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MedChemExpress hy p7158
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R&D Systems cxcl5 neutralizing antibody
Distinct immune microenvironment across LIHV-defined subgroups (A) Immune cell abundance comparison across subgroups using the indicated immune analysis tools across four independent iCCA cohorts. Circle color and size represent log 2 fold change and p value, respectively. (B) Boxplots of CD66b + neutrophils, CD68 + macrophages, CD3 + T cells, CD20 + B cells, and αSMA + fibroblasts across subgroups (Mann-Whitney U test). (C) Heatmap of immune signatures and checkpoint expression summarized as mean Z scores per subgroup across four cohorts. ∗FDR < 0.05; ∗∗FDR < 0.01; ∗∗∗FDR < 0.001. (D) Heatmap of Spearman correlations between chemokine expression and neutrophil infiltration. IHC, immunohistochemistry. (E) Boxplot comparing <t>CXCL5</t> expression across subgroups in the Fu-iCCA cohort (Mann-Whitney U test). (F) Dot heatmap of chemokine gene expression across major cell types in Xue’s scRNA-seq dataset. (G) Boxplots of average CXCL5 expression in tumor cells and macrophages across subgroups (Mann-Whitney U test). (H) Western blot validating CXCL5 knockdown and overexpression efficiency in RBE and HuCCT1 cells. (I) Quantification of migrated neutrophils in transwell assays co-cultured with modified RBE and HuCCT1 cells ( n = 4 replicates per group; mean ± SD; Student’s t test). (J) Western blot analysis of CXCL5 overexpression in KTP cells. (K) Tumor growth curves of mice injected with control or CXCL5-overexpressing KTP cells ( n = 6 per group; mean ± SEM; Student’s t test). (L) Proportion and number of infiltrated neutrophils in control and CXCL5-overexpressing KTP tumors ( n = 6 per group; Student’s t test). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. See also and and .
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Distinct immune microenvironment across LIHV-defined subgroups (A) Immune cell abundance comparison across subgroups using the indicated immune analysis tools across four independent iCCA cohorts. Circle color and size represent log 2 fold change and p value, respectively. (B) Boxplots of CD66b + neutrophils, CD68 + macrophages, CD3 + T cells, CD20 + B cells, and αSMA + fibroblasts across subgroups (Mann-Whitney U test). (C) Heatmap of immune signatures and checkpoint expression summarized as mean Z scores per subgroup across four cohorts. ∗FDR < 0.05; ∗∗FDR < 0.01; ∗∗∗FDR < 0.001. (D) Heatmap of Spearman correlations between chemokine expression and neutrophil infiltration. IHC, immunohistochemistry. (E) Boxplot comparing <t>CXCL5</t> expression across subgroups in the Fu-iCCA cohort (Mann-Whitney U test). (F) Dot heatmap of chemokine gene expression across major cell types in Xue’s scRNA-seq dataset. (G) Boxplots of average CXCL5 expression in tumor cells and macrophages across subgroups (Mann-Whitney U test). (H) Western blot validating CXCL5 knockdown and overexpression efficiency in RBE and HuCCT1 cells. (I) Quantification of migrated neutrophils in transwell assays co-cultured with modified RBE and HuCCT1 cells ( n = 4 replicates per group; mean ± SD; Student’s t test). (J) Western blot analysis of CXCL5 overexpression in KTP cells. (K) Tumor growth curves of mice injected with control or CXCL5-overexpressing KTP cells ( n = 6 per group; mean ± SEM; Student’s t test). (L) Proportion and number of infiltrated neutrophils in control and CXCL5-overexpressing KTP tumors ( n = 6 per group; Student’s t test). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. See also and and .
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Distinct immune microenvironment across LIHV-defined subgroups (A) Immune cell abundance comparison across subgroups using the indicated immune analysis tools across four independent iCCA cohorts. Circle color and size represent log 2 fold change and p value, respectively. (B) Boxplots of CD66b + neutrophils, CD68 + macrophages, CD3 + T cells, CD20 + B cells, and αSMA + fibroblasts across subgroups (Mann-Whitney U test). (C) Heatmap of immune signatures and checkpoint expression summarized as mean Z scores per subgroup across four cohorts. ∗FDR < 0.05; ∗∗FDR < 0.01; ∗∗∗FDR < 0.001. (D) Heatmap of Spearman correlations between chemokine expression and neutrophil infiltration. IHC, immunohistochemistry. (E) Boxplot comparing <t>CXCL5</t> expression across subgroups in the Fu-iCCA cohort (Mann-Whitney U test). (F) Dot heatmap of chemokine gene expression across major cell types in Xue’s scRNA-seq dataset. (G) Boxplots of average CXCL5 expression in tumor cells and macrophages across subgroups (Mann-Whitney U test). (H) Western blot validating CXCL5 knockdown and overexpression efficiency in RBE and HuCCT1 cells. (I) Quantification of migrated neutrophils in transwell assays co-cultured with modified RBE and HuCCT1 cells ( n = 4 replicates per group; mean ± SD; Student’s t test). (J) Western blot analysis of CXCL5 overexpression in KTP cells. (K) Tumor growth curves of mice injected with control or CXCL5-overexpressing KTP cells ( n = 6 per group; mean ± SEM; Student’s t test). (L) Proportion and number of infiltrated neutrophils in control and CXCL5-overexpressing KTP tumors ( n = 6 per group; Student’s t test). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. See also and and .
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Distinct immune microenvironment across LIHV-defined subgroups (A) Immune cell abundance comparison across subgroups using the indicated immune analysis tools across four independent iCCA cohorts. Circle color and size represent log 2 fold change and p value, respectively. (B) Boxplots of CD66b + neutrophils, CD68 + macrophages, CD3 + T cells, CD20 + B cells, and αSMA + fibroblasts across subgroups (Mann-Whitney U test). (C) Heatmap of immune signatures and checkpoint expression summarized as mean Z scores per subgroup across four cohorts. ∗FDR < 0.05; ∗∗FDR < 0.01; ∗∗∗FDR < 0.001. (D) Heatmap of Spearman correlations between chemokine expression and neutrophil infiltration. IHC, immunohistochemistry. (E) Boxplot comparing <t>CXCL5</t> expression across subgroups in the Fu-iCCA cohort (Mann-Whitney U test). (F) Dot heatmap of chemokine gene expression across major cell types in Xue’s scRNA-seq dataset. (G) Boxplots of average CXCL5 expression in tumor cells and macrophages across subgroups (Mann-Whitney U test). (H) Western blot validating CXCL5 knockdown and overexpression efficiency in RBE and HuCCT1 cells. (I) Quantification of migrated neutrophils in transwell assays co-cultured with modified RBE and HuCCT1 cells ( n = 4 replicates per group; mean ± SD; Student’s t test). (J) Western blot analysis of CXCL5 overexpression in KTP cells. (K) Tumor growth curves of mice injected with control or CXCL5-overexpressing KTP cells ( n = 6 per group; mean ± SEM; Student’s t test). (L) Proportion and number of infiltrated neutrophils in control and CXCL5-overexpressing KTP tumors ( n = 6 per group; Student’s t test). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. See also and and .
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R&D Systems enzyme linked immunosorbent assay elisa
Chemokine (C-X-C motif) ligand 5 (CXCL5) levels were elevated in the synovial fluid (SF) of patients with periprosthetic joint infection (PJI), especially in the Gram-positive bacterial component-associated PJI (GPC-PJI) group. a) The expression level of CXCL5 in SF from patients with aseptic loosening (AL) and PJI was measured using protein-array assays. b) ImageJ software was used to quantify signal intensity of CXCL5 expression (two patients in the AL group and three patients in the PJI group). c) CXCL5 concentrations in SF of AL, GPC-PJI, and Gram-negative bacterial PJI (GNB-PJI) patients were measured by <t>performing</t> <t>enzyme-linked</t> <t>immunosorbent</t> assays. The expression of CXCL5 in the SF of PJI patients was significantly increased (four patients in the AL group, 12 patients in the GPC group, and three patients in the GNB group). Data are presented as the mean (standard error of the mean (SEM)) and analyzed using independent-samples t -test. *p < 0.05.
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Image Search Results


Distinct immune microenvironment across LIHV-defined subgroups (A) Immune cell abundance comparison across subgroups using the indicated immune analysis tools across four independent iCCA cohorts. Circle color and size represent log 2 fold change and p value, respectively. (B) Boxplots of CD66b + neutrophils, CD68 + macrophages, CD3 + T cells, CD20 + B cells, and αSMA + fibroblasts across subgroups (Mann-Whitney U test). (C) Heatmap of immune signatures and checkpoint expression summarized as mean Z scores per subgroup across four cohorts. ∗FDR < 0.05; ∗∗FDR < 0.01; ∗∗∗FDR < 0.001. (D) Heatmap of Spearman correlations between chemokine expression and neutrophil infiltration. IHC, immunohistochemistry. (E) Boxplot comparing CXCL5 expression across subgroups in the Fu-iCCA cohort (Mann-Whitney U test). (F) Dot heatmap of chemokine gene expression across major cell types in Xue’s scRNA-seq dataset. (G) Boxplots of average CXCL5 expression in tumor cells and macrophages across subgroups (Mann-Whitney U test). (H) Western blot validating CXCL5 knockdown and overexpression efficiency in RBE and HuCCT1 cells. (I) Quantification of migrated neutrophils in transwell assays co-cultured with modified RBE and HuCCT1 cells ( n = 4 replicates per group; mean ± SD; Student’s t test). (J) Western blot analysis of CXCL5 overexpression in KTP cells. (K) Tumor growth curves of mice injected with control or CXCL5-overexpressing KTP cells ( n = 6 per group; mean ± SEM; Student’s t test). (L) Proportion and number of infiltrated neutrophils in control and CXCL5-overexpressing KTP tumors ( n = 6 per group; Student’s t test). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. See also and and .

Journal: Cell Reports Medicine

Article Title: Robust transcriptomic hallmarks targeting intratumor heterogeneity in intrahepatic cholangiocarcinoma

doi: 10.1016/j.xcrm.2026.102708

Figure Lengend Snippet: Distinct immune microenvironment across LIHV-defined subgroups (A) Immune cell abundance comparison across subgroups using the indicated immune analysis tools across four independent iCCA cohorts. Circle color and size represent log 2 fold change and p value, respectively. (B) Boxplots of CD66b + neutrophils, CD68 + macrophages, CD3 + T cells, CD20 + B cells, and αSMA + fibroblasts across subgroups (Mann-Whitney U test). (C) Heatmap of immune signatures and checkpoint expression summarized as mean Z scores per subgroup across four cohorts. ∗FDR < 0.05; ∗∗FDR < 0.01; ∗∗∗FDR < 0.001. (D) Heatmap of Spearman correlations between chemokine expression and neutrophil infiltration. IHC, immunohistochemistry. (E) Boxplot comparing CXCL5 expression across subgroups in the Fu-iCCA cohort (Mann-Whitney U test). (F) Dot heatmap of chemokine gene expression across major cell types in Xue’s scRNA-seq dataset. (G) Boxplots of average CXCL5 expression in tumor cells and macrophages across subgroups (Mann-Whitney U test). (H) Western blot validating CXCL5 knockdown and overexpression efficiency in RBE and HuCCT1 cells. (I) Quantification of migrated neutrophils in transwell assays co-cultured with modified RBE and HuCCT1 cells ( n = 4 replicates per group; mean ± SD; Student’s t test). (J) Western blot analysis of CXCL5 overexpression in KTP cells. (K) Tumor growth curves of mice injected with control or CXCL5-overexpressing KTP cells ( n = 6 per group; mean ± SEM; Student’s t test). (L) Proportion and number of infiltrated neutrophils in control and CXCL5-overexpressing KTP tumors ( n = 6 per group; Student’s t test). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. See also and and .

Article Snippet: A CXCL5 neutralizing antibody (R&D Systems, AF254) was added at 5 μg/mL.

Techniques: Comparison, MANN-WHITNEY, Expressing, Immunohistochemistry, Gene Expression, Western Blot, Knockdown, Over Expression, Cell Culture, Modification, Injection, Control

Chemokine (C-X-C motif) ligand 5 (CXCL5) levels were elevated in the synovial fluid (SF) of patients with periprosthetic joint infection (PJI), especially in the Gram-positive bacterial component-associated PJI (GPC-PJI) group. a) The expression level of CXCL5 in SF from patients with aseptic loosening (AL) and PJI was measured using protein-array assays. b) ImageJ software was used to quantify signal intensity of CXCL5 expression (two patients in the AL group and three patients in the PJI group). c) CXCL5 concentrations in SF of AL, GPC-PJI, and Gram-negative bacterial PJI (GNB-PJI) patients were measured by performing enzyme-linked immunosorbent assays. The expression of CXCL5 in the SF of PJI patients was significantly increased (four patients in the AL group, 12 patients in the GPC group, and three patients in the GNB group). Data are presented as the mean (standard error of the mean (SEM)) and analyzed using independent-samples t -test. *p < 0.05.

Journal: Bone & Joint Research

Article Title: CXCL5 suppresses osteoclastogenesis and protects against lipoteichoic acid-induced bone loss by modulating PLCγ2 and c-Fos signalling in gram-positive periprosthetic joint infection

doi: 10.1302/2046-3758.153.BJR-2025-0290.R1

Figure Lengend Snippet: Chemokine (C-X-C motif) ligand 5 (CXCL5) levels were elevated in the synovial fluid (SF) of patients with periprosthetic joint infection (PJI), especially in the Gram-positive bacterial component-associated PJI (GPC-PJI) group. a) The expression level of CXCL5 in SF from patients with aseptic loosening (AL) and PJI was measured using protein-array assays. b) ImageJ software was used to quantify signal intensity of CXCL5 expression (two patients in the AL group and three patients in the PJI group). c) CXCL5 concentrations in SF of AL, GPC-PJI, and Gram-negative bacterial PJI (GNB-PJI) patients were measured by performing enzyme-linked immunosorbent assays. The expression of CXCL5 in the SF of PJI patients was significantly increased (four patients in the AL group, 12 patients in the GPC group, and three patients in the GNB group). Data are presented as the mean (standard error of the mean (SEM)) and analyzed using independent-samples t -test. *p < 0.05.

Article Snippet: CXCL5 concentrations in SF were further measured in triplicate using enzyme-linked immunosorbent assay (ELISA) (DY254; R&D Systems).

Techniques: Infection, Expressing, Protein Array, Software