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cxcl16  (R&D Systems)


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    R&D Systems cxcl16
    ELISA was used to measure Chlamydia-infection induced (A) CCL5, (B) CXCL10, (C) IL-6, and (D) <t>CXCL16</t> secreted into the supernatants of wild-type and mutant OE cells that were either mock-treated or infected with the 10 IFU/cell C. muridarum. Supernatants were collected at the indicated time post-infection. ***= p<0.005; **= p<0.01 *= p<0.05; ns= not statistically significant when compared to mock-infected control cells. Data presented are representative .
    Cxcl16, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 49 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+cxcl16+elisa+kit/Human+CXCL16+Quantikine+ELISA+Kit/bio_rxiv__64898__2026__03__23__713660-148-6-19
    Average 94 stars, based on 49 article reviews
    cxcl16 - by Bioz Stars, 2026-09
    94/100 stars

    Images

    1) Product Images from "Examining the impact of the Chlamydia muridarum -induced synthesis of IFN-β during genital tract infection 1"

    Article Title: Examining the impact of the Chlamydia muridarum -induced synthesis of IFN-β during genital tract infection 1

    Journal: bioRxiv

    doi: 10.64898/2026.03.23.713660

    ELISA was used to measure Chlamydia-infection induced (A) CCL5, (B) CXCL10, (C) IL-6, and (D) CXCL16 secreted into the supernatants of wild-type and mutant OE cells that were either mock-treated or infected with the 10 IFU/cell C. muridarum. Supernatants were collected at the indicated time post-infection. ***= p<0.005; **= p<0.01 *= p<0.05; ns= not statistically significant when compared to mock-infected control cells. Data presented are representative .
    Figure Legend Snippet: ELISA was used to measure Chlamydia-infection induced (A) CCL5, (B) CXCL10, (C) IL-6, and (D) CXCL16 secreted into the supernatants of wild-type and mutant OE cells that were either mock-treated or infected with the 10 IFU/cell C. muridarum. Supernatants were collected at the indicated time post-infection. ***= p<0.005; **= p<0.01 *= p<0.05; ns= not statistically significant when compared to mock-infected control cells. Data presented are representative .

    Techniques Used: Enzyme-linked Immunosorbent Assay, Infection, Mutagenesis, Control

    ELISA was used to measure Chlamydia- infection-induced (A) IL-6 and (B) CXCL16 secreted into the supernatants of OE-IFNβ(-) cells that were either mock-treated, infected with the 5 IFU/cell C. muridarum in the presence or absence of 50U of recombinant IFN-βml, or treated with only 50U of recombinant IFN-β/ml. Supernatants were collected at the indicated time post-treatment. ***= p<0.005; **= p<0.01; *= p<0.05; ns= not statistically significant when compared to mock-infected control cells or where indicated. Data presented are representative .
    Figure Legend Snippet: ELISA was used to measure Chlamydia- infection-induced (A) IL-6 and (B) CXCL16 secreted into the supernatants of OE-IFNβ(-) cells that were either mock-treated, infected with the 5 IFU/cell C. muridarum in the presence or absence of 50U of recombinant IFN-βml, or treated with only 50U of recombinant IFN-β/ml. Supernatants were collected at the indicated time post-treatment. ***= p<0.005; **= p<0.01; *= p<0.05; ns= not statistically significant when compared to mock-infected control cells or where indicated. Data presented are representative .

    Techniques Used: Enzyme-linked Immunosorbent Assay, Infection, Recombinant, Control

    Related Articles

    Enzyme-linked Immunosorbent Assay:

    Article Title: LncRNA LINK‐ A Remodels Tissue Inflammatory Microenvironments to Promote Obesity
    Article Snippet: After successful induction of beige adipocytes, soluble IL‐1β inhibitor (VX‐765, MCE, 10 μ m ) or/and soluble CXCL16 inhibitor (GI254032, Selleck, 3 μ m ) was added to the medium, and cells were cultured for 24 h, followed by collecting cells for subsequent experiments. .. The concentrations of IL‐1β and CXCL16 in MCF‐10A cell supernatants after treatment with different conditions were measured using the Human IL‐1β ELISA kit (absin, abs159986) and the Human CXCL16 ELISA kit (R&D Systems, DCX160). .. The concentrations of IL‐1β and CXCL16 in mouse plasma were measured using the Mouse IL‐1β ELISA kit (absin, abs520001) and the Mouse CXCL16 ELISA kit (R&D Systems, DY503).

    Article Title: Human trophoblasts recruited T lymphocytes and monocytes into decidua by secretion of chemokine CXCL16 and interaction with CXCR6 in the first-trimester pregnancy.
    Article Snippet: .. The human CXCL16 ELISA kit (R&D Systems) was used to measure chemokine production in each supernatant and CM according to the manufacturer’s instructions. ..

    Article Title: Chemokine CXCL16 mediates acinar cell necrosis in cerulein induced acute pancreatitis in mice
    Article Snippet: .. Samples were applied to a human CXCL16 ELISA kit (R&D systems) and the levels of serum CXCL16 were measured according to the manufacturer’s instructions. ..

    Article Title: Trophoblast-derived CXCL16 induces M2 macrophage polarization that in turn inactivates NK cells at the maternal–fetal interface
    Article Snippet: .. The human CXCL16 ELISA kit (R&D Systems, MN, USA) was used to measure the levels of this secreted chemokine in each supernatant according to the manufacturer’s instructions. .. The purity of the isolated HLA-G + Cyk7 + (APC-conjugated anti-human HLA-G, 87G, Biolegend; FITC-conjugated anti-human Cyk7, CAM5.2, BD) primary human trophoblast cells and the Ki-67 (APC-conjugated anti-human Ki-67, Biolegend) expression in NK cells were analyzed by flow cytometry.

    Article Title: The clinical significance of CXCL16 in the treatment of advanced non‐small cell lung cancer
    Article Snippet: .. The value of serum CXCL16 level was measured using human CXCL16 ELISA kit (Human CXCL16 Quantikine ELISA Kit, R&D Systems, Minneapolis, MN, USA), following the manufacturer's protocol, and all analyses were performed in duplicates for the assessment of the interassay variations. ..

    Article Title: Overexpression of CXCL16 and its receptor CXCR6/Bonzo promotes growth of human schwannomas.
    Article Snippet: Chemokines and their receptors play a decisive role in tumor progression and metastasis.. Here, we describe the expression of the CXCL16-CXCR6-system in human schwannomas of different localization and in malignant peripheral nerve sheath tumors.. The transmembrane chemokine CXCL16 and its receptor CXCR6/Bonzo were overexpressed on the mRNA and protein levels in all tumor samples investigated as compared with normal peripheral or 8th cranial nerve tissues.

    Article Title: LncRNA LINK-A Remodels Tissue Inflammatory Microenvironments to Promote Obesity.
    Article Snippet: IL-1β Inhibitor or/and CXCL16 Inhibitor Treated Adipocytes: After successful induction of beige adipocytes, soluble IL-1β inhibitor (VX-765, MCE, 10 μm) or/and soluble CXCL16 inhibitor (GI254032, Selleck, 3 μm) was added to the medium, and cells were cultured for 24 h, followed by collecting cells for subsequent experiments. .. Quantitative IL-1β and CXCL16 Measurement: The concentrations of IL-1β and CXCL16 in MCF-10A cell supernatants after treatment with different conditions were measured using the Human IL-1β ELISA kit (absin, abs159986) and the Human CXCL16 ELISA kit (R&D Systems, DCX160). .. The concentrations of IL-1β and CXCL16 in mouse plasma were measured using the Mouse IL-1β ELISA kit (absin, abs520001) and the Mouse CXCL16 ELISA kit (R&D Systems, DY503).

    Article Title: NK cell-activating fusion protein, NK cell, and pharmaceutical composition including same
    Article Snippet: .. The CXCL16 ELISA was performed according to a method of Human CXCL16 ELISA kit (# DCX160) of an R&D system. .. For an ELISA analysis, the mesothelin scFv fusion polypeptide (mesothelin scFv NRP-body) was divided in an amount of 0.5 μg/mL and 50 μl/well into a 96-well plate for ELISA (R&D) and left alone at room temperature for two hours, such that a resulting absorbed one was used for that analysis.



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    A) Expansion kinetics of sorted CXCR6⁻ and CXCR6⁺ NK cells from independent peripheral blood NK-cell donors during 15 days of ex vivo culture with <t>CXCL16-expressing</t> feeder cells, irradiated allogeneic PBMC feeders, and cytokine supplementation. B) Representative post-expansion flow cytometry plots showing maintenance of CXCR6-defined NK-cell phenotypes following expansion. C) Representative intracellular HIV-Gag flow cytometry plots from the indicated culture conditions. Activated primary CD4⁺ T cells from a single peripheral blood donor were infected with HIV-1 Q23.17 at an MOI of 0.01 and cultured alone or co-cultured for 3 days with day 14-expanded CXCR6⁺ or CXCR6⁻ NK cells at a 1:1 effector-to-target ratio. HIV infection was quantified by intracellular HIV-Gag staining and flow cytometry. D) Quantification of HIV suppression assay results. CXCR6⁺ and CXCR6⁻ NK cells were tested using NK cells from five independent genetically unrelated donors, with the same HIV-infected CD4⁺ T-cell target donor used across all NK donor and subset conditions. For each NK donor and condition, the CD4 + T cell-frequency was determined by flow cytometry, triplicate technical wells per donor were averaged before statistical analysis, and the five NK donors were analyzed as biological replicates. Donor-level paired comparisons were analyzed using two-sided paired tests with Holm correction for multiple comparisons. CXCR6⁺ NK cells significantly reduced the frequency of HIV-Gag⁺ CD4⁺ T cells compared with HIV-only cultures, p = 0.000064. CXCR6⁻ NK cells also significantly reduced HIV-Gag⁺ CD4⁺ T cells compared with HIV-only cultures, p = 0.004059. CXCR6⁺ NK cells suppressed HIV significantly more effectively than paired CXCR6⁻ NK cells, p = 0.009637. Data are presented as mean ± SD, with each color representing an independent NK-cell donor. **p < 0.01, ****p < 0.0001.
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    Image Search Results


    The interaction of MDSCs and Treg by CXCL16‐CXCR6 signaling was obvious in PJI. a) The interaction plot showed the cell communications between myeloid cells and lymphocytes by ligand‐receptor pair analysis. The thicker the line represented, the stronger the interaction weights/strength, and the more the number of interactions among the cell types. b) The bar chart showed the interaction strength and the number of interactions among PJI, AF and OA. c) The bar chart showed the strength comparison of the interaction pathways among PJI, AF and OA. d) The heatmap showed relative strength of all enriched signals (outgoing and incoming) across myeloid cells and lymphocytes. e) The circle plot showed the inferred intercellular communication network for CXCL signaling pathway. f) The heatmap showed the CXCL signaling pathway among myeloid cells and lymphocytes. g) The bar chart showed the ligand‐receptor pair of CXCL signaling pathway among myeloid cells and lymphocytes. h) The bar chart showed the relative contribution of ligand‐receptor pair to the overall communication network of CXCL signaling pathway. i) The dot plot showed the incoming communication patterns of CXCL signaling pathway from M‐MDSCs among PJI, AF and OA. j) Multiplex immunofluorescence image showed the co‐location of CXCR6+ Treg and CD68+ myeloid cells with excretive CXCL16. Yellow arrow highlighted the CD68+ myeloid cells expressing CXCL16, and red arrow highlighted the CD4+FOXP3+ Treg expressing CXCR6. Scale bar, 20 mm (PJI, n = 3; AF, n = 3; OA, n = 3). Unpaired t test; ** p < 0.01, *** p < 0.001.

    Journal: Advanced Science

    Article Title: CXCL16/CXCR6/TGF‐β Feedback Loop Between M‐MDSCs and Treg Inhibits Anti‐Bacterial Immunity During Biofilm Infection

    doi: 10.1002/advs.202409537

    Figure Lengend Snippet: The interaction of MDSCs and Treg by CXCL16‐CXCR6 signaling was obvious in PJI. a) The interaction plot showed the cell communications between myeloid cells and lymphocytes by ligand‐receptor pair analysis. The thicker the line represented, the stronger the interaction weights/strength, and the more the number of interactions among the cell types. b) The bar chart showed the interaction strength and the number of interactions among PJI, AF and OA. c) The bar chart showed the strength comparison of the interaction pathways among PJI, AF and OA. d) The heatmap showed relative strength of all enriched signals (outgoing and incoming) across myeloid cells and lymphocytes. e) The circle plot showed the inferred intercellular communication network for CXCL signaling pathway. f) The heatmap showed the CXCL signaling pathway among myeloid cells and lymphocytes. g) The bar chart showed the ligand‐receptor pair of CXCL signaling pathway among myeloid cells and lymphocytes. h) The bar chart showed the relative contribution of ligand‐receptor pair to the overall communication network of CXCL signaling pathway. i) The dot plot showed the incoming communication patterns of CXCL signaling pathway from M‐MDSCs among PJI, AF and OA. j) Multiplex immunofluorescence image showed the co‐location of CXCR6+ Treg and CD68+ myeloid cells with excretive CXCL16. Yellow arrow highlighted the CD68+ myeloid cells expressing CXCL16, and red arrow highlighted the CD4+FOXP3+ Treg expressing CXCR6. Scale bar, 20 mm (PJI, n = 3; AF, n = 3; OA, n = 3). Unpaired t test; ** p < 0.01, *** p < 0.001.

    Article Snippet: CXCL16 in human synovial fluid samples was also measured by ELISA (70‐EK1254‐96, Hangzhou, China, MultiSciences).

    Techniques: Comparison, Multiplex Assay, Immunofluorescence, Expressing

    PJI patients with high CXCR6 showed a higher recurrence rate. a) The Volcano plot showed differentially expressed genes in PJI versus AF patients. The x and y axes represented the log2 fold change and p‐value, respectively, based on the Mann‐Whitney U test. Red dots: upregulated genes, blue dots: downregulated genes. b) The heatmap showed the distribution of 28 types of immune cells in PJI and AF. c) The bar chart showed the difference in proportion of M‐MDSCs and Treg between PJI and AF (PJI, n = 18; AF, n = 18). Unpaired t test; *** p < 0.001. d) The heatmap showed the characteristic genes of chemokines, PJI markers, cell markers and immune checkpoint between PJI and AF. e–l) The violin plots showed part of the differential genes (CXCL16, CXCR6, S100A8, S100A9, FOXP3, CTLA4, TIGIT and LAG3) between PJI and AF as shown in (d). Unpaired t test; ns p > 0.05, *** p < 0.001, **** p < 0.0001. m,n) Quantitative analysis of immunohistochemical staining for CXCL16 and CXCR6 (PJI, n = 80; AF, n = 25; OA = 25). 40x magnification. Scale bar, 20 mm. Unpaired t test; ** p < 0.01, *** p < 0.001. o) The Kaplan‐Meier curve showed the recurrence curves of PJI patients characterized by either low or high expression of CXCR6 (CXCR6‐high PJI, n = 30; CXCR6‐low PJI, n = 30). Significance was calculated using the log‐rank test. p,q) Quantitative analysis of Harris Hip score and HSS knee score in CXCR6‐high PJI and CXCR6‐low PJI group (CXCR6‐high PJI, n = 30; CXCR6‐low PJI, n = 30). Unpaired t test; * p < 0.05.

    Journal: Advanced Science

    Article Title: CXCL16/CXCR6/TGF‐β Feedback Loop Between M‐MDSCs and Treg Inhibits Anti‐Bacterial Immunity During Biofilm Infection

    doi: 10.1002/advs.202409537

    Figure Lengend Snippet: PJI patients with high CXCR6 showed a higher recurrence rate. a) The Volcano plot showed differentially expressed genes in PJI versus AF patients. The x and y axes represented the log2 fold change and p‐value, respectively, based on the Mann‐Whitney U test. Red dots: upregulated genes, blue dots: downregulated genes. b) The heatmap showed the distribution of 28 types of immune cells in PJI and AF. c) The bar chart showed the difference in proportion of M‐MDSCs and Treg between PJI and AF (PJI, n = 18; AF, n = 18). Unpaired t test; *** p < 0.001. d) The heatmap showed the characteristic genes of chemokines, PJI markers, cell markers and immune checkpoint between PJI and AF. e–l) The violin plots showed part of the differential genes (CXCL16, CXCR6, S100A8, S100A9, FOXP3, CTLA4, TIGIT and LAG3) between PJI and AF as shown in (d). Unpaired t test; ns p > 0.05, *** p < 0.001, **** p < 0.0001. m,n) Quantitative analysis of immunohistochemical staining for CXCL16 and CXCR6 (PJI, n = 80; AF, n = 25; OA = 25). 40x magnification. Scale bar, 20 mm. Unpaired t test; ** p < 0.01, *** p < 0.001. o) The Kaplan‐Meier curve showed the recurrence curves of PJI patients characterized by either low or high expression of CXCR6 (CXCR6‐high PJI, n = 30; CXCR6‐low PJI, n = 30). Significance was calculated using the log‐rank test. p,q) Quantitative analysis of Harris Hip score and HSS knee score in CXCR6‐high PJI and CXCR6‐low PJI group (CXCR6‐high PJI, n = 30; CXCR6‐low PJI, n = 30). Unpaired t test; * p < 0.05.

    Article Snippet: CXCL16 in human synovial fluid samples was also measured by ELISA (70‐EK1254‐96, Hangzhou, China, MultiSciences).

    Techniques: MANN-WHITNEY, Immunohistochemical staining, Staining, Expressing

    A) Expansion kinetics of sorted CXCR6⁻ and CXCR6⁺ NK cells from independent peripheral blood NK-cell donors during 15 days of ex vivo culture with CXCL16-expressing feeder cells, irradiated allogeneic PBMC feeders, and cytokine supplementation. B) Representative post-expansion flow cytometry plots showing maintenance of CXCR6-defined NK-cell phenotypes following expansion. C) Representative intracellular HIV-Gag flow cytometry plots from the indicated culture conditions. Activated primary CD4⁺ T cells from a single peripheral blood donor were infected with HIV-1 Q23.17 at an MOI of 0.01 and cultured alone or co-cultured for 3 days with day 14-expanded CXCR6⁺ or CXCR6⁻ NK cells at a 1:1 effector-to-target ratio. HIV infection was quantified by intracellular HIV-Gag staining and flow cytometry. D) Quantification of HIV suppression assay results. CXCR6⁺ and CXCR6⁻ NK cells were tested using NK cells from five independent genetically unrelated donors, with the same HIV-infected CD4⁺ T-cell target donor used across all NK donor and subset conditions. For each NK donor and condition, the CD4 + T cell-frequency was determined by flow cytometry, triplicate technical wells per donor were averaged before statistical analysis, and the five NK donors were analyzed as biological replicates. Donor-level paired comparisons were analyzed using two-sided paired tests with Holm correction for multiple comparisons. CXCR6⁺ NK cells significantly reduced the frequency of HIV-Gag⁺ CD4⁺ T cells compared with HIV-only cultures, p = 0.000064. CXCR6⁻ NK cells also significantly reduced HIV-Gag⁺ CD4⁺ T cells compared with HIV-only cultures, p = 0.004059. CXCR6⁺ NK cells suppressed HIV significantly more effectively than paired CXCR6⁻ NK cells, p = 0.009637. Data are presented as mean ± SD, with each color representing an independent NK-cell donor. **p < 0.01, ****p < 0.0001.

    Journal: bioRxiv

    Article Title: CXCR6⁺ natural killer cell immunotherapy preserves CD4⁺ T helper cells in humanized mice

    doi: 10.64898/2026.05.28.728486

    Figure Lengend Snippet: A) Expansion kinetics of sorted CXCR6⁻ and CXCR6⁺ NK cells from independent peripheral blood NK-cell donors during 15 days of ex vivo culture with CXCL16-expressing feeder cells, irradiated allogeneic PBMC feeders, and cytokine supplementation. B) Representative post-expansion flow cytometry plots showing maintenance of CXCR6-defined NK-cell phenotypes following expansion. C) Representative intracellular HIV-Gag flow cytometry plots from the indicated culture conditions. Activated primary CD4⁺ T cells from a single peripheral blood donor were infected with HIV-1 Q23.17 at an MOI of 0.01 and cultured alone or co-cultured for 3 days with day 14-expanded CXCR6⁺ or CXCR6⁻ NK cells at a 1:1 effector-to-target ratio. HIV infection was quantified by intracellular HIV-Gag staining and flow cytometry. D) Quantification of HIV suppression assay results. CXCR6⁺ and CXCR6⁻ NK cells were tested using NK cells from five independent genetically unrelated donors, with the same HIV-infected CD4⁺ T-cell target donor used across all NK donor and subset conditions. For each NK donor and condition, the CD4 + T cell-frequency was determined by flow cytometry, triplicate technical wells per donor were averaged before statistical analysis, and the five NK donors were analyzed as biological replicates. Donor-level paired comparisons were analyzed using two-sided paired tests with Holm correction for multiple comparisons. CXCR6⁺ NK cells significantly reduced the frequency of HIV-Gag⁺ CD4⁺ T cells compared with HIV-only cultures, p = 0.000064. CXCR6⁻ NK cells also significantly reduced HIV-Gag⁺ CD4⁺ T cells compared with HIV-only cultures, p = 0.004059. CXCR6⁺ NK cells suppressed HIV significantly more effectively than paired CXCR6⁻ NK cells, p = 0.009637. Data are presented as mean ± SD, with each color representing an independent NK-cell donor. **p < 0.01, ****p < 0.0001.

    Article Snippet: RPMI 8866 cells were transduced with lentiviral particles (pLenti C mGFP, Origene) carrying CXCL16 transcript variant 1 (TV1, NM_022059) or variant 2 (TV2, NM_001100812).

    Techniques: Ex Vivo, Expressing, Irradiation, Flow Cytometry, Infection, Cell Culture, Staining, HIV Inhibition Assay

    ELISA was used to measure Chlamydia-infection induced (A) CCL5, (B) CXCL10, (C) IL-6, and (D) CXCL16 secreted into the supernatants of wild-type and mutant OE cells that were either mock-treated or infected with the 10 IFU/cell C. muridarum. Supernatants were collected at the indicated time post-infection. ***= p<0.005; **= p<0.01 *= p<0.05; ns= not statistically significant when compared to mock-infected control cells. Data presented are representative .

    Journal: bioRxiv

    Article Title: Examining the impact of the Chlamydia muridarum -induced synthesis of IFN-β during genital tract infection 1

    doi: 10.64898/2026.03.23.713660

    Figure Lengend Snippet: ELISA was used to measure Chlamydia-infection induced (A) CCL5, (B) CXCL10, (C) IL-6, and (D) CXCL16 secreted into the supernatants of wild-type and mutant OE cells that were either mock-treated or infected with the 10 IFU/cell C. muridarum. Supernatants were collected at the indicated time post-infection. ***= p<0.005; **= p<0.01 *= p<0.05; ns= not statistically significant when compared to mock-infected control cells. Data presented are representative .

    Article Snippet: Levels of CCL5, CXCL10, IL-6, and CXCL16 were quantified using commercially available ELISA kits according to the manufacturer’s instructions (R&D Systems).

    Techniques: Enzyme-linked Immunosorbent Assay, Infection, Mutagenesis, Control

    ELISA was used to measure Chlamydia- infection-induced (A) IL-6 and (B) CXCL16 secreted into the supernatants of OE-IFNβ(-) cells that were either mock-treated, infected with the 5 IFU/cell C. muridarum in the presence or absence of 50U of recombinant IFN-βml, or treated with only 50U of recombinant IFN-β/ml. Supernatants were collected at the indicated time post-treatment. ***= p<0.005; **= p<0.01; *= p<0.05; ns= not statistically significant when compared to mock-infected control cells or where indicated. Data presented are representative .

    Journal: bioRxiv

    Article Title: Examining the impact of the Chlamydia muridarum -induced synthesis of IFN-β during genital tract infection 1

    doi: 10.64898/2026.03.23.713660

    Figure Lengend Snippet: ELISA was used to measure Chlamydia- infection-induced (A) IL-6 and (B) CXCL16 secreted into the supernatants of OE-IFNβ(-) cells that were either mock-treated, infected with the 5 IFU/cell C. muridarum in the presence or absence of 50U of recombinant IFN-βml, or treated with only 50U of recombinant IFN-β/ml. Supernatants were collected at the indicated time post-treatment. ***= p<0.005; **= p<0.01; *= p<0.05; ns= not statistically significant when compared to mock-infected control cells or where indicated. Data presented are representative .

    Article Snippet: Levels of CCL5, CXCL10, IL-6, and CXCL16 were quantified using commercially available ELISA kits according to the manufacturer’s instructions (R&D Systems).

    Techniques: Enzyme-linked Immunosorbent Assay, Infection, Recombinant, Control