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cxcl16 transcript variant 1  (OriGene)


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    OriGene cxcl16 transcript variant 1
    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.
    Cxcl16 Transcript Variant 1, supplied by OriGene, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cxcl16+transcript+variant+1/Human+CXCL16+ELISA+KIT/bio_rxiv__64898__2026__05__28__728486-58-13-11
    Average 94 stars, based on 2 article reviews
    cxcl16 transcript variant 1 - by Bioz Stars, 2026-11
    94/100 stars

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    1) Product Images from "CXCR6⁺ natural killer cell immunotherapy preserves CD4⁺ T helper cells in humanized mice"

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

    Journal: bioRxiv

    doi: 10.64898/2026.05.28.728486

    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.
    Figure Legend 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.

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

    Related Articles

    Expressing:

    Article Title: Phenotypic and Functional Plasticity of CXCR6 + Peripheral Blood NK Cells
    Article Snippet: .. Because CXCR6 + NK cells depend on CXCL16 expression for survival in the liver sinusoidal epithelium ( , ), we transduced a B lymphoblastoid cell line (RPMI-8866) with lentiviral particles (pLenti-C-mGFP, Origene) encoding either CXCL16 transcript variant 1 (TV1, NM_022059) or 2 (TV2, NM_001100812), thereby generating B cell lines stably expressing the ligand for CXCR6. ..

    Article Title: Phenotypic and Functional Plasticity of CXCR6 + Peripheral Blood NK Cells.
    Article Snippet: .. Because CXCR6+ NK cells depend on CXCL16 expression for survival in the liver sinusoidal epithelium (18, 25), we transduced a B lymphoblastoid cell line (RPMI-8866) with lentiviral particles (pLenti-C-mGFP, Origene) encoding either CXCL16 transcript variant 1 (TV1, NM_022059) or 2 (TV2, NM_001100812), thereby generating B cell lines stably expressing the ligand for CXCR6. ..

    Variant Assay:

    Article Title: Phenotypic and Functional Plasticity of CXCR6 + Peripheral Blood NK Cells
    Article Snippet: .. Because CXCR6 + NK cells depend on CXCL16 expression for survival in the liver sinusoidal epithelium ( , ), we transduced a B lymphoblastoid cell line (RPMI-8866) with lentiviral particles (pLenti-C-mGFP, Origene) encoding either CXCL16 transcript variant 1 (TV1, NM_022059) or 2 (TV2, NM_001100812), thereby generating B cell lines stably expressing the ligand for CXCR6. ..

    Article Title: Phenotypic and Functional Plasticity of CXCR6 + Peripheral Blood NK Cells.
    Article Snippet: .. Because CXCR6+ NK cells depend on CXCL16 expression for survival in the liver sinusoidal epithelium (18, 25), we transduced a B lymphoblastoid cell line (RPMI-8866) with lentiviral particles (pLenti-C-mGFP, Origene) encoding either CXCL16 transcript variant 1 (TV1, NM_022059) or 2 (TV2, NM_001100812), thereby generating B cell lines stably expressing the ligand for CXCR6. ..

    Article Title: CXCR6⁺ natural killer cell immunotherapy preserves CD4⁺ T helper cells in humanized mice
    Article Snippet: To support expansion of CXCR6 + NK cells in culture, the B lymphoblastoid cell line RPMI 8866 (Sigma Aldrich) was engineered to stably express CXCL16, reflecting the CXCR6 CXCL16 survival axis. .. 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). ..

    Stable Transfection:

    Article Title: Phenotypic and Functional Plasticity of CXCR6 + Peripheral Blood NK Cells
    Article Snippet: .. Because CXCR6 + NK cells depend on CXCL16 expression for survival in the liver sinusoidal epithelium ( , ), we transduced a B lymphoblastoid cell line (RPMI-8866) with lentiviral particles (pLenti-C-mGFP, Origene) encoding either CXCL16 transcript variant 1 (TV1, NM_022059) or 2 (TV2, NM_001100812), thereby generating B cell lines stably expressing the ligand for CXCR6. ..

    Article Title: Phenotypic and Functional Plasticity of CXCR6 + Peripheral Blood NK Cells.
    Article Snippet: .. Because CXCR6+ NK cells depend on CXCL16 expression for survival in the liver sinusoidal epithelium (18, 25), we transduced a B lymphoblastoid cell line (RPMI-8866) with lentiviral particles (pLenti-C-mGFP, Origene) encoding either CXCL16 transcript variant 1 (TV1, NM_022059) or 2 (TV2, NM_001100812), thereby generating B cell lines stably expressing the ligand for CXCR6. ..

    Transduction:

    Article Title: CXCR6⁺ natural killer cell immunotherapy preserves CD4⁺ T helper cells in humanized mice
    Article Snippet: To support expansion of CXCR6 + NK cells in culture, the B lymphoblastoid cell line RPMI 8866 (Sigma Aldrich) was engineered to stably express CXCL16, reflecting the CXCR6 CXCL16 survival axis. .. 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). ..



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    cxcl16 transcript variant 1  (OriGene)
    94
    OriGene cxcl16 transcript variant 1
    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.
    Cxcl16 Transcript Variant 1, supplied by OriGene, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cxcl16+transcript+variant+1/Human+CXCL16+ELISA+KIT/bio_rxiv__64898__2026__05__28__728486-58-13-11
    Average 94 stars, based on 1 article reviews
    cxcl16 transcript variant 1 - by Bioz Stars, 2026-11
    94/100 stars
    		  Buy from Supplier

    Image Search Results


    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