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Cytotoxic T cells (CD8⁺ T cells, CTLs) are lymphocytes specialized in recognizing and killing cancerous or infected cells by detecting specific antigens presented on MHC class I molecules[3][5]. Tumor-associated antigens are derived from proteins unique to or overexpressed by cancer cells, allowing CTLs to target and destroy tumor cells through release of perforin/granzymes or activation of cell death pathways[1][3]. Therapies aim to enhance this response by either modifying T cells (CAR-T cells), blocking inhibitory pathways (immune checkpoint inhibitors targeting PD-1/PD-L1 or CTLA-4), or boosting T-cell proliferation and function[2][5]. While an essential mechanism in antitumor immunity and the basis for major immunotherapies, harnessing CTLs may result in significant toxicity, including immune-related adverse events and cytokine release syndrome[1][2][5]. This entry reflects that the original phrase is an immunological process, not a molecular target—thus, it is not a canonical target suitable for drug targeting databases. It is too broad, referencing a cellular response rather than a defined molecule, and cannot be mapped to a single protein, receptor, or gene.
Blockade of inhibitory receptors (PD-1, CTLA-4) to enhance T-cell activation and cytotoxicity[2][5] Genetic modification (CAR T cells) to target tumor antigens and activate killing[1] Stimulation of T-cell proliferation and survival (cytokines)[4]
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