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Tumor-associated antigens recognized by cytokine-induced killer cells are a heterogeneous group of surface proteins and stress-induced ligands, such as those for NKG2D (e.g., MICA/B, ULBP family) and Fas/CD95, that are overexpressed or selectively presented on tumor or virus-infected cells. These antigens allow CIK cells to recognize and kill target cells via both MHC-restricted and, more notably, MHC-unrestricted mechanisms, enabling broad-spectrum antitumor cytotoxicity that is not dependent on classical antigen presentation. The recognition mechanisms involve a combination of T cell and natural killer cell pathways, mediated predominantly by activating NK cell receptors.
Recognition by immune effector receptors (primarily NKG2D, DNAM-1, NKp30); Induction of perforin- and granzyme-mediated cytotoxicity; Fas/FasL pathway-mediated apoptosis; Antibody-dependent cell-mediated cytotoxicity (when combined with antibodies, e.g., via CD16)
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