Review

cxcl13 (R&D Systems)

R&D Systems is a verified supplier

R&D Systems manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

R&D Systems cxcl13

A Schematic representation of the anti-PD1 (α-PD1), anti-TIGIT (α-TIGIT), and combined (α-PD1 + TIGIT) antibody treatments. Nf1 -OPG mice were treated (200 µg/dose/ i.p., twice per week) from 12 to 16 weeks of age, and tissues were analyzed at 16 weeks. The control group was injected with anti-IgG isotype control antibodies. Created in BioRender. Chatterjee, J. (2024) BioRender.com/r98n914. B Immunohistochemistry and quantification CD8 + T cells in the entire optic nerve (IgG, n = 10 mice; α-TIGIT, n = 10 mice; α-PD1, n = 6 mice; α-PD1 + TIGIT, n = 5 mice). Data are represented as mean ± SD. A one-way ANOVA test was performed followed by a Dunnett’s post-test correction. Exact P values are indicated (α-TIGIT, P = 0.0054; α-PD1, P = 0.0003; α-PD1 + TIGIT, P = 0.0032). Scale bar, 200 µm. C Ccl2 RNA expression in the optic nerves of Nf1 -OPG mice treated with IgG, α-TIGIT, α-PD1 or a combination of α-PD1 and α-TIGIT antibodies. Data are represented relative to the IgG control group (IgG, n = 5, 2 pooled optic nerves per sample; α-TIGIT n = 5, 2 pooled optic nerves per sample; α-PD1, n = 4, 2 pooled optic nerves per sample; α-PD1 + TIGIT, n = 4, 2 pooled optic nerves per sample). Data are represented as mean ± SD. A one-way ANOVA test was performed followed by a Dunnett’s post-test correction. Exact P values are indicated. D Volcano plot showing fold change and P value comparing Nf1 -OPG TAM to Nf1 +/ and WT monocytes in the optic nerves of 12-week-old mice. Upregulated genes in red, downregulated genes in blue. Differential analyses were performed using gene specific analysis (GSA). E Ccr2, Cxcr3 , and Cxcr5 expression in T cell populations from 12-week-old Nf1 -OPG mouse optic nerves, color-coded by T cell type. F Cxcl9, Ccl12 , and <t>Cxcl13</t> RNA expression in the optic nerves of 12-week-old WT and Nf1 -OPG mice. Data are represented relative to the WT group ( Cxcl9 ; WT n = 3, 2 pooled optic nerves per sample; Nf1 -OPG n = 4, 2 pooled optic nerves per sample; Ccl12 ; WT n = 4, 2 pooled optic nerves per sample; Nf1 -OPG n = 4, 2 pooled optic nerves per sample; Cxcl13 ; WT n = 4, 2 pooled optic nerves per sample; Nf1 -OPG n = 4, 2 pooled optic nerves per sample). Data are represented as mean ± SD. To evaluate statistical differences, a two-tailed non-parametric Mann–Whitney test was performed. Exact P values are indicated. ns, not significant. G Graph showing the percentage of migrated Nf1 +/- CD8 + T cells treated with medium (Control) ( n = 5), Ccl12 ( n = 6), or Cxcl13 ( n = 5). Data are represented as mean ± SD. A one-way ANOVA test was performed followed by a Dunnett’s post-test correction. Exact P values are indicated. Created in BioRender. Chatterjee, J. (2024) BioRender.com/r98n914. H Ccl12 RNA expression in the optic nerves of Nf1 -OPG mice treated with IgG, α-TIGIT, α-PD1 or a combination of α-PD1 and α-TIGIT antibodies. Data are represented relative to the IgG control group (IgG, n = 5, 2 pooled optic nerves per sample; α-TIGIT n = 5, 2 pooled optic nerves per sample; α-PD1, n = 4, 2 pooled optic nerves per sample; α-PD1 + TIGIT, n = 3, 2 pooled optic nerves per sample). Data are represented as mean ± SD. A one-way ANOVA test was performed followed by a Tukey’s post-test correction. Exact P values are indicated (α-TIGIT, P = 0.0012; α-PD1, P = 0.0187; α-PD1 + TIGIT, P = 0.0013). I Cxcl13 RNA expression in the optic nerves of Nf1 -OPG mice treated with IgG, α-TIGIT, α-PD1 or a combination of α-PD1 and α-TIGIT antibodies. Data are represented relative to the IgG control group (IgG, n = 4, 2 pooled optic nerves per sample; α-TIGIT n = 4, 2 pooled optic nerves per sample; α-PD1, n = 4, 2 pooled optic nerves per sample; α-PD1 + TIGIT, n = 4, 2 pooled optic nerves per sample). Data are represented as mean ± SD. A one-way ANOVA test was performed followed by a Tukey’s post test correction. Exact P values are indicated (α-TIGIT, P = 0.0003; α-PD1, P = 0.0007; α-PD1 + TIGIT, P = 0.0001).

Cxcl13, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/cxcl13/product/R&D Systems
Average 93 stars, based on 15 article reviews

cxcl13 - by Bioz Stars, 2026-03

93/100 stars

Images

1) Product Images from "Human single cell RNA-sequencing reveals a targetable CD8 + exhausted T cell population that maintains mouse low-grade glioma growth"

Article Title: Human single cell RNA-sequencing reveals a targetable CD8 + exhausted T cell population that maintains mouse low-grade glioma growth

Journal: Nature Communications

doi: 10.1038/s41467-024-54569-4

Figure Legend Snippet: A Schematic representation of the anti-PD1 (α-PD1), anti-TIGIT (α-TIGIT), and combined (α-PD1 + TIGIT) antibody treatments. Nf1 -OPG mice were treated (200 µg/dose/ i.p., twice per week) from 12 to 16 weeks of age, and tissues were analyzed at 16 weeks. The control group was injected with anti-IgG isotype control antibodies. Created in BioRender. Chatterjee, J. (2024) BioRender.com/r98n914. B Immunohistochemistry and quantification CD8 + T cells in the entire optic nerve (IgG, n = 10 mice; α-TIGIT, n = 10 mice; α-PD1, n = 6 mice; α-PD1 + TIGIT, n = 5 mice). Data are represented as mean ± SD. A one-way ANOVA test was performed followed by a Dunnett’s post-test correction. Exact P values are indicated (α-TIGIT, P = 0.0054; α-PD1, P = 0.0003; α-PD1 + TIGIT, P = 0.0032). Scale bar, 200 µm. C Ccl2 RNA expression in the optic nerves of Nf1 -OPG mice treated with IgG, α-TIGIT, α-PD1 or a combination of α-PD1 and α-TIGIT antibodies. Data are represented relative to the IgG control group (IgG, n = 5, 2 pooled optic nerves per sample; α-TIGIT n = 5, 2 pooled optic nerves per sample; α-PD1, n = 4, 2 pooled optic nerves per sample; α-PD1 + TIGIT, n = 4, 2 pooled optic nerves per sample). Data are represented as mean ± SD. A one-way ANOVA test was performed followed by a Dunnett’s post-test correction. Exact P values are indicated. D Volcano plot showing fold change and P value comparing Nf1 -OPG TAM to Nf1 +/ and WT monocytes in the optic nerves of 12-week-old mice. Upregulated genes in red, downregulated genes in blue. Differential analyses were performed using gene specific analysis (GSA). E Ccr2, Cxcr3 , and Cxcr5 expression in T cell populations from 12-week-old Nf1 -OPG mouse optic nerves, color-coded by T cell type. F Cxcl9, Ccl12 , and Cxcl13 RNA expression in the optic nerves of 12-week-old WT and Nf1 -OPG mice. Data are represented relative to the WT group ( Cxcl9 ; WT n = 3, 2 pooled optic nerves per sample; Nf1 -OPG n = 4, 2 pooled optic nerves per sample; Ccl12 ; WT n = 4, 2 pooled optic nerves per sample; Nf1 -OPG n = 4, 2 pooled optic nerves per sample; Cxcl13 ; WT n = 4, 2 pooled optic nerves per sample; Nf1 -OPG n = 4, 2 pooled optic nerves per sample). Data are represented as mean ± SD. To evaluate statistical differences, a two-tailed non-parametric Mann–Whitney test was performed. Exact P values are indicated. ns, not significant. G Graph showing the percentage of migrated Nf1 +/- CD8 + T cells treated with medium (Control) ( n = 5), Ccl12 ( n = 6), or Cxcl13 ( n = 5). Data are represented as mean ± SD. A one-way ANOVA test was performed followed by a Dunnett’s post-test correction. Exact P values are indicated. Created in BioRender. Chatterjee, J. (2024) BioRender.com/r98n914. H Ccl12 RNA expression in the optic nerves of Nf1 -OPG mice treated with IgG, α-TIGIT, α-PD1 or a combination of α-PD1 and α-TIGIT antibodies. Data are represented relative to the IgG control group (IgG, n = 5, 2 pooled optic nerves per sample; α-TIGIT n = 5, 2 pooled optic nerves per sample; α-PD1, n = 4, 2 pooled optic nerves per sample; α-PD1 + TIGIT, n = 3, 2 pooled optic nerves per sample). Data are represented as mean ± SD. A one-way ANOVA test was performed followed by a Tukey’s post-test correction. Exact P values are indicated (α-TIGIT, P = 0.0012; α-PD1, P = 0.0187; α-PD1 + TIGIT, P = 0.0013). I Cxcl13 RNA expression in the optic nerves of Nf1 -OPG mice treated with IgG, α-TIGIT, α-PD1 or a combination of α-PD1 and α-TIGIT antibodies. Data are represented relative to the IgG control group (IgG, n = 4, 2 pooled optic nerves per sample; α-TIGIT n = 4, 2 pooled optic nerves per sample; α-PD1, n = 4, 2 pooled optic nerves per sample; α-PD1 + TIGIT, n = 4, 2 pooled optic nerves per sample). Data are represented as mean ± SD. A one-way ANOVA test was performed followed by a Tukey’s post test correction. Exact P values are indicated (α-TIGIT, P = 0.0003; α-PD1, P = 0.0007; α-PD1 + TIGIT, P = 0.0001).

Techniques Used: Control, Injection, Immunohistochemistry, RNA Expression, Expressing, Two Tailed Test, MANN-WHITNEY

Image Search Results

Journal: Nature Communications

Article Title: Human single cell RNA-sequencing reveals a targetable CD8 + exhausted T cell population that maintains mouse low-grade glioma growth

doi: 10.1038/s41467-024-54569-4

Figure Lengend Snippet: A Schematic representation of the anti-PD1 (α-PD1), anti-TIGIT (α-TIGIT), and combined (α-PD1 + TIGIT) antibody treatments. Nf1 -OPG mice were treated (200 µg/dose/ i.p., twice per week) from 12 to 16 weeks of age, and tissues were analyzed at 16 weeks. The control group was injected with anti-IgG isotype control antibodies. Created in BioRender. Chatterjee, J. (2024) BioRender.com/r98n914. B Immunohistochemistry and quantification CD8 + T cells in the entire optic nerve (IgG, n = 10 mice; α-TIGIT, n = 10 mice; α-PD1, n = 6 mice; α-PD1 + TIGIT, n = 5 mice). Data are represented as mean ± SD. A one-way ANOVA test was performed followed by a Dunnett’s post-test correction. Exact P values are indicated (α-TIGIT, P = 0.0054; α-PD1, P = 0.0003; α-PD1 + TIGIT, P = 0.0032). Scale bar, 200 µm. C Ccl2 RNA expression in the optic nerves of Nf1 -OPG mice treated with IgG, α-TIGIT, α-PD1 or a combination of α-PD1 and α-TIGIT antibodies. Data are represented relative to the IgG control group (IgG, n = 5, 2 pooled optic nerves per sample; α-TIGIT n = 5, 2 pooled optic nerves per sample; α-PD1, n = 4, 2 pooled optic nerves per sample; α-PD1 + TIGIT, n = 4, 2 pooled optic nerves per sample). Data are represented as mean ± SD. A one-way ANOVA test was performed followed by a Dunnett’s post-test correction. Exact P values are indicated. D Volcano plot showing fold change and P value comparing Nf1 -OPG TAM to Nf1 +/ and WT monocytes in the optic nerves of 12-week-old mice. Upregulated genes in red, downregulated genes in blue. Differential analyses were performed using gene specific analysis (GSA). E Ccr2, Cxcr3 , and Cxcr5 expression in T cell populations from 12-week-old Nf1 -OPG mouse optic nerves, color-coded by T cell type. F Cxcl9, Ccl12 , and Cxcl13 RNA expression in the optic nerves of 12-week-old WT and Nf1 -OPG mice. Data are represented relative to the WT group ( Cxcl9 ; WT n = 3, 2 pooled optic nerves per sample; Nf1 -OPG n = 4, 2 pooled optic nerves per sample; Ccl12 ; WT n = 4, 2 pooled optic nerves per sample; Nf1 -OPG n = 4, 2 pooled optic nerves per sample; Cxcl13 ; WT n = 4, 2 pooled optic nerves per sample; Nf1 -OPG n = 4, 2 pooled optic nerves per sample). Data are represented as mean ± SD. To evaluate statistical differences, a two-tailed non-parametric Mann–Whitney test was performed. Exact P values are indicated. ns, not significant. G Graph showing the percentage of migrated Nf1 +/- CD8 + T cells treated with medium (Control) ( n = 5), Ccl12 ( n = 6), or Cxcl13 ( n = 5). Data are represented as mean ± SD. A one-way ANOVA test was performed followed by a Dunnett’s post-test correction. Exact P values are indicated. Created in BioRender. Chatterjee, J. (2024) BioRender.com/r98n914. H Ccl12 RNA expression in the optic nerves of Nf1 -OPG mice treated with IgG, α-TIGIT, α-PD1 or a combination of α-PD1 and α-TIGIT antibodies. Data are represented relative to the IgG control group (IgG, n = 5, 2 pooled optic nerves per sample; α-TIGIT n = 5, 2 pooled optic nerves per sample; α-PD1, n = 4, 2 pooled optic nerves per sample; α-PD1 + TIGIT, n = 3, 2 pooled optic nerves per sample). Data are represented as mean ± SD. A one-way ANOVA test was performed followed by a Tukey’s post-test correction. Exact P values are indicated (α-TIGIT, P = 0.0012; α-PD1, P = 0.0187; α-PD1 + TIGIT, P = 0.0013). I Cxcl13 RNA expression in the optic nerves of Nf1 -OPG mice treated with IgG, α-TIGIT, α-PD1 or a combination of α-PD1 and α-TIGIT antibodies. Data are represented relative to the IgG control group (IgG, n = 4, 2 pooled optic nerves per sample; α-TIGIT n = 4, 2 pooled optic nerves per sample; α-PD1, n = 4, 2 pooled optic nerves per sample; α-PD1 + TIGIT, n = 4, 2 pooled optic nerves per sample). Data are represented as mean ± SD. A one-way ANOVA test was performed followed by a Tukey’s post test correction. Exact P values are indicated (α-TIGIT, P = 0.0003; α-PD1, P = 0.0007; α-PD1 + TIGIT, P = 0.0001).

Article Snippet: 500 μl of chemoattractant media (Ccl12 [25 ng/ml, 428-P5-025- R&D systems ] and Cxcl13 [1 µg/ml, 470-BC-025- R&D systems] ) was added to the lower chamber, and the number of T cells in the lower chambers counted 6 h later.

Techniques: Control, Injection, Immunohistochemistry, RNA Expression, Expressing, Two Tailed Test, MANN-WHITNEY

Identification of CXCL13 binding to syndecan-1 (SDC-1). ( A ) Co-expression of SDC-1 and CXCL13 in submandibular gland tissues of NOD/ShiLtJ mice. Each section was double-stained with immunofluorescent antibodies to determine the distribution of SDC-1 (CD138, red) and CXCL13 (green) on the epithelial cells. The sections were counterstained with 4′,6-diamidino-2-phenylindole (DAPI, blue). The merged images obtained by confocal microscopy show the yellow co-localization of both molecules. Magnified views of the boxed areas are shown in the right column. Scale bars = 50 and 25 µm. ( B ) Co-expression of SDC-1 and CXCL13 on normal murine mammary gland (NMuMG) cells. NMuMG cells were double-stained with anti-CXCL13 mAb (green) and anti-SDC-1 mAb (red). The sections were counterstained with DAPI (blue). Scale bar = 25 µm. ( C ) Association of SDC-1 with CXCL13 at the cell surface of NMuMG cells. NMuMG cells were incubated with 0, 50, 100, and 150 nM recombinant mouse CXCL13 for 18 h. The cell pellets of NMuMG cells were harvested following the protocol outlined in the Pierce™ Classic Magnetic IP/Co-IP Kit. The cell lysates were incubated with mouse anti-SDC-1 antibody, and anti-SDC-1 antibody binding complexes were analyzed by Western blotting assay with antibody against CXCL13 (Novus Biologicals, Centennial, CO, USA) or rat immunoglobulin G (control, Santacruz, Dallas, TX, USA).

Journal: International Journal of Molecular Sciences

Article Title: Syndecan-1 Plays a Role in the Pathogenesis of Sjögren’s Disease by Inducing B-Cell Chemotaxis through CXCL13–Heparan Sulfate Interaction

doi: 10.3390/ijms25179375

Figure Lengend Snippet: Identification of CXCL13 binding to syndecan-1 (SDC-1). ( A ) Co-expression of SDC-1 and CXCL13 in submandibular gland tissues of NOD/ShiLtJ mice. Each section was double-stained with immunofluorescent antibodies to determine the distribution of SDC-1 (CD138, red) and CXCL13 (green) on the epithelial cells. The sections were counterstained with 4′,6-diamidino-2-phenylindole (DAPI, blue). The merged images obtained by confocal microscopy show the yellow co-localization of both molecules. Magnified views of the boxed areas are shown in the right column. Scale bars = 50 and 25 µm. ( B ) Co-expression of SDC-1 and CXCL13 on normal murine mammary gland (NMuMG) cells. NMuMG cells were double-stained with anti-CXCL13 mAb (green) and anti-SDC-1 mAb (red). The sections were counterstained with DAPI (blue). Scale bar = 25 µm. ( C ) Association of SDC-1 with CXCL13 at the cell surface of NMuMG cells. NMuMG cells were incubated with 0, 50, 100, and 150 nM recombinant mouse CXCL13 for 18 h. The cell pellets of NMuMG cells were harvested following the protocol outlined in the Pierce™ Classic Magnetic IP/Co-IP Kit. The cell lysates were incubated with mouse anti-SDC-1 antibody, and anti-SDC-1 antibody binding complexes were analyzed by Western blotting assay with antibody against CXCL13 (Novus Biologicals, Centennial, CO, USA) or rat immunoglobulin G (control, Santacruz, Dallas, TX, USA).

Article Snippet: Recombinant mouse CXCL13 was purchased from R&D Systems (Minneapolis, MN, USA), and Pierce™ Classic Magnetic IP/Co-IP Kit was obtained from Thermo Fisher Scientific (Waltham, MA, USA).

Techniques: Binding Assay, Expressing, Staining, Confocal Microscopy, Incubation, Recombinant, Co-Immunoprecipitation Assay, Western Blot, Control

(A) Representative TLS in tissues stained by H&E and CXCL13 (Fast RED) by RNA ISH. Scale bars indicate 100 µm. (B) TLS presence ratio based on CXCL13 gene expression. Analysis by Fisher’s exact test in 28 cases with microarray data. (C) Characterization of the immune infiltrate in tumors according to CXCL13 gene expression (n=28). Correlation was determined by Spearman’s correlation test. (D) (E) The distribution of infiltrating immune cells into the tumor site and CXCL13 gene expression using CIBERSORT (n=522). Correlation was determined by Spearman’s correlation test. (F) Overall survival of patients with HGSC by CXCL13 gene expression (TCGA n=217, KOV n=28). Patients with CXCL13 high defined if CXCL13 gene expression was above the median. Analyses were performed with Kaplan-Meier estimates, log-rank tests and Wilcoxon tests. The level of significance was set as * P <0.05, ** P <0.01, and **** P <0.0001.

Journal: bioRxiv

Article Title: Tertiary lymphoid structures induced by CXCL13-producing CD4 + T cells increase tumor infiltrating CD8 + T cells and B cells in ovarian cancer

doi: 10.1101/2021.12.01.470493

Figure Lengend Snippet: (A) Representative TLS in tissues stained by H&E and CXCL13 (Fast RED) by RNA ISH. Scale bars indicate 100 µm. (B) TLS presence ratio based on CXCL13 gene expression. Analysis by Fisher’s exact test in 28 cases with microarray data. (C) Characterization of the immune infiltrate in tumors according to CXCL13 gene expression (n=28). Correlation was determined by Spearman’s correlation test. (D) (E) The distribution of infiltrating immune cells into the tumor site and CXCL13 gene expression using CIBERSORT (n=522). Correlation was determined by Spearman’s correlation test. (F) Overall survival of patients with HGSC by CXCL13 gene expression (TCGA n=217, KOV n=28). Patients with CXCL13 high defined if CXCL13 gene expression was above the median. Analyses were performed with Kaplan-Meier estimates, log-rank tests and Wilcoxon tests. The level of significance was set as * P <0.05, ** P <0.01, and **** P <0.0001.

Article Snippet: Mouse recombinant CXCL13 (R&D Systems) treatment was initiated one day after the tumor inoculation and administered intraperitoneally at 1 μg/mouse every other day for five times.

Techniques: Staining, Gene Expression, Microarray

(A) Fluorescent double staining of CXCL13 (red) and CD4 (green), and CXCL13 (red) and CD8 (white) by RNA ISH in TLS. Images of four representative TLS are shown. (B) Fluorescent double staining of CXCL13 (red) and CD4 (green), and CXCL13 (red) and CD8 (white) by RNA ISH in TIL. The upper and lower pictures are representative TIL images from the same patient. Nuclei are stained with DAPI (blue). Scale bars indicate 100 µm. Co-localization of CXCL13 with CD4 or CD8 is shown in the bar graph as the relative positive ratio quantified using BZ-H4C/hybrid cell count software.

Journal: bioRxiv

Article Title: Tertiary lymphoid structures induced by CXCL13-producing CD4 + T cells increase tumor infiltrating CD8 + T cells and B cells in ovarian cancer

doi: 10.1101/2021.12.01.470493

Figure Lengend Snippet: (A) Fluorescent double staining of CXCL13 (red) and CD4 (green), and CXCL13 (red) and CD8 (white) by RNA ISH in TLS. Images of four representative TLS are shown. (B) Fluorescent double staining of CXCL13 (red) and CD4 (green), and CXCL13 (red) and CD8 (white) by RNA ISH in TIL. The upper and lower pictures are representative TIL images from the same patient. Nuclei are stained with DAPI (blue). Scale bars indicate 100 µm. Co-localization of CXCL13 with CD4 or CD8 is shown in the bar graph as the relative positive ratio quantified using BZ-H4C/hybrid cell count software.

Techniques: Double Staining, Staining, Cell Counting, Software

(A) Representative images of early TLS. (B) Representative images of follicle-formed TLS. Upper panels show CXCL13 (RNA ISH, Fast RED) and lower panels show FDC (CD21 IHC, DAB). (C) Fluorescence double staining of CXCL13 (red) and CD4 (green), CXCL13 (red) and CD8 (white), and CXCL13 (red) and CD21 (light blue) in representative early TLS and follicle-formed TLS. Nuclei are stained with DAPI (blue). Scale bar indicates 100 µm. Co-localization of CXCL13 with CD4, CD8, or CD21 is shown in the bar graph as the relative positive ratio quantified using BZ-H4C/hybrid cell count software.

Journal: bioRxiv

Article Title: Tertiary lymphoid structures induced by CXCL13-producing CD4 + T cells increase tumor infiltrating CD8 + T cells and B cells in ovarian cancer

doi: 10.1101/2021.12.01.470493

Figure Lengend Snippet: (A) Representative images of early TLS. (B) Representative images of follicle-formed TLS. Upper panels show CXCL13 (RNA ISH, Fast RED) and lower panels show FDC (CD21 IHC, DAB). (C) Fluorescence double staining of CXCL13 (red) and CD4 (green), CXCL13 (red) and CD8 (white), and CXCL13 (red) and CD21 (light blue) in representative early TLS and follicle-formed TLS. Nuclei are stained with DAPI (blue). Scale bar indicates 100 µm. Co-localization of CXCL13 with CD4, CD8, or CD21 is shown in the bar graph as the relative positive ratio quantified using BZ-H4C/hybrid cell count software.

Techniques: Fluorescence, Double Staining, Staining, Cell Counting, Software

(A) Correlation between CXCL13 and TGF-β1 expression in TCGA (n=217) and KOV (n=28). Correlation was determined by Spearman’s correlation test. (B) Human naïve CD4 + and CD8 + T cells from a healthy donor were differentiated by TCR stimulation and TGF-β1 in the presence or absence of a TGF signal inhibitor, SB431542. The proportion of CXCL13 + cells was determined by flow cytometry. Data are shown as the mean ± SEM of four samples. Statistical significance was determined by two-tailed Student’s t -test, * P <0.05, ** P <0.01, *** P <0.001, n.s.: not significant. (C) The concentration of TGF-β1 in conditioned medium obtained from three human ovarian cancer cell lines was measured by ELISA. Data are shown as the mean ± SEM of three samples. (D) Human naïve CD4 + and CD8 + T cells from a healthy donor were differentiated with TCR stimulation and conditioned medium obtained from three human ovarian cancer cell lines in the presence or absence of a TGF signal inhibitor, SB431542. The proportion of CXCL13 + cells was determined by flow cytometry. Data are shown as the mean ± SEM of triplicates. (E) (F) (G) Human naïve CD4 + and CD8 + T cells from a healthy donor were differentiated with TCR stimulation and the indicated cytokines. The proportion of CXCL13 + cells was determined by flow cytometry (E) . The concentration of CXCL13 in the culture supernatant was measured by ELISA (F) . Data are shown as the mean ± SEM of four samples in CD4 and three samples in CD8. Statistical significance was determined by two-tailed Student’s t -test, * P <0.05, ** P < 0.01, *** P < 0.001, **** P <0.0001, n.s.: not significant. Representative dot plots of PD-1 (upper row), CXCR5 (lower row), and intracellular CXCL13 in healthy human naïve CD4 + T cells are shown (G) . a IL-2 Ab indicates anti IL-2 antibody.

Journal: bioRxiv

Article Title: Tertiary lymphoid structures induced by CXCL13-producing CD4 + T cells increase tumor infiltrating CD8 + T cells and B cells in ovarian cancer

doi: 10.1101/2021.12.01.470493

Figure Lengend Snippet: (A) Correlation between CXCL13 and TGF-β1 expression in TCGA (n=217) and KOV (n=28). Correlation was determined by Spearman’s correlation test. (B) Human naïve CD4 + and CD8 + T cells from a healthy donor were differentiated by TCR stimulation and TGF-β1 in the presence or absence of a TGF signal inhibitor, SB431542. The proportion of CXCL13 + cells was determined by flow cytometry. Data are shown as the mean ± SEM of four samples. Statistical significance was determined by two-tailed Student’s t -test, * P <0.05, ** P <0.01, *** P <0.001, n.s.: not significant. (C) The concentration of TGF-β1 in conditioned medium obtained from three human ovarian cancer cell lines was measured by ELISA. Data are shown as the mean ± SEM of three samples. (D) Human naïve CD4 + and CD8 + T cells from a healthy donor were differentiated with TCR stimulation and conditioned medium obtained from three human ovarian cancer cell lines in the presence or absence of a TGF signal inhibitor, SB431542. The proportion of CXCL13 + cells was determined by flow cytometry. Data are shown as the mean ± SEM of triplicates. (E) (F) (G) Human naïve CD4 + and CD8 + T cells from a healthy donor were differentiated with TCR stimulation and the indicated cytokines. The proportion of CXCL13 + cells was determined by flow cytometry (E) . The concentration of CXCL13 in the culture supernatant was measured by ELISA (F) . Data are shown as the mean ± SEM of four samples in CD4 and three samples in CD8. Statistical significance was determined by two-tailed Student’s t -test, * P <0.05, ** P < 0.01, *** P < 0.001, **** P <0.0001, n.s.: not significant. Representative dot plots of PD-1 (upper row), CXCR5 (lower row), and intracellular CXCL13 in healthy human naïve CD4 + T cells are shown (G) . a IL-2 Ab indicates anti IL-2 antibody.

Techniques: Expressing, Flow Cytometry, Two Tailed Test, Concentration Assay, Enzyme-linked Immunosorbent Assay

(A) Mouse rCXCL13 was administered intraperitoneally to induce TLS in a mouse ovarian cancer model. Representative H&E images of TLS formed in an omental tumor. The area of TLS per tumor area was compared between the control group and the rCXCL13 treated group (n=7, each). Statistical significance was determined by two-tailed Student’s t -test, * P <0.05. (B) TLS induced by mouse rCXCL13 (H&E) and expression of mouse CXCL13 corresponding to TLS (RNA ISH, Fast RED). (C) CD8 + T cell IHC images (DAB) in the rCXCL13 treated group and control group. Scale bars indicate 100 µm. (D) (E) The effect of rCXCL13 administration on the survival of tumor-bearing mice was compared between immunocompetent mice (D) and immunodeficient mice (E). Analyses were performed using Kaplan-Meier estimates and log-rank tests.

Journal: bioRxiv

Article Title: Tertiary lymphoid structures induced by CXCL13-producing CD4 + T cells increase tumor infiltrating CD8 + T cells and B cells in ovarian cancer

doi: 10.1101/2021.12.01.470493

Figure Lengend Snippet: (A) Mouse rCXCL13 was administered intraperitoneally to induce TLS in a mouse ovarian cancer model. Representative H&E images of TLS formed in an omental tumor. The area of TLS per tumor area was compared between the control group and the rCXCL13 treated group (n=7, each). Statistical significance was determined by two-tailed Student’s t -test, * P <0.05. (B) TLS induced by mouse rCXCL13 (H&E) and expression of mouse CXCL13 corresponding to TLS (RNA ISH, Fast RED). (C) CD8 + T cell IHC images (DAB) in the rCXCL13 treated group and control group. Scale bars indicate 100 µm. (D) (E) The effect of rCXCL13 administration on the survival of tumor-bearing mice was compared between immunocompetent mice (D) and immunodeficient mice (E). Analyses were performed using Kaplan-Meier estimates and log-rank tests.

Techniques: Control, Two Tailed Test, Expressing

CXCL13, regulated by HDAC6, mediates AD. (A) Serum of each Nc/Nga mouse of each experimental group was employed for cytokine array analysis. AD was induced as described. Nc/Nga mice were given an intravenous injection of the indicated siRNA (100 nM). (B) ELISA was performed to determine serum CXCL13 level. ***, p < 0.001. Average values of three independent experiments were shown. (C) Skin mast cells from DNCB-untreated Nc/Nga mouse were treated with CXCL13 as indicated. (D) Effect of CXCL13 on clinical symptoms associated with AD was shown. **, p < 0.01; ***, p < 0.001. (E) Serum and tissue lysates were subjected to ELISA and qRT-PCR, respectively. *, p < 0.05; **, p < 0.01; ***, p < 0.001. Average values of three independent experiments were shown. (F) Immunoblot analysis employing skin tissue lysates (left) or skin mast cell lysates isolated from skin tissue of Nc/Nga mouse of each experimental group was performed (right). Representative blots of three independent experiments were shown. (G) H&E staining, toluidine blue staining, and immunohistochemical staining were performed. Closed rectangle represents degranulated mast cells. ***, p < 0.001. Quantification was performed using ImageJ (NIH).

Journal: Frontiers in Pharmacology

Article Title: HDAC6 and CXCL13 Mediate Atopic Dermatitis by Regulating Cellular Interactions and Expression Levels of miR-9 and SIRT1

doi: 10.3389/fphar.2021.691279

Figure Lengend Snippet: CXCL13, regulated by HDAC6, mediates AD. (A) Serum of each Nc/Nga mouse of each experimental group was employed for cytokine array analysis. AD was induced as described. Nc/Nga mice were given an intravenous injection of the indicated siRNA (100 nM). (B) ELISA was performed to determine serum CXCL13 level. ***, p < 0.001. Average values of three independent experiments were shown. (C) Skin mast cells from DNCB-untreated Nc/Nga mouse were treated with CXCL13 as indicated. (D) Effect of CXCL13 on clinical symptoms associated with AD was shown. **, p < 0.01; ***, p < 0.001. (E) Serum and tissue lysates were subjected to ELISA and qRT-PCR, respectively. *, p < 0.05; **, p < 0.01; ***, p < 0.001. Average values of three independent experiments were shown. (F) Immunoblot analysis employing skin tissue lysates (left) or skin mast cell lysates isolated from skin tissue of Nc/Nga mouse of each experimental group was performed (right). Representative blots of three independent experiments were shown. (G) H&E staining, toluidine blue staining, and immunohistochemical staining were performed. Closed rectangle represents degranulated mast cells. ***, p < 0.001. Quantification was performed using ImageJ (NIH).

Article Snippet: Mouse recombinant CXCL13 protein was purchased from R&D Systems.

Techniques: Injection, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR, Western Blot, Isolation, Staining, Immunohistochemical staining

Sirtinol suppresses AD. (A) Sirtinol suppresses AD. Nc/Nga mice were given an intraperitoneal injection of sirtinol (0.5 mg/kg). Each experimental group comprised four Nc/Nga mice. ***, p < 0.001. Blue triangle denotes intraperitoneal injection with sirtinol. Black triangle denotes topical treatment with DNCB. (B) Skin tissue lysates were subjected to qRT-PCR. Serum PGE2 level, and serum CXCL13 level were also determined. **, p < 0.01; ***, p < 0.001. Average values of three independent experiments were shown. (C) Skin tissue lysates were subjected to immunoblot (left). Skin mast cell lysates from Nc/Nga mouse of each experimental group were subjected to immunoblot (right). Representative blots of three independent experiments were shown. (D) H&E staining, toluidine blue staining, and immunohistochemical staining were performed. Closed triangle represents degranulated mast cells. *, p < 0.05; **, p < 0.01; ***, p < 0.001. Quantification was performed using ImageJ (NIH).

Journal: Frontiers in Pharmacology

Article Title: HDAC6 and CXCL13 Mediate Atopic Dermatitis by Regulating Cellular Interactions and Expression Levels of miR-9 and SIRT1

doi: 10.3389/fphar.2021.691279

Figure Lengend Snippet: Sirtinol suppresses AD. (A) Sirtinol suppresses AD. Nc/Nga mice were given an intraperitoneal injection of sirtinol (0.5 mg/kg). Each experimental group comprised four Nc/Nga mice. ***, p < 0.001. Blue triangle denotes intraperitoneal injection with sirtinol. Black triangle denotes topical treatment with DNCB. (B) Skin tissue lysates were subjected to qRT-PCR. Serum PGE2 level, and serum CXCL13 level were also determined. **, p < 0.01; ***, p < 0.001. Average values of three independent experiments were shown. (C) Skin tissue lysates were subjected to immunoblot (left). Skin mast cell lysates from Nc/Nga mouse of each experimental group were subjected to immunoblot (right). Representative blots of three independent experiments were shown. (D) H&E staining, toluidine blue staining, and immunohistochemical staining were performed. Closed triangle represents degranulated mast cells. *, p < 0.05; **, p < 0.01; ***, p < 0.001. Quantification was performed using ImageJ (NIH).

Article Snippet: Mouse recombinant CXCL13 protein was purchased from R&D Systems.

Techniques: Injection, Quantitative RT-PCR, Western Blot, Staining, Immunohistochemical staining

CXCL13 mediates cellular interactions. (A) Dermal fibroblast cells were treated with mouse recombinant CXCL13 protein (20 ng) for 2 h (left). Culture medium of dermal fibroblast cells was then added to HaCaT cells for 16 h (middle). HaCaT cells were treated with DNCB (5 μM) for various time intervals (right, upper). HaCaT cells were pretreated with tubastain A (10 μM) for 2 h, and treatment with DNCB (5 μM) for 1 h was followed (right, lower). Immunoblot was performed. Representative blots of three independent experiments were shown. (B) Twenty-four hours after treatment with CXCL13 protein, invasion potential of dermal fibroblast cells was determined (upper). Twenty-four hours after treatment with culture medium of skin dermal fibroblast cells treated with recombinant CXCL13 protein for 2 h, invasion potential of HaCaT cells was determined (lower). ***, p < 0.001. Average values of three independent experiments were shown. (C) Skin mast cells from DNCB-untreated Nc/Nga mouse were treated with mouse recombinant CXCL13 protein (20 ng) for 2 h (left). Culture medium of skin mast cells was then added to HaCaT cells or dermal fibroblast cells for 16 h (right). Immunoblot was performed. Representative blots of three independent experiments were shown. (D) Same as (C) except that invasion assays were performed as described. Average values of three independent experiments were shown. (E) Culture medium of skin mast cells from Nc/Nga mouse of each experimental group was employed. Culture medium of skin mast cells was added to HaCaT cells or dermal fibroblast cells for 16 h. Immunoblot was performed. Representative blots of three independent experiments were shown. (F) Indicated siRNA (10 nM) was transfected into dermal fibroblast cells. The next day, cells were then treated with DNCB (5 μM) for 1 h followed by immunoblot (left). Culture medium of dermal fibroblast cells was added to HaCaT cells (middle) or skin mast cells (right) for 16 h followed by immunoblot (right). Representative blots of three independent experiments were shown.

Journal: Frontiers in Pharmacology

Article Title: HDAC6 and CXCL13 Mediate Atopic Dermatitis by Regulating Cellular Interactions and Expression Levels of miR-9 and SIRT1

doi: 10.3389/fphar.2021.691279

Figure Lengend Snippet: CXCL13 mediates cellular interactions. (A) Dermal fibroblast cells were treated with mouse recombinant CXCL13 protein (20 ng) for 2 h (left). Culture medium of dermal fibroblast cells was then added to HaCaT cells for 16 h (middle). HaCaT cells were treated with DNCB (5 μM) for various time intervals (right, upper). HaCaT cells were pretreated with tubastain A (10 μM) for 2 h, and treatment with DNCB (5 μM) for 1 h was followed (right, lower). Immunoblot was performed. Representative blots of three independent experiments were shown. (B) Twenty-four hours after treatment with CXCL13 protein, invasion potential of dermal fibroblast cells was determined (upper). Twenty-four hours after treatment with culture medium of skin dermal fibroblast cells treated with recombinant CXCL13 protein for 2 h, invasion potential of HaCaT cells was determined (lower). ***, p < 0.001. Average values of three independent experiments were shown. (C) Skin mast cells from DNCB-untreated Nc/Nga mouse were treated with mouse recombinant CXCL13 protein (20 ng) for 2 h (left). Culture medium of skin mast cells was then added to HaCaT cells or dermal fibroblast cells for 16 h (right). Immunoblot was performed. Representative blots of three independent experiments were shown. (D) Same as (C) except that invasion assays were performed as described. Average values of three independent experiments were shown. (E) Culture medium of skin mast cells from Nc/Nga mouse of each experimental group was employed. Culture medium of skin mast cells was added to HaCaT cells or dermal fibroblast cells for 16 h. Immunoblot was performed. Representative blots of three independent experiments were shown. (F) Indicated siRNA (10 nM) was transfected into dermal fibroblast cells. The next day, cells were then treated with DNCB (5 μM) for 1 h followed by immunoblot (left). Culture medium of dermal fibroblast cells was added to HaCaT cells (middle) or skin mast cells (right) for 16 h followed by immunoblot (right). Representative blots of three independent experiments were shown.

Article Snippet: Mouse recombinant CXCL13 protein was purchased from R&D Systems.

Techniques: Recombinant, Western Blot, Transfection

Exosomes of skin mast cells induce features of AD in HaCaT and dermal fibroblast cells. (A) Skin mast cells were pretreated with GW4869 (20 μM) for 2 h, and treatment with DNCB (5 μM) for 1 h was followed. HaCaT cells and dermal fibroblast cells were treated with the culture medium of skin mast cells for 12 h. Immunoblot was performed. Representative blots of three independent experiments were shown. (B) Exosomes isolated from skin mast cells treated with or without DNCB (5 μM) for 24 h were visualized by negative staining electron microscopy. (C) Shows size distributions of exosomes employing nanoparticle tracking analysis (NTA). (D) Immunoblot shows the presence of CXCL13 in the exosomes of DNCB-treated skin mast cells. Representative blots of three independent experiments were shown. (E) Exosomes were isolated from skin mast cells treated with or without DNCB for 1 h. Exosomes (5 μg) were then added to HaCaT cells or skin dermal fibroblast cells for 24 h followed by immunoblot and invasion assays. *, p < 0.05; ***, p < 0.001. Average values of three independent experiments were shown. (F) Immuno-gold staining images using anti-TSG101, a known membrane marker for the exosomes, and anti-CXCL13 antibody. Twenty-five and 10 nm gold particles show the presence of TSG101 and CXCL13, respectively.

Journal: Frontiers in Pharmacology

Article Title: HDAC6 and CXCL13 Mediate Atopic Dermatitis by Regulating Cellular Interactions and Expression Levels of miR-9 and SIRT1

doi: 10.3389/fphar.2021.691279

Figure Lengend Snippet: Exosomes of skin mast cells induce features of AD in HaCaT and dermal fibroblast cells. (A) Skin mast cells were pretreated with GW4869 (20 μM) for 2 h, and treatment with DNCB (5 μM) for 1 h was followed. HaCaT cells and dermal fibroblast cells were treated with the culture medium of skin mast cells for 12 h. Immunoblot was performed. Representative blots of three independent experiments were shown. (B) Exosomes isolated from skin mast cells treated with or without DNCB (5 μM) for 24 h were visualized by negative staining electron microscopy. (C) Shows size distributions of exosomes employing nanoparticle tracking analysis (NTA). (D) Immunoblot shows the presence of CXCL13 in the exosomes of DNCB-treated skin mast cells. Representative blots of three independent experiments were shown. (E) Exosomes were isolated from skin mast cells treated with or without DNCB for 1 h. Exosomes (5 μg) were then added to HaCaT cells or skin dermal fibroblast cells for 24 h followed by immunoblot and invasion assays. *, p < 0.05; ***, p < 0.001. Average values of three independent experiments were shown. (F) Immuno-gold staining images using anti-TSG101, a known membrane marker for the exosomes, and anti-CXCL13 antibody. Twenty-five and 10 nm gold particles show the presence of TSG101 and CXCL13, respectively.

Article Snippet: Mouse recombinant CXCL13 protein was purchased from R&D Systems.

Techniques: Western Blot, Isolation, Negative Staining, Electron Microscopy, Staining, Membrane, Marker

Journal: Frontiers in Pharmacology

Article Title: HDAC6 and CXCL13 Mediate Atopic Dermatitis by Regulating Cellular Interactions and Expression Levels of miR-9 and SIRT1

doi: 10.3389/fphar.2021.691279

Figure Lengend Snippet: Primer sequences used for qRT-PCR.

Article Snippet: Mouse recombinant CXCL13 protein was purchased from R&D Systems.

Techniques:

Primary antibodies used for immunoblot and immunohistochemical staining.

Journal: Frontiers in Pharmacology

Article Title: HDAC6 and CXCL13 Mediate Atopic Dermatitis by Regulating Cellular Interactions and Expression Levels of miR-9 and SIRT1

doi: 10.3389/fphar.2021.691279

Figure Lengend Snippet: Primary antibodies used for immunoblot and immunohistochemical staining.

Article Snippet: Mouse recombinant CXCL13 protein was purchased from R&D Systems.

Techniques: Western Blot, Immunohistochemical staining, Staining

CXCL13 concentration increases in the allo lipo α‐GC group and is correlated with the proportion of Tfh cells. (A) Concentrations of CXCL13 in the plasma of syngeneic/vehicle ( n = 2, one experiment), syngeneic/lipo α‐GC ( n = 2, one experiment), allogeneic/vehicle ( n = 8, data combined from two independently performed experiments with four mice per experiments), and allogeneic/lipo α‐GC ( n = 8, data combined from two independently performed experiments with four mice per experiments) mice on Day 56. Data are expressed as means ± SEM . (B–D) Each orange, green, red, and blue marker indicates the result from syngeneic/vehicle, syngeneic/lipo α‐GC, allogeneic/vehicle, and allogeneic/lipo α‐GC, respectively. (B) Spearman's rank correlation between the percentage of Tfh cells in MLNs and the plasma concentration of CXCL13 on Day 56 ( r = .853, p < 10 −6 ). (C) Spearman's rank correlation between the percentage of Tfh cells in MLNs and the skin cGVHD score on Day 56 ( r = .775, p < 10 −5 ). (D) Spearman's rank correlation between the percentage of Tfh cells in MLNs and the skin pathological score on Day 56 ( r = .766, p < 10 −5 ). cGVHD, chronic graft‐versus‐host disease; MLN, mesenteric lymph nodes; Tfh, follicular helper T cell; α‐GC, α‐Galactosylceramide

Journal: Immunity, Inflammation and Disease

Article Title: Donor Treg expansion by liposomal α‐galactosylceramide modulates Tfh cells and prevents sclerodermatous chronic graft‐versus‐host disease

doi: 10.1002/iid3.425

Figure Lengend Snippet: CXCL13 concentration increases in the allo lipo α‐GC group and is correlated with the proportion of Tfh cells. (A) Concentrations of CXCL13 in the plasma of syngeneic/vehicle ( n = 2, one experiment), syngeneic/lipo α‐GC ( n = 2, one experiment), allogeneic/vehicle ( n = 8, data combined from two independently performed experiments with four mice per experiments), and allogeneic/lipo α‐GC ( n = 8, data combined from two independently performed experiments with four mice per experiments) mice on Day 56. Data are expressed as means ± SEM . (B–D) Each orange, green, red, and blue marker indicates the result from syngeneic/vehicle, syngeneic/lipo α‐GC, allogeneic/vehicle, and allogeneic/lipo α‐GC, respectively. (B) Spearman's rank correlation between the percentage of Tfh cells in MLNs and the plasma concentration of CXCL13 on Day 56 ( r = .853, p < 10 −6 ). (C) Spearman's rank correlation between the percentage of Tfh cells in MLNs and the skin cGVHD score on Day 56 ( r = .775, p < 10 −5 ). (D) Spearman's rank correlation between the percentage of Tfh cells in MLNs and the skin pathological score on Day 56 ( r = .766, p < 10 −5 ). cGVHD, chronic graft‐versus‐host disease; MLN, mesenteric lymph nodes; Tfh, follicular helper T cell; α‐GC, α‐Galactosylceramide

Article Snippet: Mouse plasma was collected on Day 56 following HSCT, and plasma samples were assayed for CXCL13 via sandwich enzyme‐linked immunosorbent assay using the Quantikine mouse CXCL13/BLC/BCA‐1 immunoassay (R&D Systems).

Techniques: Concentration Assay, Marker

Review

Structured Review

Images

1) Product Images from "Human single cell RNA-sequencing reveals a targetable CD8 + exhausted T cell population that maintains mouse low-grade glioma growth"

Similar Products

Image Search Results