il 2 dy202 (R&D Systems)
Structured Review

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
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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
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
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
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