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R&D Systems dcx130
Dcx130, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 84 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cxcl13/Human+CXCL13%2FBLC%2FBCA-1+Quantikine+ELISA+Kit/pmc13041753-237-22-27
Average 95 stars, based on 84 article reviews

dcx130 - by Bioz Stars, 2026-11

95/100 stars

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Clinical Proteomics:

Article Title: Reprogramming of stroma-derived chemokine networks drives the loss of tissue organization in nodal B cell lymphoma.
Article Snippet: .. Absolute CXCL13 plasma levels were quantified in duplicates using the Human CXCL13 Quantikine ELISA Kit (R&D Systems) according to the manufacturer’s instructions. .. Absorbance was measured using a FLUOstar Omega microplate reader (BMG Labtech) and the associated software (Omega version 6.2, BMG Labtech).

Article Title: CXCL13 as a simple and promising blood biomarker for differentiating Sézary syndrome from mycosis fungoides and other confounding chronic inflammatory skin diseases
Article Snippet: .. Plasma CXCL13 concentrations were measured using a Human CXCL13 Quantikine ELISA kit (DCX130; R&D Systems), following the manufacturer’s instructions. ..

Enzyme-linked Immunosorbent Assay:

Article Title: Inflammatory arthritis irAE may represent a unique autoimmune disease primarily driven by T cells but likely not autoantibodies.
Article Snippet: Human naïve B cells were isolated from PBMCs using the EasySep Human Naïve B Cell Isolation Kit (STEMCELL Technologies, catalog no. 17254), and only the samples with the percentage of IgD+CD27− more than 95% were used for the culture experiment. .. For CXCL13, IL- 21, and CX3CL1 measurements, the following kits were used: Human CXCL13/BLC/BCA- 1 Quantikine Enzyme- Linked Immunosorbent Assay (ELISA) (R&D Systems, catalog no. DCX130), Human IL- 21 DuoSet ELISA (R&D Systems, catalog no. DY887905), and Human CX3CL1/Fractalkine DuoSet ELISA (R&D Systems, DY365); all steps were performed according to the manufacturer’s instructions. .. Condition 1: anti–human Ig (M + G + A) (2.5 μg/ml; Jackson ImmunoResearch, catalog no. 109- 006- 064), CpG oligodeoxynucleotide (ODN) (2.5 μg/ ml; Invivogen, catalog no. tlrl- 2006- 1), anti–human CD40 (10 μg/ml; Bio X Cell, catalog no. BE0189), rhIL- 21 (20 ng/ml; Peprotech, catalog no. 200- 21- 50UG), rhIL- 4 (10 ng/ml; BioLegend, catalog no. 574004), and rhIL- 2 (10 ng/ml; Peprotech, catalog no. 200- 02- 250UG).

other:

Article Title: Inflammatory arthritis irAE may represent a unique autoimmune disease primarily driven by T cells but likely not autoantibodies
Article Snippet: The data were acquired on the Attune NxT system (Life Technologies) and analyzed using cloud-based software from Qognit.

Image Search Results

Structural characteristics of tertiary lymphoid structures in periodontitis tissues with different severity. a Representative H&E and mIHC images of TLSs in healthy tissues and periodontitis patients (stages/grades: IIIC, IVB, IVC, n = 3). Magnified images of TLSs in periodontitis tissues of IIIC ( b ) and IVB ( c ) showed close spatial co-localization of B cells, Th cells, and HEVs; white dotted lines outlined the TLS boundaries; white triangles pointed to HEVs. d Magnified images of TLSs in IVC periodontitis tissues (left to right): spatial relationships of B cells, Th cells, and CXCL13, with the prominent HEVs. e Comparison of mean density of TLS-related cells across stages/grades. Statistical significance in e was determined using the Kruskal-Wallis test with post-hoc Bonferroni multiple comparison tests. TLSs: Tertiary lymphoid structures; PNAd: Peripheral node addressin; IIIC: Stage III grade C; IVB: Stage IV grade B; IVC: Stage IV grade C; Th cells: T helper cells; HEVs: High endothelial venules. * P < 0.05, ** P < 0.01, *** P < 0.001

Journal: International Journal of Oral Science

Article Title: Targeting IFN-I driven tertiary lymphoid structures halts B cell-mediated bone loss in periodontitis

doi: 10.1038/s41368-026-00450-7

Figure Lengend Snippet: Structural characteristics of tertiary lymphoid structures in periodontitis tissues with different severity. a Representative H&E and mIHC images of TLSs in healthy tissues and periodontitis patients (stages/grades: IIIC, IVB, IVC, n = 3). Magnified images of TLSs in periodontitis tissues of IIIC ( b ) and IVB ( c ) showed close spatial co-localization of B cells, Th cells, and HEVs; white dotted lines outlined the TLS boundaries; white triangles pointed to HEVs. d Magnified images of TLSs in IVC periodontitis tissues (left to right): spatial relationships of B cells, Th cells, and CXCL13, with the prominent HEVs. e Comparison of mean density of TLS-related cells across stages/grades. Statistical significance in e was determined using the Kruskal-Wallis test with post-hoc Bonferroni multiple comparison tests. TLSs: Tertiary lymphoid structures; PNAd: Peripheral node addressin; IIIC: Stage III grade C; IVB: Stage IV grade B; IVC: Stage IV grade C; Th cells: T helper cells; HEVs: High endothelial venules. * P < 0.05, ** P < 0.01, *** P < 0.001

Article Snippet: CXCL13 levels in HGF supernatants were quantified using Human CXCL13 ELISA kits (MULTI SCIENCES, EK1105) following the manufacturer’s instructions.

Techniques: Comparison

Single-cell atlas of human periodontitis tissues revealed CXCL13 + fibroblast characteristics and functions. a UMAP plot of six fibroblast clusters. b Stacked violin plots of differentially expressed genes across clusters. c Fibroblast cluster proportions in healthy ( n = 8) vs periodontitis ( n = 13). d Dot plots of TLS hallmark gene expression across clusters. e qPCR analysis of CXCL13 mRNA levels in healthy and periodontitis tissues (Healthy: n = 16; Periodontitis: n = 25). f Representative immunofluorescence images and quantitative analysis ( n = 5) of CXCL13 + fibroblast in healthy and periodontitis tissues. g Hierarchical diagram showed CXCL signaling network between fibroblasts and CD4 + T/B cells. h Heatmaps showed altered CXCL signaling to T-cell subsets, red arrows: increased recruitment of Th17/Treg cells and Tfh cells in periodontitis state. Statistical significance in c , e , f was determined using the Mann–Whitney U test. UMAP: Uniform manifold approximation and projection; nCells: number of cells in each cluster; FB: Fibroblasts; B: B cells; T: T cells; Th1: T helper cell type 1; Th2: T helper cell type 2; Tn: naïve T cells; Th17: T helper cell type 17; Treg: Regulatory T cells; Tfh: Follicular helper T cells; GC B: Germinal center B cells. * P < 0.05, ** P < 0.01, *** P < 0.001

Journal: International Journal of Oral Science

Article Title: Targeting IFN-I driven tertiary lymphoid structures halts B cell-mediated bone loss in periodontitis

doi: 10.1038/s41368-026-00450-7

Figure Lengend Snippet: Single-cell atlas of human periodontitis tissues revealed CXCL13 + fibroblast characteristics and functions. a UMAP plot of six fibroblast clusters. b Stacked violin plots of differentially expressed genes across clusters. c Fibroblast cluster proportions in healthy ( n = 8) vs periodontitis ( n = 13). d Dot plots of TLS hallmark gene expression across clusters. e qPCR analysis of CXCL13 mRNA levels in healthy and periodontitis tissues (Healthy: n = 16; Periodontitis: n = 25). f Representative immunofluorescence images and quantitative analysis ( n = 5) of CXCL13 + fibroblast in healthy and periodontitis tissues. g Hierarchical diagram showed CXCL signaling network between fibroblasts and CD4 + T/B cells. h Heatmaps showed altered CXCL signaling to T-cell subsets, red arrows: increased recruitment of Th17/Treg cells and Tfh cells in periodontitis state. Statistical significance in c , e , f was determined using the Mann–Whitney U test. UMAP: Uniform manifold approximation and projection; nCells: number of cells in each cluster; FB: Fibroblasts; B: B cells; T: T cells; Th1: T helper cell type 1; Th2: T helper cell type 2; Tn: naïve T cells; Th17: T helper cell type 17; Treg: Regulatory T cells; Tfh: Follicular helper T cells; GC B: Germinal center B cells. * P < 0.05, ** P < 0.01, *** P < 0.001

Article Snippet: CXCL13 levels in HGF supernatants were quantified using Human CXCL13 ELISA kits (MULTI SCIENCES, EK1105) following the manufacturer’s instructions.

Techniques: Single Cell, Gene Expression, Immunofluorescence, MANN-WHITNEY

IRF7-driven overproduction of IFNβ activated gingival fibroblasts into a CXCL13 + inflammatory phenotype. a Relative mRNA expression levels of CXCL13 and CCL19 in HGFs stimulated by P. gingivalis LPS at 2, 4, 8, 16 and 24 h; target gene expression was normalized to GAPDH and showed as fold change of unstimulated cells; dotted lines indicating the gene expression of unstimulated cells at each time point. b ELISA detection of CXCL13 levels in cell supernatants of HGFs stimulated by various inflammatory cytokines ( n = 3 per group). c qPCR results of IFNA1 , IFNΒ1 , and CXCL13 expression levels in HGFs stimulated by P. gingivalis LPS and IFNβ at 2, 4, 8, 16 and 24 h; target gene expression was normalized to GAPDH and showed as fold change of unstimulated cells; dotted lines indicating the gene expression of unstimulated cells at each time point. d SCENIC transcription factor analysis results showed highly active transcription factors in the CXCL13 + FB. e qPCR results of PRDM1 , and IRF7 expression levels in HGFs stimulated by P. gingivalis LPS and IFNβ at 2, 4, 8, 16 and 24 h; target gene expression was normalized to GAPDH and showed as fold change of unstimulated cells, dotted lines indicating the gene expression of unstimulated cells at each time point. Representative western blot images ( f ) and quantitative analysis ( g ) of PRDM1, IRF7 and IFNB1 in HGFs stimulated by P. gingivalis LPS or IFNβ, protein levels were normalized to GAPDH. Statistical significance in a - c , e , g was determined using one-way ANOVA followed by post-hoc Dunn test. * P < 0.05, ** P < 0.01, *** P < 0.001, ns: non-significant

Journal: International Journal of Oral Science

Article Title: Targeting IFN-I driven tertiary lymphoid structures halts B cell-mediated bone loss in periodontitis

doi: 10.1038/s41368-026-00450-7

Figure Lengend Snippet: IRF7-driven overproduction of IFNβ activated gingival fibroblasts into a CXCL13 + inflammatory phenotype. a Relative mRNA expression levels of CXCL13 and CCL19 in HGFs stimulated by P. gingivalis LPS at 2, 4, 8, 16 and 24 h; target gene expression was normalized to GAPDH and showed as fold change of unstimulated cells; dotted lines indicating the gene expression of unstimulated cells at each time point. b ELISA detection of CXCL13 levels in cell supernatants of HGFs stimulated by various inflammatory cytokines ( n = 3 per group). c qPCR results of IFNA1 , IFNΒ1 , and CXCL13 expression levels in HGFs stimulated by P. gingivalis LPS and IFNβ at 2, 4, 8, 16 and 24 h; target gene expression was normalized to GAPDH and showed as fold change of unstimulated cells; dotted lines indicating the gene expression of unstimulated cells at each time point. d SCENIC transcription factor analysis results showed highly active transcription factors in the CXCL13 + FB. e qPCR results of PRDM1 , and IRF7 expression levels in HGFs stimulated by P. gingivalis LPS and IFNβ at 2, 4, 8, 16 and 24 h; target gene expression was normalized to GAPDH and showed as fold change of unstimulated cells, dotted lines indicating the gene expression of unstimulated cells at each time point. Representative western blot images ( f ) and quantitative analysis ( g ) of PRDM1, IRF7 and IFNB1 in HGFs stimulated by P. gingivalis LPS or IFNβ, protein levels were normalized to GAPDH. Statistical significance in a - c , e , g was determined using one-way ANOVA followed by post-hoc Dunn test. * P < 0.05, ** P < 0.01, *** P < 0.001, ns: non-significant

Article Snippet: CXCL13 levels in HGF supernatants were quantified using Human CXCL13 ELISA kits (MULTI SCIENCES, EK1105) following the manufacturer’s instructions.

Techniques: Expressing, Targeted Gene Expression, Gene Expression, Enzyme-linked Immunosorbent Assay, Western Blot

Anti-IFNAR1 blockade or knockdown of IRF7 attenuates IFNβ and CXCL13 expression in HGFs. a Schematic diagram of the in vitro experiment using anti-IFNAR1 to block IFN-I signaling in HGFs. b Relative mRNA expression levels of CXCL13 , IFNΒ1 , IRF7 , and PRDM1 in HGFs treated with anti-IFNAR1 and stimulated with P. gingivalis LPS. c Western blot results and quantitative analysis of IRF7 and IFNβ production in HGFs treated with anti-IFNAR1 and stimulated with P. gingivalis LPS. d Schematic diagram of the in vitro experiment using siRNA to knock down transcription factors IRF7 and PRDM1 in HGFs. e Relative mRNA expression levels of CXCL13 , IFNΒ1 mRNA in HGFs with siRNA knockdown of IRF7 or PRDM1 and stimulated with IFNβ. f Western blot results and quantitative analysis of IFNβ production and PRDM1 protein level in HGFs with siRNA knockdown of IRF7 and stimulated with IFNβ. Statistical significance in b, e was determined using one-way ANOVA followed by post-hoc Tukey test, and statistical significance in c, f was determined using unpaired two-tailed Student’s t -test. * P < 0.05, ** P < 0.01, *** P < 0.001, ns: non-significant

Journal: International Journal of Oral Science

Article Title: Targeting IFN-I driven tertiary lymphoid structures halts B cell-mediated bone loss in periodontitis

doi: 10.1038/s41368-026-00450-7

Figure Lengend Snippet: Anti-IFNAR1 blockade or knockdown of IRF7 attenuates IFNβ and CXCL13 expression in HGFs. a Schematic diagram of the in vitro experiment using anti-IFNAR1 to block IFN-I signaling in HGFs. b Relative mRNA expression levels of CXCL13 , IFNΒ1 , IRF7 , and PRDM1 in HGFs treated with anti-IFNAR1 and stimulated with P. gingivalis LPS. c Western blot results and quantitative analysis of IRF7 and IFNβ production in HGFs treated with anti-IFNAR1 and stimulated with P. gingivalis LPS. d Schematic diagram of the in vitro experiment using siRNA to knock down transcription factors IRF7 and PRDM1 in HGFs. e Relative mRNA expression levels of CXCL13 , IFNΒ1 mRNA in HGFs with siRNA knockdown of IRF7 or PRDM1 and stimulated with IFNβ. f Western blot results and quantitative analysis of IFNβ production and PRDM1 protein level in HGFs with siRNA knockdown of IRF7 and stimulated with IFNβ. Statistical significance in b, e was determined using one-way ANOVA followed by post-hoc Tukey test, and statistical significance in c, f was determined using unpaired two-tailed Student’s t -test. * P < 0.05, ** P < 0.01, *** P < 0.001, ns: non-significant

Article Snippet: CXCL13 levels in HGF supernatants were quantified using Human CXCL13 ELISA kits (MULTI SCIENCES, EK1105) following the manufacturer’s instructions.

Techniques: Knockdown, Expressing, In Vitro, Blocking Assay, Western Blot, Two Tailed Test

Blocking IFN-I signaling reduced tertiary lymphoid structures development and osteoclast formation in LIP mice. a Representative micro-CT images among groups ( n = 6); between the white dotted lines is the area of bone destruction; red vertical lines represent the five pre-determined measurement sites of bone destruction. b Bone destruction quantification among groups ( n = 6). c Representative TRAP staining, and Masson staining images among groups ( n = 6). d Quantitative analysis of osteoclast number among groups ( n = 6). Representative images ( e ) and quantitative analysis ( f ) of immunofluorescence staining of HEVs (PNAd) and surrounding B cells (CD19 + ), CXCL13 + fibroblasts and RANKL + B cells in LIP mice ( n = 6–9); the white curved dotted line delineates the outline of the teeth. Statistical significance in b , d , f was determined using one-way ANOVA followed by post-hoc Tukey test. * P < 0.05, ** P < 0.01, *** P < 0.001, ns: non-significant

Journal: International Journal of Oral Science

Article Title: Targeting IFN-I driven tertiary lymphoid structures halts B cell-mediated bone loss in periodontitis

doi: 10.1038/s41368-026-00450-7

Figure Lengend Snippet: Blocking IFN-I signaling reduced tertiary lymphoid structures development and osteoclast formation in LIP mice. a Representative micro-CT images among groups ( n = 6); between the white dotted lines is the area of bone destruction; red vertical lines represent the five pre-determined measurement sites of bone destruction. b Bone destruction quantification among groups ( n = 6). c Representative TRAP staining, and Masson staining images among groups ( n = 6). d Quantitative analysis of osteoclast number among groups ( n = 6). Representative images ( e ) and quantitative analysis ( f ) of immunofluorescence staining of HEVs (PNAd) and surrounding B cells (CD19 + ), CXCL13 + fibroblasts and RANKL + B cells in LIP mice ( n = 6–9); the white curved dotted line delineates the outline of the teeth. Statistical significance in b , d , f was determined using one-way ANOVA followed by post-hoc Tukey test. * P < 0.05, ** P < 0.01, *** P < 0.001, ns: non-significant

Article Snippet: CXCL13 levels in HGF supernatants were quantified using Human CXCL13 ELISA kits (MULTI SCIENCES, EK1105) following the manufacturer’s instructions.

Techniques: Blocking Assay, Micro-CT, Staining, Immunofluorescence

CXCL13 mRNA expression in PBMCs from patients with Sézary syndrome and other confounding skin diseases. (A) Box-and-whisker plots showing individual CXCL13 ΔCt values in PBMCs from patients with Sézary syndrome (SS), mycosis fungoides (MF), atopic dermatitis (AD), psoriasis (PS) and healthy donors (HD). ΔCt values were calculated using GAPDH as housekeeping gene. Statistical significance was assessed using the Kruskal–Wallis test followed by Dunn’s multiple comparisons test. ***p ≤ 0.001; *p ≤ 0.05. (B) Relative CXCL13 expression levels expressed as fold change (RQ) for each disease group relative to HD, calculated using the mean ΔCt value of HD as reference. RQmin and RQmax represent the minimum and maximum relative quantities obtained by adding or subtracting, respectively, the standard deviation of ΔCt values to ΔΔCt.

Journal: Frontiers in Immunology

Article Title: CXCL13 as a simple and promising blood biomarker for differentiating Sézary syndrome from mycosis fungoides and other confounding chronic inflammatory skin diseases

doi: 10.3389/fimmu.2026.1804103

Figure Lengend Snippet: CXCL13 mRNA expression in PBMCs from patients with Sézary syndrome and other confounding skin diseases. (A) Box-and-whisker plots showing individual CXCL13 ΔCt values in PBMCs from patients with Sézary syndrome (SS), mycosis fungoides (MF), atopic dermatitis (AD), psoriasis (PS) and healthy donors (HD). ΔCt values were calculated using GAPDH as housekeeping gene. Statistical significance was assessed using the Kruskal–Wallis test followed by Dunn’s multiple comparisons test. ***p ≤ 0.001; *p ≤ 0.05. (B) Relative CXCL13 expression levels expressed as fold change (RQ) for each disease group relative to HD, calculated using the mean ΔCt value of HD as reference. RQmin and RQmax represent the minimum and maximum relative quantities obtained by adding or subtracting, respectively, the standard deviation of ΔCt values to ΔΔCt.

Article Snippet: Plasma CXCL13 concentrations were measured using a Human CXCL13 Quantikine ELISA kit (DCX130; R&D Systems), following the manufacturer’s instructions.

Techniques: Expressing, Whisker Assay, Standard Deviation

CXCL13 immunohistochemical expression in skin biopsies from Sézary syndrome, mycosis fungoides and inflammatory skin diseases. Representative immunohistochemical staining for CXCL13 in skin lesions from patients with Sézary syndrome [SS; (A) ] and mycosis fungoides [MF; (B) ], showing CXCL13 expression in endothelial cells and neoplastic lymphocytes infiltrating the dermis, frequently displaying a dot-like staining pattern. In atopic dermatitis [AD; (C) ], psoriasis [PS; (D) ], eczema [EC; (E) ] and healthy donor skin [HD; (F) ], CXCL13 immunoreactivity is mainly confined to endothelial cells and scattered non-neoplastic lymphocytes. Sections were counterstained with haematoxylin. Original magnification: ×10; inserts ×40.

Journal: Frontiers in Immunology

Article Title: CXCL13 as a simple and promising blood biomarker for differentiating Sézary syndrome from mycosis fungoides and other confounding chronic inflammatory skin diseases

doi: 10.3389/fimmu.2026.1804103

Figure Lengend Snippet: CXCL13 immunohistochemical expression in skin biopsies from Sézary syndrome, mycosis fungoides and inflammatory skin diseases. Representative immunohistochemical staining for CXCL13 in skin lesions from patients with Sézary syndrome [SS; (A) ] and mycosis fungoides [MF; (B) ], showing CXCL13 expression in endothelial cells and neoplastic lymphocytes infiltrating the dermis, frequently displaying a dot-like staining pattern. In atopic dermatitis [AD; (C) ], psoriasis [PS; (D) ], eczema [EC; (E) ] and healthy donor skin [HD; (F) ], CXCL13 immunoreactivity is mainly confined to endothelial cells and scattered non-neoplastic lymphocytes. Sections were counterstained with haematoxylin. Original magnification: ×10; inserts ×40.

Article Snippet: Plasma CXCL13 concentrations were measured using a Human CXCL13 Quantikine ELISA kit (DCX130; R&D Systems), following the manufacturer’s instructions.

Techniques: Immunohistochemical staining, Expressing, Staining

Plasma CXCL13 levels and diagnostic performance in Sézary syndrome. (A) Box-and-whisker plots showing individual plasma CXCL13 concentrations in patients with Sézary syndrome (SS), mycosis fungoides (MF), atopic dermatitis (AD), psoriasis (PS), eczema (EC) and healthy donors (HD). Statistical significance was assessed using the Kruskal–Wallis test followed by Dunn’s multiple comparisons test. (B) Plasma CXCL13 concentrations in MF patients stratified according to disease stage at sampling (stage IB/IIA vs . advanced stages IIB and III). Statistical significance was assessed using the Mann–Whitney U test. (C) Receiver operating characteristic (ROC) curve analysis evaluating the ability of plasma CXCL13 to discriminate SS patients from all non-SS individuals (MF, AD, PS, EC and HD). The red cross indicates the selected cut-off value (151.1 pg/mL) maximising sensitivity (87%) and specificity (88%). (D) Box-and-whisker plots showing individual plasma CXCL13 concentrations in SS (right) and non-SS (left) patients. The dotted line indicates the ROC-derived cut-off value. Statistical significance was assessed using the Mann–Whitney U test. ****p ≤ 0.0001; **p ≤ 0.01; *p ≤ 0.05.

Journal: Frontiers in Immunology

Article Title: CXCL13 as a simple and promising blood biomarker for differentiating Sézary syndrome from mycosis fungoides and other confounding chronic inflammatory skin diseases

doi: 10.3389/fimmu.2026.1804103

Figure Lengend Snippet: Plasma CXCL13 levels and diagnostic performance in Sézary syndrome. (A) Box-and-whisker plots showing individual plasma CXCL13 concentrations in patients with Sézary syndrome (SS), mycosis fungoides (MF), atopic dermatitis (AD), psoriasis (PS), eczema (EC) and healthy donors (HD). Statistical significance was assessed using the Kruskal–Wallis test followed by Dunn’s multiple comparisons test. (B) Plasma CXCL13 concentrations in MF patients stratified according to disease stage at sampling (stage IB/IIA vs . advanced stages IIB and III). Statistical significance was assessed using the Mann–Whitney U test. (C) Receiver operating characteristic (ROC) curve analysis evaluating the ability of plasma CXCL13 to discriminate SS patients from all non-SS individuals (MF, AD, PS, EC and HD). The red cross indicates the selected cut-off value (151.1 pg/mL) maximising sensitivity (87%) and specificity (88%). (D) Box-and-whisker plots showing individual plasma CXCL13 concentrations in SS (right) and non-SS (left) patients. The dotted line indicates the ROC-derived cut-off value. Statistical significance was assessed using the Mann–Whitney U test. ****p ≤ 0.0001; **p ≤ 0.01; *p ≤ 0.05.

Article Snippet: Plasma CXCL13 concentrations were measured using a Human CXCL13 Quantikine ELISA kit (DCX130; R&D Systems), following the manufacturer’s instructions.

Techniques: Clinical Proteomics, Diagnostic Assay, Whisker Assay, Sampling, MANN-WHITNEY, Derivative Assay

Journal: Frontiers in Immunology

Article Title: CXCL13 as a simple and promising blood biomarker for differentiating Sézary syndrome from mycosis fungoides and other confounding chronic inflammatory skin diseases

doi: 10.3389/fimmu.2026.1804103

Article Snippet: Sections were then incubated overnight at 4 °C with a goat polyclonal anti-CXCL13 antibody (AF801; R&D Systems) at a concentration of 2.5 μg/mL in 2% bovine serum albumin (BSA).

Techniques: Expressing, Whisker Assay, Standard Deviation

Journal: Frontiers in Immunology

Article Title: CXCL13 as a simple and promising blood biomarker for differentiating Sézary syndrome from mycosis fungoides and other confounding chronic inflammatory skin diseases

doi: 10.3389/fimmu.2026.1804103

Techniques: Immunohistochemical staining, Expressing, Staining

Journal: Frontiers in Immunology

Article Title: CXCL13 as a simple and promising blood biomarker for differentiating Sézary syndrome from mycosis fungoides and other confounding chronic inflammatory skin diseases

doi: 10.3389/fimmu.2026.1804103

Techniques: Clinical Proteomics, Diagnostic Assay, Whisker Assay, Sampling, MANN-WHITNEY, Derivative Assay

( A ) Expression of CD27 and IgD on CD19 + B cells. Right: Percentage of IgD + CD27 − naïve B cells and IgD − CD27 − DN B cells. ( B ) Expression of CD27 and CD38 on CD19 + B cells. Right: Percentages of CD27 hi CD38 hi ASCs and CD27 + CD38 − memory B cells. ( C ) Expression of CD138 on CD27 hi CD38 hi ASCs. Right: Percentage of CD138 + ASCs and CD138 − ASCs. ( D ) Expression of CD11c and CD21 on CD19 + B cells. Right: Percentage of CD11c + CD21 − CD19 + B cells. [(A) to (D)] HC ( n = 63), irAE ( n = 33), RAC ( n = 46), and ICI ( n = 20). ( E to G ) GSEA was performed on the B cells between irAE and ICI. (E) Significantly enriched pathways in B cells from irAE and ICI. GSEA plots of IFN-α and IFN-γ response (F), and oxidative phosphorylation (G). ( H ) The volcano plots of the citrullinated or noncitrullinated relative IgG or IgM isotype autoantigen levels comparing RA versus HC, irAE versus ICI, irAE versus HC, or irAE versus RA. The autoantigens were labeled when P < 0.01. TNF-α reactivities resulted from the administration of anti–TNF-α therapy for the treatment of RA. ( I ) Immunoglobulin isotype levels in the plasma were measured by multiplex assay. HC ( n = 22), irAE ( n = 34), RAC ( n = 46), and ICI ( n = 26). ( J ) CXCL13 levels in the plasma were measured by enzyme-linked immunosorbent assay (ELISA). HC ( n = 20), irAE ( n = 34) RAC ( n = 47), and ICI ( n = 23). ( K ) B-cell activating factor (BAFF) levels in the plasma were measured by multiplex assay. HC ( n = 21), irAE ( n = 34), RAC ( n = 47), and ICI ( n = 18). Data in graphs represent mean ± SEM. Significance was tested by one-way ANOVA [(A) to (D) and (I) to (K)] and logistic regression (H). [(A) to (D) and (F) to (K)] ICI, ICI control.

Journal: Science Advances

Article Title: Inflammatory arthritis irAE may represent a unique autoimmune disease primarily driven by T cells but likely not autoantibodies

doi: 10.1126/sciadv.aea4262

Figure Lengend Snippet: ( A ) Expression of CD27 and IgD on CD19 + B cells. Right: Percentage of IgD + CD27 − naïve B cells and IgD − CD27 − DN B cells. ( B ) Expression of CD27 and CD38 on CD19 + B cells. Right: Percentages of CD27 hi CD38 hi ASCs and CD27 + CD38 − memory B cells. ( C ) Expression of CD138 on CD27 hi CD38 hi ASCs. Right: Percentage of CD138 + ASCs and CD138 − ASCs. ( D ) Expression of CD11c and CD21 on CD19 + B cells. Right: Percentage of CD11c + CD21 − CD19 + B cells. [(A) to (D)] HC ( n = 63), irAE ( n = 33), RAC ( n = 46), and ICI ( n = 20). ( E to G ) GSEA was performed on the B cells between irAE and ICI. (E) Significantly enriched pathways in B cells from irAE and ICI. GSEA plots of IFN-α and IFN-γ response (F), and oxidative phosphorylation (G). ( H ) The volcano plots of the citrullinated or noncitrullinated relative IgG or IgM isotype autoantigen levels comparing RA versus HC, irAE versus ICI, irAE versus HC, or irAE versus RA. The autoantigens were labeled when P < 0.01. TNF-α reactivities resulted from the administration of anti–TNF-α therapy for the treatment of RA. ( I ) Immunoglobulin isotype levels in the plasma were measured by multiplex assay. HC ( n = 22), irAE ( n = 34), RAC ( n = 46), and ICI ( n = 26). ( J ) CXCL13 levels in the plasma were measured by enzyme-linked immunosorbent assay (ELISA). HC ( n = 20), irAE ( n = 34) RAC ( n = 47), and ICI ( n = 23). ( K ) B-cell activating factor (BAFF) levels in the plasma were measured by multiplex assay. HC ( n = 21), irAE ( n = 34), RAC ( n = 47), and ICI ( n = 18). Data in graphs represent mean ± SEM. Significance was tested by one-way ANOVA [(A) to (D) and (I) to (K)] and logistic regression (H). [(A) to (D) and (F) to (K)] ICI, ICI control.

Article Snippet: For CXCL13, IL-21, and CX3CL1 measurements, the following kits were used: Human CXCL13/BLC/BCA-1 Quantikine Enzyme-Linked Immunosorbent Assay (ELISA) (R&D Systems, catalog no. DCX130), Human IL-21 DuoSet ELISA (R&D Systems, catalog no. DY8879-05), and Human CX3CL1/Fractalkine DuoSet ELISA (R&D Systems, DY365); all steps were performed according to the manufacturer’s instructions.

Techniques: Expressing, Phospho-proteomics, Immunopeptidomics, Labeling, Clinical Proteomics, Multiplex Assay, Enzyme-linked Immunosorbent Assay, Control

( A to C ) Human naïve B cells were isolated from PBMCs and cultured under indicated conditions for 7 days; pembrolizumab or isotype control IgG4 (IgG4 Iso) was added on day 2; n = 8. (A) Expression of CD38 and CD27 on B cells. Right: Percentages of CD27 + CD38 − and CD27 + CD38 + B cells. (B) Expression of CD138 on CD27 + CD38 + B cells. Right: Percentage of CD138 + CD27 + CD38 + B cells. (C) Different immunoglobulin isotypes were measured in the culture supernatant of (A) and (B) by multiplex assay. ( D to F ) B cells from Humanized PD-1 (HuPD-1) mice were isolated and cultured with LPS, IL-4, BAFF, or ODN 2006, anti-IgM, IL-21, IL-4 or R848, anti-IgM, anti-CD40, IL-21, and IFN-γ for 3 days; pembrolizumab or isotype control was added on day 1. (D) Expression of IgG2c on activated B cells. FSC-H, Forward scatter height. Right: Percentage of IgG2c + B cells; n = 5. (E) Expression of IgG1 on activated B cells. Right: Percentage of IgG1 + B cells; n = 5. (F) Different immunoglobulin isotypes in the supernatant were measured by multiplex assay; n = 5. Data in graphs represent mean ± SEM. Significance was tested by two-way ANOVA.

Journal: Science Advances

Article Title: Inflammatory arthritis irAE may represent a unique autoimmune disease primarily driven by T cells but likely not autoantibodies

doi: 10.1126/sciadv.aea4262

Figure Lengend Snippet: ( A to C ) Human naïve B cells were isolated from PBMCs and cultured under indicated conditions for 7 days; pembrolizumab or isotype control IgG4 (IgG4 Iso) was added on day 2; n = 8. (A) Expression of CD38 and CD27 on B cells. Right: Percentages of CD27 + CD38 − and CD27 + CD38 + B cells. (B) Expression of CD138 on CD27 + CD38 + B cells. Right: Percentage of CD138 + CD27 + CD38 + B cells. (C) Different immunoglobulin isotypes were measured in the culture supernatant of (A) and (B) by multiplex assay. ( D to F ) B cells from Humanized PD-1 (HuPD-1) mice were isolated and cultured with LPS, IL-4, BAFF, or ODN 2006, anti-IgM, IL-21, IL-4 or R848, anti-IgM, anti-CD40, IL-21, and IFN-γ for 3 days; pembrolizumab or isotype control was added on day 1. (D) Expression of IgG2c on activated B cells. FSC-H, Forward scatter height. Right: Percentage of IgG2c + B cells; n = 5. (E) Expression of IgG1 on activated B cells. Right: Percentage of IgG1 + B cells; n = 5. (F) Different immunoglobulin isotypes in the supernatant were measured by multiplex assay; n = 5. Data in graphs represent mean ± SEM. Significance was tested by two-way ANOVA.

Techniques: Isolation, Cell Culture, Control, Expressing, Multiplex Assay

( A to G ) CD8 + T cells isolated from healthy donor were cultured in the plate coated with anti–human CD3/CD28 (10 μg/ml) for indicated days in the presence of vehicle control (control), IFN-α (100 ng/ml), IL-6 (100 ng/ml), IL-12 (100 ng/ml), or the combination. (A) Summaries of the percentage of CD38 + CD127 − CD8 + T cells at days 1 and 5. (B) MFI of CD69 (day 5). (C) MFI of CD25 (day 5). (D) Activated CD8 + T cells were restimulated with PMA, ionomycin, and monensin for 5 hours; expression of granzyme B and IFN-γ in CD8 + T cells was examined. [(E) to (G)] CD8 + T cells were cultured for 5 days. MFIs (all relative to those under control condition) of MTDR (E), MTG (F), and GluCy5 (G) were summarized. ( H to L ) CD4 + T cells were isolated from HC, cultured in the plate coated with anti–human CD3/CD28 (10 μg/ml) for indicated days in the presence of IFN-α (100 ng/ml), IL-6 (100 ng/ml), IL-12 (100 ng/ml), control, or the combination of them. (H) Activated CD4 + T cells were restimulated with PMA, ionomycin, and monensin for 5 hours, and IL-21 level was examined in the CD45RA − CD4 + T cells. (I) Activated CD4 + T cells were restimulated with plate-coated anti–human CD3/CD28 (10 μg/ml) with monensin for 6 hours, and expression of CXCL13 was measured in CD45RA − CD4 + T cells. (J) CD38 and CXCR5 were examined on CD4 + T cells at day 5. (K) Percentage of CXCL13 + cells in indicated T cells at day 5. (L) Percentage of IL-21 + cells in indicated T cells at day 5. Data in graphs represent mean ± SEM. Significance was tested by one-way ANOVA.

Journal: Science Advances

Article Title: Inflammatory arthritis irAE may represent a unique autoimmune disease primarily driven by T cells but likely not autoantibodies

doi: 10.1126/sciadv.aea4262

Figure Lengend Snippet: ( A to G ) CD8 + T cells isolated from healthy donor were cultured in the plate coated with anti–human CD3/CD28 (10 μg/ml) for indicated days in the presence of vehicle control (control), IFN-α (100 ng/ml), IL-6 (100 ng/ml), IL-12 (100 ng/ml), or the combination. (A) Summaries of the percentage of CD38 + CD127 − CD8 + T cells at days 1 and 5. (B) MFI of CD69 (day 5). (C) MFI of CD25 (day 5). (D) Activated CD8 + T cells were restimulated with PMA, ionomycin, and monensin for 5 hours; expression of granzyme B and IFN-γ in CD8 + T cells was examined. [(E) to (G)] CD8 + T cells were cultured for 5 days. MFIs (all relative to those under control condition) of MTDR (E), MTG (F), and GluCy5 (G) were summarized. ( H to L ) CD4 + T cells were isolated from HC, cultured in the plate coated with anti–human CD3/CD28 (10 μg/ml) for indicated days in the presence of IFN-α (100 ng/ml), IL-6 (100 ng/ml), IL-12 (100 ng/ml), control, or the combination of them. (H) Activated CD4 + T cells were restimulated with PMA, ionomycin, and monensin for 5 hours, and IL-21 level was examined in the CD45RA − CD4 + T cells. (I) Activated CD4 + T cells were restimulated with plate-coated anti–human CD3/CD28 (10 μg/ml) with monensin for 6 hours, and expression of CXCL13 was measured in CD45RA − CD4 + T cells. (J) CD38 and CXCR5 were examined on CD4 + T cells at day 5. (K) Percentage of CXCL13 + cells in indicated T cells at day 5. (L) Percentage of IL-21 + cells in indicated T cells at day 5. Data in graphs represent mean ± SEM. Significance was tested by one-way ANOVA.

Techniques: Isolation, Cell Culture, Control, Expressing

( A to G ) PBMCs from the patients with irAE were cultured in the plate coated with anti-CD3 and anti-CD28 (10 μg/ml) in the presence of IgG1 isotype control or anti–human IL-6R (50 μg/ml), anti–human IL-12p40 (50 μg/ml), and anti–human IFNAR1 (50 μg/ml) for 3 days; n = 9. (A) Expression of CD38 and CD127 on CD8 + T cells. Right: Percentage of CD38 + CD127 − CD8 + T cells. (B and C) CD8 + T cells activated for 5 days were restimulated with PMA, ionomycin, and monensin for 5 hours. (B) Expression of granzyme B and IFN-γ. Right: Percentage of granzyme B + IFN-γ + CD8 + T cells. (C) Expression of perforin and IFN-γ. Right: Percentage of perforin + IFN-γ + CD8 + T cells. [(D) and (E)] MFIs of GluCy5 (D), TMRM, and MTDR (E) in CD8 + T cells were presented. [(F) and (G)] CD4 + T cells activated for 5 days were restimulated with PMA, ionomycin, and monensin for 5 hours. (F) Expression of IL-21 and IL-2. Right: Percentage of IL-21 + IL-2 + CD4 + T cells. (G) Expression of CD38 and CXCR5 on CD4 + T cells. Right: Percentage of CD38 + CXCR5 − CD4 + T cells. Data in graphs represent mean ± SEM. Significance was tested paired Student’s t test [(A) to (G)].

Journal: Science Advances

Article Title: Inflammatory arthritis irAE may represent a unique autoimmune disease primarily driven by T cells but likely not autoantibodies

doi: 10.1126/sciadv.aea4262

Figure Lengend Snippet: ( A to G ) PBMCs from the patients with irAE were cultured in the plate coated with anti-CD3 and anti-CD28 (10 μg/ml) in the presence of IgG1 isotype control or anti–human IL-6R (50 μg/ml), anti–human IL-12p40 (50 μg/ml), and anti–human IFNAR1 (50 μg/ml) for 3 days; n = 9. (A) Expression of CD38 and CD127 on CD8 + T cells. Right: Percentage of CD38 + CD127 − CD8 + T cells. (B and C) CD8 + T cells activated for 5 days were restimulated with PMA, ionomycin, and monensin for 5 hours. (B) Expression of granzyme B and IFN-γ. Right: Percentage of granzyme B + IFN-γ + CD8 + T cells. (C) Expression of perforin and IFN-γ. Right: Percentage of perforin + IFN-γ + CD8 + T cells. [(D) and (E)] MFIs of GluCy5 (D), TMRM, and MTDR (E) in CD8 + T cells were presented. [(F) and (G)] CD4 + T cells activated for 5 days were restimulated with PMA, ionomycin, and monensin for 5 hours. (F) Expression of IL-21 and IL-2. Right: Percentage of IL-21 + IL-2 + CD4 + T cells. (G) Expression of CD38 and CXCR5 on CD4 + T cells. Right: Percentage of CD38 + CXCR5 − CD4 + T cells. Data in graphs represent mean ± SEM. Significance was tested paired Student’s t test [(A) to (G)].

Techniques: Cell Culture, Control, Expressing

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