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The term "immune effector cell-mediated cytotoxicity pathways" encompasses multiple biological processes by which immune cells such as NK cells, cytotoxic T lymphocytes, macrophages, neutrophils, and eosinophils destroy target cells through a variety of mechanisms. Key pathways include direct cytotoxic granule exocytosis (e.g., perforin/granzyme release), engagement of death receptors (e.g., FasL/Fas, TRAIL), and antibody-dependent cell-mediated cytotoxicity (ADCC), where antibodies direct effector cells to targets via Fc receptors[1][2][4][5][6]. These mechanisms are central to the immune system’s ability to eliminate malignant, infected, or otherwise dysfunctional cells. The molecular effectors include perforin, granzymes, Fas ligand, TRAIL, and various cytokines. Crucial receptors involved are FcγRIIIa (CD16), NKG2D, and the killer cell immunoglobulin-like receptor (KIR) family[1][2][5][6]. The pathways are modulated by a balance of activating and inhibitory signals, integrating input from the immune context, and can be exploited in immunotherapies but may also lead to immune-mediated toxicity.
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