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il 2 dy202  (R&D Systems)


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    R&D Systems il 2 dy202
    Effects of nivolumab–relatlimab combined with ipilimumab or atezolizumab on secretion of cytokines in the supernatant of cocultures of hPBMCs with HFC cells. HFC cells were cocultured with lymphocytes (effector–target ratio 5:1) and treated for 48 hours at 37°C with the combination of nivolumab + relatlimab (light gray bars), ipilimumab or atezolizumab (dark gray bars) used alone, or in combinations (black bars) at the indicated <t>concentration.</t> <t>IL-2</t> (A) and granzyme B (B) levels (pg/mL) were obtained by using the duoset ELISA kit from R & D Systems performed on cell supernatants. Cells untreated or treated with an unrelated hIgG (with bars) were used as negative controls. Error bars depict means ± SD. P -values for the combinations relative to respective single agents are *** P < 0.001; ** P < 0.01.
    Il 2 Dy202, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 211 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/il+2+dy202/Human+IL-2+DuoSet+ELISA/pmc13043227-36-11-22
    Average 96 stars, based on 211 article reviews
    il 2 dy202 - by Bioz Stars, 2026-10
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    Images

    1) Product Images from "Evidence of Cardiotoxic Immune Activation by Triple Immune Checkpoint Blockade: A Translational Alert for Clinical Surveillance in Patients With Cancer"

    Article Title: Evidence of Cardiotoxic Immune Activation by Triple Immune Checkpoint Blockade: A Translational Alert for Clinical Surveillance in Patients With Cancer

    Journal: Journal of Cardiovascular Pharmacology

    doi: 10.1097/FJC.0000000000001798

    Effects of nivolumab–relatlimab combined with ipilimumab or atezolizumab on secretion of cytokines in the supernatant of cocultures of hPBMCs with HFC cells. HFC cells were cocultured with lymphocytes (effector–target ratio 5:1) and treated for 48 hours at 37°C with the combination of nivolumab + relatlimab (light gray bars), ipilimumab or atezolizumab (dark gray bars) used alone, or in combinations (black bars) at the indicated concentration. IL-2 (A) and granzyme B (B) levels (pg/mL) were obtained by using the duoset ELISA kit from R & D Systems performed on cell supernatants. Cells untreated or treated with an unrelated hIgG (with bars) were used as negative controls. Error bars depict means ± SD. P -values for the combinations relative to respective single agents are *** P < 0.001; ** P < 0.01.
    Figure Legend Snippet: Effects of nivolumab–relatlimab combined with ipilimumab or atezolizumab on secretion of cytokines in the supernatant of cocultures of hPBMCs with HFC cells. HFC cells were cocultured with lymphocytes (effector–target ratio 5:1) and treated for 48 hours at 37°C with the combination of nivolumab + relatlimab (light gray bars), ipilimumab or atezolizumab (dark gray bars) used alone, or in combinations (black bars) at the indicated concentration. IL-2 (A) and granzyme B (B) levels (pg/mL) were obtained by using the duoset ELISA kit from R & D Systems performed on cell supernatants. Cells untreated or treated with an unrelated hIgG (with bars) were used as negative controls. Error bars depict means ± SD. P -values for the combinations relative to respective single agents are *** P < 0.001; ** P < 0.01.

    Techniques Used: Concentration Assay, Enzyme-linked Immunosorbent Assay

    Proposed mechanism of immune checkpoint inhibitor (ICI)-driven disruption of immune tolerance and cardiomyocyte injury. Under physiologic conditions, regulatory T cells (Tregs) and inhibitory checkpoint pathways—including cytotoxic T-lymphocyte–associated protein 4 (CTLA-4), lymphocyte activation gene-3 (LAG-3), and programmed cell death-1/programmed cell death-ligand 1 (PD-1/PD-L1)—cooperate to maintain peripheral tolerance and protect cardiac tissue from autoreactive immune responses. ICI therapy blocks these inhibitory signals at multiple levels: (I) anti-CTLA-4 antibodies prevent CTLA-4 engagement on both activated T cells and Tregs, thereby dampening Treg-mediated suppression and enhancing effector T-cell activation; (ii) anti-LAG-3 antibodies abrogate an additional inhibitory checkpoint on activated T cells, further potentiating T-cell cytotoxicity; and (iii) antibodies targeting PD-1 or PD-L1 disrupt the PD-1/PD-L1 axis, which normally delivers inhibitory signals on engagement of PD-1 on activated T cells with PD-L1 expressed on cardiomyocytes. Cumulative blockade of these checkpoints removes critical layers of peripheral tolerance and unleashes effector T cells that recognize cardiac antigens as targets, leading to immune attack against cardiomyocytes. This loss of tolerance contributes to proinflammatory cytokine secretion (eg, IL-2, IL-1β, IL-6, IL-8, CCL2, IL-17), enhanced cytotoxic mediator release such as granzyme B, and activation of the cardiomyocyte NLRP3–MyD88–NF-κB axis, ultimately driving myocardial inflammation and injury. The figure summarizes the central paradigm supported by our coculture experiments, wherein triplet checkpoint blockade (anti-CTLA-4 + anti-PD-1 + anti-LAG-3 or anti-PD-L1) produced the strongest disruption of immune tolerance and the most pronounced cardiotoxic effects.
    Figure Legend Snippet: Proposed mechanism of immune checkpoint inhibitor (ICI)-driven disruption of immune tolerance and cardiomyocyte injury. Under physiologic conditions, regulatory T cells (Tregs) and inhibitory checkpoint pathways—including cytotoxic T-lymphocyte–associated protein 4 (CTLA-4), lymphocyte activation gene-3 (LAG-3), and programmed cell death-1/programmed cell death-ligand 1 (PD-1/PD-L1)—cooperate to maintain peripheral tolerance and protect cardiac tissue from autoreactive immune responses. ICI therapy blocks these inhibitory signals at multiple levels: (I) anti-CTLA-4 antibodies prevent CTLA-4 engagement on both activated T cells and Tregs, thereby dampening Treg-mediated suppression and enhancing effector T-cell activation; (ii) anti-LAG-3 antibodies abrogate an additional inhibitory checkpoint on activated T cells, further potentiating T-cell cytotoxicity; and (iii) antibodies targeting PD-1 or PD-L1 disrupt the PD-1/PD-L1 axis, which normally delivers inhibitory signals on engagement of PD-1 on activated T cells with PD-L1 expressed on cardiomyocytes. Cumulative blockade of these checkpoints removes critical layers of peripheral tolerance and unleashes effector T cells that recognize cardiac antigens as targets, leading to immune attack against cardiomyocytes. This loss of tolerance contributes to proinflammatory cytokine secretion (eg, IL-2, IL-1β, IL-6, IL-8, CCL2, IL-17), enhanced cytotoxic mediator release such as granzyme B, and activation of the cardiomyocyte NLRP3–MyD88–NF-κB axis, ultimately driving myocardial inflammation and injury. The figure summarizes the central paradigm supported by our coculture experiments, wherein triplet checkpoint blockade (anti-CTLA-4 + anti-PD-1 + anti-LAG-3 or anti-PD-L1) produced the strongest disruption of immune tolerance and the most pronounced cardiotoxic effects.

    Techniques Used: Disruption, Activation Assay, Produced

    Related Articles

    Enzyme-linked Immunosorbent Assay:

    Article Title: Evidence of Cardiotoxic Immune Activation by Triple Immune Checkpoint Blockade: A Translational Alert for Clinical Surveillance in Patients With Cancer
    Article Snippet: .. Supernatants were collected after 48 hours of coculture and analyzed for IL-2 (DY202) and granzyme B (DY2906) concentrations using DuoSet ELISA kits (R&D Systems, Minneapolis, MN) endowed with a sensitivity of 50 pg/mL. ..

    Article Title: Generation of novel human anti-OX-40 mAbs endowed with different biological properties as tools for cancer therapy
    Article Snippet: .. The IL-2 (DY202) and IFNγ (DY285B) DuoSet ELISA kits by R&D Systems were used to measure the release of cytokines from cell culture supernatants. ..

    Article Title: Activation of the Innate Immune Checkpoint CLEC5A on Myeloid Cells in the Absence of Danger Signals Modulates Macrophages' Function but Does Not Trigger the Adaptive T Cell Immune Response
    Article Snippet: .. ELISA kits to measure MMP1 (DY901B), MIP1-a (DY270), MIP1-b (DY271), and IL-2 (DY202) were obtained from R&D Systems. ..

    Article Title: Tri-specific tribodies targeting 5T4, CD3, and immune checkpoint drive stronger functional T-cell responses than combinations of antibody therapeutics.
    Article Snippet: Thus, after the collection of cell supernatant, the level of LDH released by the cells was evaluated to accurately and quantitatively measure the percentage of lysis of tumor cells treated [36, 51], following the manufacturer’s recommendations (C20300, Thermofisher Scientific, Rockford, IL, USA). .. The IL-2 (DY202) and IFNγ (DY285B) DuoSet ELISA Development kits (DuoSet ELISA, R&D Systems, Minneapolis, MN, USA) were used to measure the release of cytokines from cell culture supernatants. .. The IL-2 (DY202) and IFNγ (DY285B) DuoSet ELISA Development kits (DuoSet ELISA, R&D Systems, Minneapolis, MN, USA) were used to measure the release of cytokines from cell culture supernatants.

    Article Title: Ligand-receptor interactions of V-domain Ig-containing suppressor of T cell activation and programmed death-1 suppress the anticancer activities of T cells
    Article Snippet: Goat anti-mouse (925-32210 and 926-68070) and anti-rabbit (926-3211 and 926-68071) secondary antibodies were obtained from Li-COR (Lincoln, Nebraska). .. ELISA-based assay kits for the detection of PD-L1 (DY156), VISTA (DY7126) and IL-2 (DY202) as well as carrier-free recombinant human VISTA, PD-1 and PD-L1 were purchased from Bio-Techne (R&D Systems, Abingdon, UK). ..

    Article Title: Tri-specific tribodies targeting 5T4, CD3, and immune checkpoint drive stronger functional T-cell responses than combinations of antibody therapeutics
    Article Snippet: Thus, after the collection of cell supernatant, the level of LDH released by the cells was evaluated to accurately and quantitatively measure the percentage of lysis of tumor cells treated [ , ], following the manufacturer’s recommendations (C20300, Thermofisher Scientific, Rockford, IL, USA). .. The IL-2 (DY202) and IFNγ (DY285B) DuoSet ELISA Development kits (DuoSet ELISA, R&D Systems, Minneapolis, MN, USA) were used to measure the release of cytokines from cell culture supernatants. .. The IL-2 (DY202) and IFNγ (DY285B) DuoSet ELISA Development kits (DuoSet ELISA, R&D Systems, Minneapolis, MN, USA) were used to measure the release of cytokines from cell culture supernatants.

    Cell Culture:

    Article Title: Generation of novel human anti-OX-40 mAbs endowed with different biological properties as tools for cancer therapy
    Article Snippet: .. The IL-2 (DY202) and IFNγ (DY285B) DuoSet ELISA kits by R&D Systems were used to measure the release of cytokines from cell culture supernatants. ..

    Article Title: Tri-specific tribodies targeting 5T4, CD3, and immune checkpoint drive stronger functional T-cell responses than combinations of antibody therapeutics.
    Article Snippet: Thus, after the collection of cell supernatant, the level of LDH released by the cells was evaluated to accurately and quantitatively measure the percentage of lysis of tumor cells treated [36, 51], following the manufacturer’s recommendations (C20300, Thermofisher Scientific, Rockford, IL, USA). .. The IL-2 (DY202) and IFNγ (DY285B) DuoSet ELISA Development kits (DuoSet ELISA, R&D Systems, Minneapolis, MN, USA) were used to measure the release of cytokines from cell culture supernatants. .. The IL-2 (DY202) and IFNγ (DY285B) DuoSet ELISA Development kits (DuoSet ELISA, R&D Systems, Minneapolis, MN, USA) were used to measure the release of cytokines from cell culture supernatants.

    Article Title: Tri-specific tribodies targeting 5T4, CD3, and immune checkpoint drive stronger functional T-cell responses than combinations of antibody therapeutics
    Article Snippet: Thus, after the collection of cell supernatant, the level of LDH released by the cells was evaluated to accurately and quantitatively measure the percentage of lysis of tumor cells treated [ , ], following the manufacturer’s recommendations (C20300, Thermofisher Scientific, Rockford, IL, USA). .. The IL-2 (DY202) and IFNγ (DY285B) DuoSet ELISA Development kits (DuoSet ELISA, R&D Systems, Minneapolis, MN, USA) were used to measure the release of cytokines from cell culture supernatants. .. The IL-2 (DY202) and IFNγ (DY285B) DuoSet ELISA Development kits (DuoSet ELISA, R&D Systems, Minneapolis, MN, USA) were used to measure the release of cytokines from cell culture supernatants.

    Recombinant:

    Article Title: Ligand-receptor interactions of V-domain Ig-containing suppressor of T cell activation and programmed death-1 suppress the anticancer activities of T cells
    Article Snippet: Goat anti-mouse (925-32210 and 926-68070) and anti-rabbit (926-3211 and 926-68071) secondary antibodies were obtained from Li-COR (Lincoln, Nebraska). .. ELISA-based assay kits for the detection of PD-L1 (DY156), VISTA (DY7126) and IL-2 (DY202) as well as carrier-free recombinant human VISTA, PD-1 and PD-L1 were purchased from Bio-Techne (R&D Systems, Abingdon, UK). ..



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    Image Search Results


    Effects of nivolumab–relatlimab combined with ipilimumab or atezolizumab on secretion of cytokines in the supernatant of cocultures of hPBMCs with HFC cells. HFC cells were cocultured with lymphocytes (effector–target ratio 5:1) and treated for 48 hours at 37°C with the combination of nivolumab + relatlimab (light gray bars), ipilimumab or atezolizumab (dark gray bars) used alone, or in combinations (black bars) at the indicated concentration. IL-2 (A) and granzyme B (B) levels (pg/mL) were obtained by using the duoset ELISA kit from R & D Systems performed on cell supernatants. Cells untreated or treated with an unrelated hIgG (with bars) were used as negative controls. Error bars depict means ± SD. P -values for the combinations relative to respective single agents are *** P < 0.001; ** P < 0.01.

    Journal: Journal of Cardiovascular Pharmacology

    Article Title: Evidence of Cardiotoxic Immune Activation by Triple Immune Checkpoint Blockade: A Translational Alert for Clinical Surveillance in Patients With Cancer

    doi: 10.1097/FJC.0000000000001798

    Figure Lengend Snippet: Effects of nivolumab–relatlimab combined with ipilimumab or atezolizumab on secretion of cytokines in the supernatant of cocultures of hPBMCs with HFC cells. HFC cells were cocultured with lymphocytes (effector–target ratio 5:1) and treated for 48 hours at 37°C with the combination of nivolumab + relatlimab (light gray bars), ipilimumab or atezolizumab (dark gray bars) used alone, or in combinations (black bars) at the indicated concentration. IL-2 (A) and granzyme B (B) levels (pg/mL) were obtained by using the duoset ELISA kit from R & D Systems performed on cell supernatants. Cells untreated or treated with an unrelated hIgG (with bars) were used as negative controls. Error bars depict means ± SD. P -values for the combinations relative to respective single agents are *** P < 0.001; ** P < 0.01.

    Article Snippet: Supernatants were collected after 48 hours of coculture and analyzed for IL-2 (DY202) and granzyme B (DY2906) concentrations using DuoSet ELISA kits (R&D Systems, Minneapolis, MN) endowed with a sensitivity of 50 pg/mL.

    Techniques: Concentration Assay, Enzyme-linked Immunosorbent Assay

    Proposed mechanism of immune checkpoint inhibitor (ICI)-driven disruption of immune tolerance and cardiomyocyte injury. Under physiologic conditions, regulatory T cells (Tregs) and inhibitory checkpoint pathways—including cytotoxic T-lymphocyte–associated protein 4 (CTLA-4), lymphocyte activation gene-3 (LAG-3), and programmed cell death-1/programmed cell death-ligand 1 (PD-1/PD-L1)—cooperate to maintain peripheral tolerance and protect cardiac tissue from autoreactive immune responses. ICI therapy blocks these inhibitory signals at multiple levels: (I) anti-CTLA-4 antibodies prevent CTLA-4 engagement on both activated T cells and Tregs, thereby dampening Treg-mediated suppression and enhancing effector T-cell activation; (ii) anti-LAG-3 antibodies abrogate an additional inhibitory checkpoint on activated T cells, further potentiating T-cell cytotoxicity; and (iii) antibodies targeting PD-1 or PD-L1 disrupt the PD-1/PD-L1 axis, which normally delivers inhibitory signals on engagement of PD-1 on activated T cells with PD-L1 expressed on cardiomyocytes. Cumulative blockade of these checkpoints removes critical layers of peripheral tolerance and unleashes effector T cells that recognize cardiac antigens as targets, leading to immune attack against cardiomyocytes. This loss of tolerance contributes to proinflammatory cytokine secretion (eg, IL-2, IL-1β, IL-6, IL-8, CCL2, IL-17), enhanced cytotoxic mediator release such as granzyme B, and activation of the cardiomyocyte NLRP3–MyD88–NF-κB axis, ultimately driving myocardial inflammation and injury. The figure summarizes the central paradigm supported by our coculture experiments, wherein triplet checkpoint blockade (anti-CTLA-4 + anti-PD-1 + anti-LAG-3 or anti-PD-L1) produced the strongest disruption of immune tolerance and the most pronounced cardiotoxic effects.

    Journal: Journal of Cardiovascular Pharmacology

    Article Title: Evidence of Cardiotoxic Immune Activation by Triple Immune Checkpoint Blockade: A Translational Alert for Clinical Surveillance in Patients With Cancer

    doi: 10.1097/FJC.0000000000001798

    Figure Lengend Snippet: Proposed mechanism of immune checkpoint inhibitor (ICI)-driven disruption of immune tolerance and cardiomyocyte injury. Under physiologic conditions, regulatory T cells (Tregs) and inhibitory checkpoint pathways—including cytotoxic T-lymphocyte–associated protein 4 (CTLA-4), lymphocyte activation gene-3 (LAG-3), and programmed cell death-1/programmed cell death-ligand 1 (PD-1/PD-L1)—cooperate to maintain peripheral tolerance and protect cardiac tissue from autoreactive immune responses. ICI therapy blocks these inhibitory signals at multiple levels: (I) anti-CTLA-4 antibodies prevent CTLA-4 engagement on both activated T cells and Tregs, thereby dampening Treg-mediated suppression and enhancing effector T-cell activation; (ii) anti-LAG-3 antibodies abrogate an additional inhibitory checkpoint on activated T cells, further potentiating T-cell cytotoxicity; and (iii) antibodies targeting PD-1 or PD-L1 disrupt the PD-1/PD-L1 axis, which normally delivers inhibitory signals on engagement of PD-1 on activated T cells with PD-L1 expressed on cardiomyocytes. Cumulative blockade of these checkpoints removes critical layers of peripheral tolerance and unleashes effector T cells that recognize cardiac antigens as targets, leading to immune attack against cardiomyocytes. This loss of tolerance contributes to proinflammatory cytokine secretion (eg, IL-2, IL-1β, IL-6, IL-8, CCL2, IL-17), enhanced cytotoxic mediator release such as granzyme B, and activation of the cardiomyocyte NLRP3–MyD88–NF-κB axis, ultimately driving myocardial inflammation and injury. The figure summarizes the central paradigm supported by our coculture experiments, wherein triplet checkpoint blockade (anti-CTLA-4 + anti-PD-1 + anti-LAG-3 or anti-PD-L1) produced the strongest disruption of immune tolerance and the most pronounced cardiotoxic effects.

    Article Snippet: Supernatants were collected after 48 hours of coculture and analyzed for IL-2 (DY202) and granzyme B (DY2906) concentrations using DuoSet ELISA kits (R&D Systems, Minneapolis, MN) endowed with a sensitivity of 50 pg/mL.

    Techniques: Disruption, Activation Assay, Produced

    Withaferin A (WA) Reduces TNF-α-Induced Inflammation and Matrix Metalloproteinase levels in HUVEC and HDFa’s. (A) IL-6 secretion in HUVECs and HDFa’s and treatment with Withaferin A-loaded liposomes (either 1 mg/mL noted as WA-L or 5 mg/mL noted as WA-H), resulted in a concentration-dependent reduction of IL-6 levels. (B) MMP-9 secretion in HDFa’s was significantly elevated by TNF-α stimulation however treatment with Withaferin A-loaded liposomal gel reduced MMP-9 levels. Cells were stimulated with 5 ng/mL TNF-α for 3 h and treated with Withaferin A-loaded liposomal gels (WA-L and WA-H corresponding to a Withaferin A loading to 1 and 5 mg/mL) for 24 h followed by appropriate ELISA analysis. Data are presented as mean ± standard deviation, n = 3 independent experiments. Statistical significance was assessed by One-way ANOVA: **p < 0.01, ***p < 0.001, ****p < 0.0001.

    Journal: British Journal of Biomedical Science

    Article Title: Formulation and In Vitro Characterisation of Withaferin A-Loaded Liposomal Gels for the Topical Management of Chronic Inflammatory Skin Conditions

    doi: 10.3389/bjbs.2025.14847

    Figure Lengend Snippet: Withaferin A (WA) Reduces TNF-α-Induced Inflammation and Matrix Metalloproteinase levels in HUVEC and HDFa’s. (A) IL-6 secretion in HUVECs and HDFa’s and treatment with Withaferin A-loaded liposomes (either 1 mg/mL noted as WA-L or 5 mg/mL noted as WA-H), resulted in a concentration-dependent reduction of IL-6 levels. (B) MMP-9 secretion in HDFa’s was significantly elevated by TNF-α stimulation however treatment with Withaferin A-loaded liposomal gel reduced MMP-9 levels. Cells were stimulated with 5 ng/mL TNF-α for 3 h and treated with Withaferin A-loaded liposomal gels (WA-L and WA-H corresponding to a Withaferin A loading to 1 and 5 mg/mL) for 24 h followed by appropriate ELISA analysis. Data are presented as mean ± standard deviation, n = 3 independent experiments. Statistical significance was assessed by One-way ANOVA: **p < 0.01, ***p < 0.001, ****p < 0.0001.

    Article Snippet: To assess the anti-inflammatory and matrix remodelling regulatory potential of Withaferin A, levels of IL-6 and MMP9 were quantified in cell culture supernatants using the Human DuoSet enzyme-linked immunosorbent assay (ELISA) (R&D Systems, Minneapolis, USA, DY202 and DY911 respectively).

    Techniques: Liposomes, Concentration Assay, Enzyme-linked Immunosorbent Assay, Standard Deviation