Natural killer cell cytotoxicity via stress-induced ligand recognition on tumor cells

Natural killer (NK) cell cytotoxicity via stress-induced ligand recognition on tumor cells is a process wherein NK cells detect and kill abnormal cells, such as tumor or virus-infected cells, by recognizing ligands (such as MICA, MICB, and ULBPs) upregulated in response to cellular stress or transformation. These ligands are recognized by activating receptors on NK cells (e.g., NKG2D, NKp30, NKp44, NKp46), leading to NK cell activation, degranulation, and target cell lysis through perforin and granzymes, or through death receptor ligands (such as Fas ligand and TRAIL)[1][2][3][4][5]. This innate immune process is critical for tumor surveillance and the effectiveness of various antibody-based therapies, but is subject to tumor escape mechanisms such as downregulation of ligands, secretion of soluble decoys, and local immune suppression[3][4][5]. Important caveat: This entry should not be treated as a specific molecular entity but as an immunological phenomenon involving multiple receptors (such as NKG2D and other natural cytotoxicity receptors) and their corresponding ligands[4][5]. For structured databases, it is recommended to instead catalog individual receptors (e.g., “NKG2D receptor”, “Natural cytotoxicity receptor 1 [NKp46]”) or cytolytic effector molecules (e.g., “Perforin”, “Granzyme B”).

Other names

NK cell cytotoxicityStress-induced ligand recognition by NK cellsNK cell tumor surveillanceNK cell-mediated cytolysis

Immune-mediated direct tumor cell lysis; Antibody-dependent cellular cytotoxicity (ADCC) via CD16 (FcγRIIIa) on NK cells; Activation or inhibition via NK cell receptors (e.g., activating receptors NKG2D, NKp30, NKp44, NKp46; inhibitory receptors KIR, NKG2A)