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Natural killer cell-like cytotoxicity refers to the ability of natural killer (NK) cells, a subset of lymphocytes in the innate immune system, to recognize and destroy infected, stressed, or transformed cells without prior sensitization[5][7]. NK cells mediate cytotoxicity primarily through two mechanisms: granule exocytosis (releasing perforin and granzymes to induce apoptosis in target cells) and the engagement of death receptor pathways (such as Fas ligand or TRAIL)[1][2][4]. NK cells also mediate antibody-dependent cellular cytotoxicity (ADCC) via their CD16 (FcγRIII) receptor, recognizing and killing antibody-coated target cells[4][5]. NK cell-mediated cytotoxicity is vital for immune surveillance against tumors and infection, and is subject to regulation by activating and inhibitory receptors that sense the presence or absence of MHC class I molecules and stress-induced ligands on target cells[2][3][7]. Measuring this cytotoxicity underpins the development and monitoring of NK cell-based immunotherapies in cancer, infection, and other diseases[6]. "Natural killer cell-like cytotoxicity" should not be considered a canonical drug target—it is a cellular function, not a molecular entity. If you intend to refer to a specific NK cell receptor or effector molecule (such as "NKp30," "CD16," or "perforin"), providing a more precise target name will allow for structured information retrieval[1][4][6].
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