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. 2023 Sep 20;6(3):642–655. doi: 10.20517/cdr.2023.47

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© The Author(s) 2023.

© The Author(s) 2023. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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Mechanism of action of immune checkpoint inhibitors. The monoclonal antibodies against PD-1/PD-L1 and CTLA-4 abolish the T-cell inhibitory responses that are stimulated by the interaction of PD-1 with PD-L1 and CTLA-4 with its ligand CD 80/86 and thereby enhance antitumor immunity. Ab: Antibody; CD 80/86: cluster of differentiation 80/86; CEACAM: carcinoembryonic antigen-related cell adhesion molecule; CTLA-4: cytotoxic T lymphocyte-associated protein 4; IFN-γ: interferon-γ; LAG3: lymphocyte-activation gene 3; MHC: major histocompatibility complex; PD-1: programmed death-1; PD-L1: programmed death ligand-1; RCC: renal cell carcinoma; TCR: T cell receptor; TIGIT: T cell immunoglobulin and ITIM domain; TIM3: T cell immunoglobulin and mucin domain 3. (Figure credits: Roy AM).