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CD8+ cytotoxic T lymphocytes (CTLs) specifically recognize and destroy virus-infected or tumor cells presenting antigenic peptides via MHC class I molecules on their surface[1][7][9]. This recognition is mediated by the T cell receptor (TCR) on CD8+ T cells binding to the peptide-MHC I complex and is stabilized by the CD8 co-receptor[1][3][8]. Upon activation, CTLs induce target cell lysis through the release of cytotoxic granules containing perforin and granzymes, as well as through death receptor engagement[5][7]. This process underpins the immune system’s defense against intracellular pathogens and tumor cells, and is central to the efficacy of immunotherapies targeting cancer and infection[5][9]. The phrase itself, however, refers broadly to this cellular mechanism and not a single druggable target.
Immune checkpoint inhibitors (e.g., anti-PD-1/PD-L1, anti-CTLA-4) can enhance CD8+ T cell function by removing inhibitory signals. Cancer vaccines increase presentation of tumor antigens on MHC I to drive CD8+ T cell responses. Adoptive T cell therapies provide ex vivo expanded or engineered T cells with enhanced cytolytic capabilities.
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