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Cytotoxic T lymphocyte-mediated tumor killing refers to the process by which **CD8+ cytotoxic T lymphocytes** (CTLs) recognize and destroy cancerous cells. This is a key mechanism in the immune system’s defense against tumors. The process involves direct recognition of tumor antigens presented on major histocompatibility complex class I molecules by the target cell. Upon recognition, CTLs induce apoptosis in target cells through two main mechanisms: 1. **Granule exocytosis pathway:** Release of perforin forms pores in the target cell membrane, allowing granzymes to enter and trigger apoptosis. 2. **Death receptor pathway:** Engagement of Fas ligand on the CTL with Fas on the target cell induces caspase-dependent apoptosis. CTLs can also mediate indirect killing via cytokine secretion that affects neighboring tumor cells[1][2][4]. This biological function is central to many cancer immunotherapies that aim to enhance or restore effective cytotoxic responses against tumors—such as immune checkpoint blockade therapies targeting PD‑1/PD-L1 or CTLA‑4 pathways[3]. However, "cytotoxic T lymphocyte-mediated tumor killing" is not a specific molecular entity but rather describes an immune effector mechanism involving multiple molecules and cellular interactions; therefore it should not be considered a canonical therapeutic "target" like a receptor or enzyme. **Note:** There is something incorrect about this entry as it does not refer to a single molecule/receptor but rather an entire biological process involving several components including CD8+ T-cell receptors, co-receptors like CD8, signaling proteins such as perforin/granzymes/Fas ligand, etc.[2]
Enhancement of CTL activation and function by blocking inhibitory pathways such as PD‑1/PD‑L1 or CTLA‑4[3]
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