Ligands for Natural Killer cell receptors on tumor cells

Ligands for NK cell receptors on tumor cells constitute a diverse set of cell surface molecules that interact with both *activating* and *inhibitory* receptors on NK cells, determining whether a tumor cell will be targeted for destruction or allowed to persist. Key activating ligands include the *NKG2D ligand family* (MICA, MICB, ULBPs), which are frequently upregulated in response to cellular stress, transformation, or DNA damage, while inhibitory ligands often consist of MHC class I family members and related molecules such as HLA-E and CD155 that interact with receptors like KIRs, NKG2A, TIGIT, and others. Tumors often manipulate the expression or shedding of these ligands to evade immune surveillance. Therapeutic strategies target these ligand-receptor interactions to boost NK cell-mediated anti-tumor immunity. Because the entry refers to a large family of molecules rather than a specific ligand, further refinement is necessary for structured database use[1][2][3][4].

Other names

NK cell activating ligandsNK cell inhibitory ligandsNKG2D ligands (e.g. MICA, MICB, ULBP)Tumor-associated NK cell ligandsStress-induced ligands (context-dependent)

Blockade of inhibitory receptors to relieve NK suppression (e.g. KIR, NKG2A inhibitors) Upregulation of activating ligands on tumor cells to promote NK cell killing Antibody-dependent cellular cytotoxicity (ADCC) via Fc receptor binding Enhanced immune synapse formation resulting in targeted cell lysis via granzyme and perforin release