human cxcl13 quantikine elisa kit  (R&D Systems)

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

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

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

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: 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

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: 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: 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

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

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

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.

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

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.

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: Isolation, Cell Culture, Control, Expressing

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)].

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: Cell Culture, Control, Expressing

Journal: Journal of Neurology

Article Title: Soluble TIM-3 and galectin-9 serve as additional diagnostic biomarkers in primary central nervous system lymphoma

doi: 10.1007/s00415-026-13791-4

Figure Lengend Snippet: Accuracy of CSF diagnostic markers for PCNSL. Boxplots depicted the distribution of CSF IL-10 ( A ), CXCL13 ( B ), IL-2RA ( C ), FasL ( D ), TIM-3 ( E ), and galectin-9 ( F ) levels in PCNSL, neuroimmunological diseases, other brain tumors, and iNPH patients. Median values were represented by the horizontal bar, IQR by boxes, 1.5 × IQR by whiskers, and individual values by dots. IL-10 and IL-2RA are shown on a logarithmic scale due to the highly skewed distribution with a large proportion of zero or low values and a small number of extremely high values. The y -axis is displayed on a logarithmic scale after log10 transformation of IL-10 and IL-2RA concentrations with the addition of a constant of 1, while tick labels indicate the original values in pg/mL. **, adjusted p < 0.01. ***, adjusted p < 0.001. n.s., not significant. Holm-adjusted Dunn’s tests were used to compare PCNSL with the other groups. G–I ROC curves showed the diagnostic performance of CSF IL-10, CXCL13, IL-2RA, FasL, TIM-3, and galectin-9 for distinguishing PCNSL from different disease groups. The corresponding AUC values were shown. G PCNSL versus all other diseases. H PCNSL versus neuroimmunological diseases. (I) PCNSL versus other brain tumors. AUC values were shown in the legends of each panel AUC, area under the curve; CSF, cerebrospinal fluid; CXCL13, C–X–C motif chemokine ligand 13; FasL, Fas ligand; IL-2RA, interleukin-2 receptor chain alpha; IL-10, interleukin-10; iNPH, idiopathic normal pressure hydrocephalus; IQR, interquartile range; PCNSL, primary central nervous system lymphoma; ROC, Receiver operating characteristic; TIM-3, T-cell immunoglobulin and mucin domain 3

Article Snippet: CXCL13 + Galectin-9 , 55.1 , 63.4 , 0.940 , 0.223 , 0.735 , .

Techniques: Diagnostic Assay, Transformation Assay

Journal: Journal of Neurology

Article Title: Soluble TIM-3 and galectin-9 serve as additional diagnostic biomarkers in primary central nervous system lymphoma

doi: 10.1007/s00415-026-13791-4

Figure Lengend Snippet: Correlations and clustering of diagnostic markers in PCNSL. Scatter plots and correlation analyses showed correlations between IL-10 and CXCL13 ( A ), IL-10 and IL-2RA ( B ), IL-10 and FasL ( C ), IL-10 and TIM-3 ( D ), IL-10 and galectin-9 ( E ), CXCL13 and IL-2RA ( F ), CXCL13 and FasL ( G ), CXCL13 and TIM-3 ( H ), CXCL13 and galectin-9 ( I ), IL-2RA and FasL ( J ), IL-2RA and TIM-3 ( K ), IL-2RA and galectin-9 (L), FasL and TIM-3 ( M ), FasL and galectin-9 ( N ), and TIM-3 and galectin-9 ( O ). Spearman’s rank correlation was used to measure the degree of correlation between CSF diagnostic markers. P Correlation matrix showed Spearman’s rank correlation coefficients between CSF diagnostic markers in PCNSL patients. Q Hierarchical clustering of CSF diagnostic markers in PCNSL patients based on Spearman’s rank correlation coefficients. Clustering was performed using 1 − Spearman’s correlation coefficient as the distance metric with the complete linkage method. CSF, cerebrospinal fluid; CXCL13, C–X–C motif chemokine ligand 13; FasL, Fas ligand; IL-2RA, interleukin-2 receptor chain alpha; IL-10, interleukin-10; PCNSL, primary central nervous system lymphoma; TIM-3, T-cell immunoglobulin and mucin domain 3

Article Snippet: CXCL13 + Galectin-9 , 55.1 , 63.4 , 0.940 , 0.223 , 0.735 , .

Techniques: Diagnostic Assay

Journal: Journal of Neurology

Article Title: Soluble TIM-3 and galectin-9 serve as additional diagnostic biomarkers in primary central nervous system lymphoma

doi: 10.1007/s00415-026-13791-4

Figure Lengend Snippet: Comparison of PFS in PCNSL according to diagnostic marker levels. Kaplan–Meier curves for PFS in PCNSL patients were compared according to CSF IL-10 ( A ), CXCL13 ( B ), IL-2RA ( C ), FasL ( D ), TIM-3 ( E ), and galectin-9 ( F ) levels. PFS was compared using the log-rank test. CSF, cerebrospinal fluid; CXCL13, C–X–C motif chemokine ligand 13; FasL, Fas ligand; IL-2RA, interleukin-2 receptor chain alpha; IL-10, interleukin-10; PCNSL, primary central nervous system lymphoma; PFS, progression-free survival; TIM-3, T-cell immunoglobulin and mucin domain 3

Article Snippet: CXCL13 + Galectin-9 , 55.1 , 63.4 , 0.940 , 0.223 , 0.735 , .

Techniques: Comparison, Diagnostic Assay, Marker