Regulatory function of cell surface molecules CD2-, LFA- and β2-microglobulin in natural killer cell activity

Differential Adhesion Molecule Expression on Porcine Mononuclear Cell Populations

“…Porcine NK cells contrast with blood lymphocytes in having relatively high b 1 and b 2 integrin expression. Such a phenotype has been noted with other species [32,35], relating to the importance of integrin expression in adhesion/migration [5,[26][27][28] and target-effector cell interactions [35,36]. Both b 1 and b 2 integrins are also required for NK cell infiltration into tumours [37] and tissues [38].…”

Human leukocyte antigen-G, a ligand for the natural killer receptor KIR2DL4, is expressed by eutopic endometrium only in the menstrual phase

“…Within the past decade NK receptors that can recognize self-antigens and regulate cytotoxicity, such as KIR (10)(11)(12), immunoglobulin-like transcript (ILT) (20), and lectin-like receptor CD94/NKG2 (21), have been identified apart from conventional receptors such as CD2, lymphocyte function-associated antigen-1, and CD16 (22)(23)(24). Increased inhibitory KIR2DL1 þ NK cells in PB and PF…”

Genomic alterations underlying immune privilege in malignant lymphomas

“…A recent study investigating the genetic mechanisms underlying transformation of FL has further demonstrated that B2M mutations are enriched in the transformed lymphomas with mutation patterns similar to the one observed in de-novo DLBCL, providing evidence for the existence of immune selection pressure during evolution to a high-grade malignancy [16 & ]. Interestingly, mutations of CD58, a member of the immunoglobulin superfamily and ligand for the CD2 receptor on natural killer (NK) cells [75,76], have been found to co-occur frequently with B2M aberrations in de-novo DLBCL as well as in transformed FL (tFL), suggesting that B2M and CD58 mutations represent complementary mechanisms to establish immune privilege [16 & ,26]. Specifically, the co-occurrence was attributed to the potentially synergistic effects of reduced recognition by cytotoxic T cells and inactivating NK cells, since it has been described in earlier studies that escape from CTLs triggers NK cell recognition as part of a compensation mechanism [26,77].…”