test with Holm correction was used for statistical testing and only significant comparisons are shown. e Experimental approach for in vitro induction of CD8 low cells. CD8 + T cells were activated with anti-CD3/CD28 beads and cultured with 150 U/ml IL-2 alone or IL-2 with 100 ng/ml CXCL16 for 7 days. Upon harvest, CD8 high , CD8 mid and CD8 low CD3 + T cells were sorted and processed for low-input RNA-seq using the Smart-seq2 protocol . f , Heatmap of scaled normalized expression of low-input RNA-seq using the Smart-seq2 protocol of genes in the DNαβ T cell transcriptome score for in vitro induced CD8 high ( n = 3), CD8 mid ( n = 4) and CD8 low T cells at day7 in the absence ( n = 2) or presence ( n = 4) of CXCL16. g Heatmap of regulon activity (RScenic ) of top DNαβ T cell regulons shown in Fig. for sorted CD8 high , CD8 mid and CD8 low T cells from cultured CD8 + T cells harvested at day 7. h Boxplots showing regulon activity for in vitro induced CD8 low T cells at day 7 in the presence or absence of CXCL16 shown in ( g ) for each hierarchical cluster ( n = 3, n = 3 and n = 5 regulons in each cluster, respectively). A paired t-test was used for statistical analysis; n.s.: not significant.
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    Image Search Results


    The interaction of MDSCs and Treg by CXCL16‐CXCR6 signaling was obvious in PJI. a) The interaction plot showed the cell communications between myeloid cells and lymphocytes by ligand‐receptor pair analysis. The thicker the line represented, the stronger the interaction weights/strength, and the more the number of interactions among the cell types. b) The bar chart showed the interaction strength and the number of interactions among PJI, AF and OA. c) The bar chart showed the strength comparison of the interaction pathways among PJI, AF and OA. d) The heatmap showed relative strength of all enriched signals (outgoing and incoming) across myeloid cells and lymphocytes. e) The circle plot showed the inferred intercellular communication network for CXCL signaling pathway. f) The heatmap showed the CXCL signaling pathway among myeloid cells and lymphocytes. g) The bar chart showed the ligand‐receptor pair of CXCL signaling pathway among myeloid cells and lymphocytes. h) The bar chart showed the relative contribution of ligand‐receptor pair to the overall communication network of CXCL signaling pathway. i) The dot plot showed the incoming communication patterns of CXCL signaling pathway from M‐MDSCs among PJI, AF and OA. j) Multiplex immunofluorescence image showed the co‐location of CXCR6+ Treg and CD68+ myeloid cells with excretive CXCL16. Yellow arrow highlighted the CD68+ myeloid cells expressing CXCL16, and red arrow highlighted the CD4+FOXP3+ Treg expressing CXCR6. Scale bar, 20 mm (PJI, n = 3; AF, n = 3; OA, n = 3). Unpaired t test; ** p < 0.01, *** p < 0.001.

    Journal: Advanced Science

    Article Title: CXCL16/CXCR6/TGF‐β Feedback Loop Between M‐MDSCs and Treg Inhibits Anti‐Bacterial Immunity During Biofilm Infection

    doi: 10.1002/advs.202409537

    Figure Lengend Snippet: The interaction of MDSCs and Treg by CXCL16‐CXCR6 signaling was obvious in PJI. a) The interaction plot showed the cell communications between myeloid cells and lymphocytes by ligand‐receptor pair analysis. The thicker the line represented, the stronger the interaction weights/strength, and the more the number of interactions among the cell types. b) The bar chart showed the interaction strength and the number of interactions among PJI, AF and OA. c) The bar chart showed the strength comparison of the interaction pathways among PJI, AF and OA. d) The heatmap showed relative strength of all enriched signals (outgoing and incoming) across myeloid cells and lymphocytes. e) The circle plot showed the inferred intercellular communication network for CXCL signaling pathway. f) The heatmap showed the CXCL signaling pathway among myeloid cells and lymphocytes. g) The bar chart showed the ligand‐receptor pair of CXCL signaling pathway among myeloid cells and lymphocytes. h) The bar chart showed the relative contribution of ligand‐receptor pair to the overall communication network of CXCL signaling pathway. i) The dot plot showed the incoming communication patterns of CXCL signaling pathway from M‐MDSCs among PJI, AF and OA. j) Multiplex immunofluorescence image showed the co‐location of CXCR6+ Treg and CD68+ myeloid cells with excretive CXCL16. Yellow arrow highlighted the CD68+ myeloid cells expressing CXCL16, and red arrow highlighted the CD4+FOXP3+ Treg expressing CXCR6. Scale bar, 20 mm (PJI, n = 3; AF, n = 3; OA, n = 3). Unpaired t test; ** p < 0.01, *** p < 0.001.

    Article Snippet: CXCL16 in human synovial fluid samples was also measured by ELISA (70‐EK1254‐96, Hangzhou, China, MultiSciences).

    Techniques: Comparison, Multiplex Assay, Immunofluorescence, Expressing

    PJI patients with high CXCR6 showed a higher recurrence rate. a) The Volcano plot showed differentially expressed genes in PJI versus AF patients. The x and y axes represented the log2 fold change and p‐value, respectively, based on the Mann‐Whitney U test. Red dots: upregulated genes, blue dots: downregulated genes. b) The heatmap showed the distribution of 28 types of immune cells in PJI and AF. c) The bar chart showed the difference in proportion of M‐MDSCs and Treg between PJI and AF (PJI, n = 18; AF, n = 18). Unpaired t test; *** p < 0.001. d) The heatmap showed the characteristic genes of chemokines, PJI markers, cell markers and immune checkpoint between PJI and AF. e–l) The violin plots showed part of the differential genes (CXCL16, CXCR6, S100A8, S100A9, FOXP3, CTLA4, TIGIT and LAG3) between PJI and AF as shown in (d). Unpaired t test; ns p > 0.05, *** p < 0.001, **** p < 0.0001. m,n) Quantitative analysis of immunohistochemical staining for CXCL16 and CXCR6 (PJI, n = 80; AF, n = 25; OA = 25). 40x magnification. Scale bar, 20 mm. Unpaired t test; ** p < 0.01, *** p < 0.001. o) The Kaplan‐Meier curve showed the recurrence curves of PJI patients characterized by either low or high expression of CXCR6 (CXCR6‐high PJI, n = 30; CXCR6‐low PJI, n = 30). Significance was calculated using the log‐rank test. p,q) Quantitative analysis of Harris Hip score and HSS knee score in CXCR6‐high PJI and CXCR6‐low PJI group (CXCR6‐high PJI, n = 30; CXCR6‐low PJI, n = 30). Unpaired t test; * p < 0.05.

    Journal: Advanced Science

    Article Title: CXCL16/CXCR6/TGF‐β Feedback Loop Between M‐MDSCs and Treg Inhibits Anti‐Bacterial Immunity During Biofilm Infection

    doi: 10.1002/advs.202409537

    Figure Lengend Snippet: PJI patients with high CXCR6 showed a higher recurrence rate. a) The Volcano plot showed differentially expressed genes in PJI versus AF patients. The x and y axes represented the log2 fold change and p‐value, respectively, based on the Mann‐Whitney U test. Red dots: upregulated genes, blue dots: downregulated genes. b) The heatmap showed the distribution of 28 types of immune cells in PJI and AF. c) The bar chart showed the difference in proportion of M‐MDSCs and Treg between PJI and AF (PJI, n = 18; AF, n = 18). Unpaired t test; *** p < 0.001. d) The heatmap showed the characteristic genes of chemokines, PJI markers, cell markers and immune checkpoint between PJI and AF. e–l) The violin plots showed part of the differential genes (CXCL16, CXCR6, S100A8, S100A9, FOXP3, CTLA4, TIGIT and LAG3) between PJI and AF as shown in (d). Unpaired t test; ns p > 0.05, *** p < 0.001, **** p < 0.0001. m,n) Quantitative analysis of immunohistochemical staining for CXCL16 and CXCR6 (PJI, n = 80; AF, n = 25; OA = 25). 40x magnification. Scale bar, 20 mm. Unpaired t test; ** p < 0.01, *** p < 0.001. o) The Kaplan‐Meier curve showed the recurrence curves of PJI patients characterized by either low or high expression of CXCR6 (CXCR6‐high PJI, n = 30; CXCR6‐low PJI, n = 30). Significance was calculated using the log‐rank test. p,q) Quantitative analysis of Harris Hip score and HSS knee score in CXCR6‐high PJI and CXCR6‐low PJI group (CXCR6‐high PJI, n = 30; CXCR6‐low PJI, n = 30). Unpaired t test; * p < 0.05.

    Article Snippet: CXCL16 in human synovial fluid samples was also measured by ELISA (70‐EK1254‐96, Hangzhou, China, MultiSciences).

    Techniques: MANN-WHITNEY, Immunohistochemical staining, Staining, Expressing

    a Interaction specificity weights of ligand-receptor interactions between NC monocytes and DNαβ T cells in T-ALL group 2 patients (NATMI ). b Bubble heatmap showing expression of genes involved in the CXCL16-CXCR6 axis in group 2 T-ALL patients at diagnosis. c mRNA expression of CXCL16 , ADAM10 and ADAM17 in peripheral blood NC monocytes for group 2 T-ALL patients at diagnosis ( n = 1603 cells), prophase ( n = 740 cells) and remission ( n = 103 cells) and healthy donors ( n = 168 cells). A Kruskal-Wallis test followed by Dunn’s post-hoc test with Holm correction was used for statistical testing and only significant comparisons are shown. d Barplot showing concentration of soluble CXCL16 in serum of primary peripheral blood samples grouped by percentage of NC monocytes of monocytes. Data are presented as mean values +/- SEM (0-30%: n = 3, 30-60%: n = 2, 60–100%: n = 2) including technical duplicates. A Kruskal-Wallis test followed by Dunn’s post-hoc test with Holm correction was used for statistical testing and only significant comparisons are shown. e Experimental approach for in vitro induction of CD8 low cells. CD8 + T cells were activated with anti-CD3/CD28 beads and cultured with 150 U/ml IL-2 alone or IL-2 with 100 ng/ml CXCL16 for 7 days. Upon harvest, CD8 high , CD8 mid and CD8 low CD3 + T cells were sorted and processed for low-input RNA-seq using the Smart-seq2 protocol . f , Heatmap of scaled normalized expression of low-input RNA-seq using the Smart-seq2 protocol of genes in the DNαβ T cell transcriptome score for in vitro induced CD8 high ( n = 3), CD8 mid ( n = 4) and CD8 low T cells at day7 in the absence ( n = 2) or presence ( n = 4) of CXCL16. g Heatmap of regulon activity (RScenic ) of top DNαβ T cell regulons shown in Fig. for sorted CD8 high , CD8 mid and CD8 low T cells from cultured CD8 + T cells harvested at day 7. h Boxplots showing regulon activity for in vitro induced CD8 low T cells at day 7 in the presence or absence of CXCL16 shown in ( g ) for each hierarchical cluster ( n = 3, n = 3 and n = 5 regulons in each cluster, respectively). A paired t-test was used for statistical analysis; n.s.: not significant.

    Journal: Nature Communications

    Article Title: Remodeling of the immune microenvironment is linked to adverse outcome in pediatric T cell acute lymphoblastic leukemia

    doi: 10.1038/s41467-025-65134-y

    Figure Lengend Snippet: a Interaction specificity weights of ligand-receptor interactions between NC monocytes and DNαβ T cells in T-ALL group 2 patients (NATMI ). b Bubble heatmap showing expression of genes involved in the CXCL16-CXCR6 axis in group 2 T-ALL patients at diagnosis. c mRNA expression of CXCL16 , ADAM10 and ADAM17 in peripheral blood NC monocytes for group 2 T-ALL patients at diagnosis ( n = 1603 cells), prophase ( n = 740 cells) and remission ( n = 103 cells) and healthy donors ( n = 168 cells). A Kruskal-Wallis test followed by Dunn’s post-hoc test with Holm correction was used for statistical testing and only significant comparisons are shown. d Barplot showing concentration of soluble CXCL16 in serum of primary peripheral blood samples grouped by percentage of NC monocytes of monocytes. Data are presented as mean values +/- SEM (0-30%: n = 3, 30-60%: n = 2, 60–100%: n = 2) including technical duplicates. A Kruskal-Wallis test followed by Dunn’s post-hoc test with Holm correction was used for statistical testing and only significant comparisons are shown. e Experimental approach for in vitro induction of CD8 low cells. CD8 + T cells were activated with anti-CD3/CD28 beads and cultured with 150 U/ml IL-2 alone or IL-2 with 100 ng/ml CXCL16 for 7 days. Upon harvest, CD8 high , CD8 mid and CD8 low CD3 + T cells were sorted and processed for low-input RNA-seq using the Smart-seq2 protocol . f , Heatmap of scaled normalized expression of low-input RNA-seq using the Smart-seq2 protocol of genes in the DNαβ T cell transcriptome score for in vitro induced CD8 high ( n = 3), CD8 mid ( n = 4) and CD8 low T cells at day7 in the absence ( n = 2) or presence ( n = 4) of CXCL16. g Heatmap of regulon activity (RScenic ) of top DNαβ T cell regulons shown in Fig. for sorted CD8 high , CD8 mid and CD8 low T cells from cultured CD8 + T cells harvested at day 7. h Boxplots showing regulon activity for in vitro induced CD8 low T cells at day 7 in the presence or absence of CXCL16 shown in ( g ) for each hierarchical cluster ( n = 3, n = 3 and n = 5 regulons in each cluster, respectively). A paired t-test was used for statistical analysis; n.s.: not significant.

    Article Snippet: Human CXCL16 was measured in duplicates using a multiplex assay (BosterBio, #SEST004-P0004) by BosterBio ( https://www.bosterbio.com/ Pleasenton, CA).

    Techniques: Expressing, Biomarker Discovery, Concentration Assay, In Vitro, Cell Culture, RNA Sequencing, Activity Assay