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Natural killer (NK) cell receptor–tumor ligand interactions represent a complex system of activating and inhibitory signals that determine the immune system's ability to identify and destroy malignant cells. NK cells utilize a variety of germline-encoded receptors, such as NKG2D, Natural Cytotoxicity Receptors (NCRs), and Killer-cell Immunoglobulin-like Receptors (KIRs), to sense ligands that are often upregulated or downregulated on the surface of stressed or transformed tumor cells. In the context of cancer, tumors frequently exploit these pathways by overexpressing inhibitory ligands or shedding activating ligands to evade immune detection. Therapeutic strategies currently under investigation aim to block inhibitory interactions (e.g., Monalizumab targeting NKG2A) or enhance activating signals to restore NK cell-mediated surveillance. Because this entry refers to a broad category of interactions rather than a single molecular entity, it is classified as an incorrect target specification for structured drug-target mapping.
Modulation of NK cell activation or inhibition through the targeting of specific receptor-ligand pairs to enhance anti-tumor immunity.
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