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Tumor cell antigen-specific T lymphocyte-mediated cytotoxicity refers to the immune process by which cytotoxic T lymphocytes (CTLs; typically CD8+ T cells) recognize and kill tumor cells that display tumor-specific or tumor-associated peptide antigens on their surface via major histocompatibility complex class I (MHC-I)[1][2][3]. This process is central to anti-tumor immunity and is a foundational mechanism of action for many immunotherapies such as checkpoint inhibitors and CAR-T cells. Effector CTLs, upon recognizing their cognate antigen on tumor cells, induce apoptosis by release of cytotoxic granules containing perforin and granzymes. In some conditions, CD4+ T cells may also mediate cytotoxic effects, particularly if relieved from suppression by regulatory T cells[4]. This entity is not a discrete molecule but a complex biological process essential to cancer immunosurveillance and immunotherapy efficacy.
T cell receptor (TCR)-mediated recognition of tumor peptides presented on MHC class I molecules triggers release of perforin, granzymes, and granulysin to induce apoptosis in target tumor cells by cytotoxic T lymphocytes[1][2][3]. Under some conditions, tumor-specific CD4+ T cells may also develop cytotoxic effector functions, especially when regulatory T cells (Tregs) are depleted[4].
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