human cxcl13 quantikine elisa kit (R&D Systems)
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human cxcl13 quantikine elisa kit
Human Cxcl13 Quantikine Elisa Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 82 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+cxcl13/Human+CXCL13%2FBLC%2FBCA-1+Quantikine+ELISA+Kit/pmc13106335-76-7-13
Average 95 stars, based on 82 article reviews
Human Cxcl13 Quantikine Elisa Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 82 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+cxcl13/Human+CXCL13%2FBLC%2FBCA-1+Quantikine+ELISA+Kit/pmc13106335-76-7-13
Average 95 stars, based on 82 article reviews
human cxcl13 quantikine elisa kit - by Bioz Stars,
2026-09
95/100 stars
Images
1) Product Images from "CXCL13 as a simple and promising blood biomarker for differentiating Sézary syndrome from mycosis fungoides and other confounding chronic inflammatory skin diseases"
Article Title: CXCL13 as a simple and promising blood biomarker for differentiating Sézary syndrome from mycosis fungoides and other confounding chronic inflammatory skin diseases
Journal: Frontiers in Immunology
doi: 10.3389/fimmu.2026.1804103
Figure Legend 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.
Techniques Used: 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.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_6335/pmc13106335/pmc13106335__fimmu-17-1804103-g002.jpg "CXCL13 immunohistochemical expression in skin biopsies from Sézary syndrome, ...")
Figure Legend 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.
Techniques Used: Immunohistochemical staining, Expressing, Staining
Figure Legend 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.
Techniques Used: Clinical Proteomics, Diagnostic Assay, Whisker Assay, Sampling, MANN-WHITNEY, Derivative Assay
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![( 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 <t>by</t> <t>enzyme-linked</t> 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.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_1753/pmc13041753/pmc13041753__sciadv.aea4262-f3.jpg)
![( 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.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_1753/pmc13041753/pmc13041753__sciadv.aea4262-f6.jpg)
![( 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)].](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_1753/pmc13041753/pmc13041753__sciadv.aea4262-f7.jpg)