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CD3+CD56+ cytokine-induced killer (CIK) cells are a unique immune effector population derived from T cells cultured ex vivo with cytokines. They display both T cell (CD3+) and natural killer cell (CD56+) features, combining the major histocompatibility complex (MHC)-restricted cytotoxicity of conventional T cells with MHC-unrestricted tumor cell killing seen in NK cells. Their cytolytic activity against tumor and virus-infected cells is primarily mediated through a direct cytolysis pathway that involves exocytosis of perforin and granzymes, leading to apoptosis of target cells[3][4][6][8]. CIK cell therapy has shown clinical promise in the treatment of cancers and infections, due to their dual targeting mechanisms and favorable safety profile. However, "direct cytolysis via perforin/granzyme pathway by CD3+CD56+ CIK effectors" refers to a function of this immune population, not a discrete druggable molecular target[6][3][5].
Perforin/granzyme-dependent lysis of target cells. MHC-restricted and MHC-unrestricted cytotoxicity. Cytokine secretion (e.g., interferon-γ, tumor necrosis factor-α).
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