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Cytotoxic T cell-mediated cell death is a fundamental immune process where CD8+ cytotoxic T lymphocytes (CTLs) identify and eliminate virally infected, stressed, or malignant cells. This process is initiated when the T-cell receptor (TCR) recognizes specific antigenic peptides presented by Major Histocompatibility Complex (MHC) class I molecules on the surface of target cells (StatPearls, 2023). Upon activation, CTLs employ two primary pathways to induce apoptosis: the granule exocytosis pathway, involving the release of perforin and granzymes, and the death receptor pathway, primarily through Fas/FasL interactions (Nature Reviews Immunology, 2018). While not a single molecular target itself, this mechanism is the primary effector arm for many modern immunotherapies, including immune checkpoint inhibitors, CAR-T cell therapies, and bispecific T-cell engagers (BiTEs). Enhancing this process is a cornerstone of oncology, though overactivation can lead to severe safety concerns such as cytokine release syndrome or systemic autoimmunity (NIH, 2022).
Induction of target cell apoptosis through the release of perforin and granzymes or via the Fas/FasL signaling pathway following TCR recognition of MHC-I/peptide complexes.
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