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goat polyclonal anti cxcl13 antibody  (R&D Systems)


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    Structured Review

    R&D Systems goat polyclonal anti cxcl13 antibody
    <t>CXCL13</t> 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.
    Goat Polyclonal Anti Cxcl13 Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 69 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 93 stars, based on 69 article reviews
    goat polyclonal anti cxcl13 antibody - by Bioz Stars, 2026-06
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    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

    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.
    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.
    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

    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.
    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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    <t>CXCL13</t> 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.
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    <t>CXCL13</t> 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.
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    Image Search Results


    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: 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

    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: 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

    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: 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

    (A) TFH (CD3 + CD8 - CD19 - CXCR5 hi PD-1 hi ) were spinoculated with X4-HIV GFP reporter virus (X4-HIV) and cultured with autologous uninfected, CellTrace Blue labeled TFH or GCB (CD19 + CD3 - CD38 mid IgD - ) for 3 days in R-15 and 5μM saquinavir. CXCR5 MFI of CellTrace - GFP + and GFP - TFH was determined by flow cytometry (n = 11). (B) Supernatant from cultures of TFH spinoculated with X4-HIV and cultured with autologous uninfected CellTrace Blue labeled TFH or GCB were collected after three days. Live, CellTrace Blue - TFH cell counts were determined by flow cytometry. CXCL13 concentrations were determined by ELISA and normalized to pg/TFH (n = 6). (C) CXCR5 MFI was determined by flow cytometry on GFP + CellTrace - TFH from cultures of X4-HIV spinoculated TFH cultured with autologous uninfected, CellTrace Blue labeled TFH or GCB in the presence or absence of CXCL13 blocking antibody after 3 days (n = 10). (D) TFH (CD3 + CD8 - PD-1 hi ICOS hi ) were spinoculated with X4-HIV, then recovered for 1 hour in R-15 with 5μM saquinavir. Half of the cells were cultured 3 days in R-15 with 5μM saquinavir, while the other half were washed and subjected to a CXCL13 chemotaxis assay using 5 μm transwells. After 4 hours, cells were collected from both top and bottom wells, washed, and cultured 3 days in R-15 containing 5μM saquinavir. On day 3, the chemotaxis assay was performed on the remaining TFH untouched post spinoculation. GFP expression was determined in TFH from top and bottom wells and total GFP + and GFP - cells counts were determined using absolute count beads by flow cytometry to determine chemotactic indexes (n = 5). Horizontal bars indicate medians (A). Wilcoxon matched paired tests were performed using Graphpad Prism v10 and significance indicated: ns, not significant; *p < 0.05; **p < 0.01; ***p < 0.001.

    Journal: PLOS Pathogens

    Article Title: Lymphoid B cells upregulate HIV-1 ex vivo and are linked to its expression in vivo

    doi: 10.1371/journal.ppat.1013661

    Figure Lengend Snippet: (A) TFH (CD3 + CD8 - CD19 - CXCR5 hi PD-1 hi ) were spinoculated with X4-HIV GFP reporter virus (X4-HIV) and cultured with autologous uninfected, CellTrace Blue labeled TFH or GCB (CD19 + CD3 - CD38 mid IgD - ) for 3 days in R-15 and 5μM saquinavir. CXCR5 MFI of CellTrace - GFP + and GFP - TFH was determined by flow cytometry (n = 11). (B) Supernatant from cultures of TFH spinoculated with X4-HIV and cultured with autologous uninfected CellTrace Blue labeled TFH or GCB were collected after three days. Live, CellTrace Blue - TFH cell counts were determined by flow cytometry. CXCL13 concentrations were determined by ELISA and normalized to pg/TFH (n = 6). (C) CXCR5 MFI was determined by flow cytometry on GFP + CellTrace - TFH from cultures of X4-HIV spinoculated TFH cultured with autologous uninfected, CellTrace Blue labeled TFH or GCB in the presence or absence of CXCL13 blocking antibody after 3 days (n = 10). (D) TFH (CD3 + CD8 - PD-1 hi ICOS hi ) were spinoculated with X4-HIV, then recovered for 1 hour in R-15 with 5μM saquinavir. Half of the cells were cultured 3 days in R-15 with 5μM saquinavir, while the other half were washed and subjected to a CXCL13 chemotaxis assay using 5 μm transwells. After 4 hours, cells were collected from both top and bottom wells, washed, and cultured 3 days in R-15 containing 5μM saquinavir. On day 3, the chemotaxis assay was performed on the remaining TFH untouched post spinoculation. GFP expression was determined in TFH from top and bottom wells and total GFP + and GFP - cells counts were determined using absolute count beads by flow cytometry to determine chemotactic indexes (n = 5). Horizontal bars indicate medians (A). Wilcoxon matched paired tests were performed using Graphpad Prism v10 and significance indicated: ns, not significant; *p < 0.05; **p < 0.01; ***p < 0.001.

    Article Snippet: In some experiments 5μg/ml CXCL13 blocking antibody (clone AF801, R&D systems), 10μg/ml anti-IL-2 (clone 5334, R&D systems), 10μg/ml anti-GITRL (clone 109114, R&D systems), 5μg/ml 4–1BB-Fc (R&D systems), 10μg/ml anti-MHC-II (clone IVA12, Raybiotech), 10μg/ml sICOS (Biolegend), 10μg/ml sCD40L (Biolegend), 10μg/ml anti-CD40 (clone 82102, R&D systems), 100nM AZD5582 (SelleckChem), 5μM NIK-SMI1 (Sigma), 0.1-1μM tofocitinib (SelleckChem), 0.1-1μM ruxolitinib (SelleckChem), or DMSO as an appropriate vehicle control when necessary were added.

    Techniques: Virus, Cell Culture, Labeling, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Blocking Assay, Chemotaxis Assay, Expressing

    CXCL13 is upregulated in infected MDMs specifically. (A) Volcano plot showing considerably upregulated (red dots) and downregulated genes (blue dots) in M. leprae -infected FMs vs M. leprae-infected MDMs. KEGG enrichment analysis of upregulated (B) and downregulated (C) DEGs in M. leprae -infected FMs vs M. leprae -infected MDMs. (D) Expression of CXCL13 in different groups (n=10 per group). Expression abundance of CXCL13 in the supernatants of MDMs, FMs, M. leprae -infected MDMs and FMs (n=10 per group) (E) , and in the serum of HCs and leprosy patients (n=5 per group) (F) . (G) mIHC showing the co-localization of CXCL13 and FMs marker ADRP in leprosy lesions from BT and LL subtypes (n=5 per group). BT, borderline tuberculoid leprosy; LL, lepromatous leprosy; HC, healthy control; KEGG, Kyoto Encyclopedia of Genes and Genomes; DEG, Differential expressed gene. Differences between the mean of experimental groups were analyzed using the two-tailed Student t-test . *, **, *** or N.S. indicates p-value <0.05, <0.01, <0.001 or no statistical significance respectively.

    Journal: Frontiers in Immunology

    Article Title: Insufficient CXCL13 secretion in leprosy foamy macrophages attenuates lymphocyte recruitment and antimicrobial protein production

    doi: 10.3389/fimmu.2025.1541954

    Figure Lengend Snippet: CXCL13 is upregulated in infected MDMs specifically. (A) Volcano plot showing considerably upregulated (red dots) and downregulated genes (blue dots) in M. leprae -infected FMs vs M. leprae-infected MDMs. KEGG enrichment analysis of upregulated (B) and downregulated (C) DEGs in M. leprae -infected FMs vs M. leprae -infected MDMs. (D) Expression of CXCL13 in different groups (n=10 per group). Expression abundance of CXCL13 in the supernatants of MDMs, FMs, M. leprae -infected MDMs and FMs (n=10 per group) (E) , and in the serum of HCs and leprosy patients (n=5 per group) (F) . (G) mIHC showing the co-localization of CXCL13 and FMs marker ADRP in leprosy lesions from BT and LL subtypes (n=5 per group). BT, borderline tuberculoid leprosy; LL, lepromatous leprosy; HC, healthy control; KEGG, Kyoto Encyclopedia of Genes and Genomes; DEG, Differential expressed gene. Differences between the mean of experimental groups were analyzed using the two-tailed Student t-test . *, **, *** or N.S. indicates p-value <0.05, <0.01, <0.001 or no statistical significance respectively.

    Article Snippet: Rabbit anti–human ADRP (1:200, 15294-1-AP, proteintech), antibody and CXCL13 (1:200, 10927-1-AP, proteintech) antibody were used.

    Techniques: Infection, Expressing, Marker, Control, Two Tailed Test