Abstract
Natural killer (NK) cells are important for host defense against malignancy and infection. At a cellular level NK cells are activated when signals from activating receptors exceed signaling from inhibitory receptors. At a molecular level NK cells undergo an education process to both prevent autoimmunity and acquire lytic capacity. Mouse models have shown important roles for inositol phospholipid signaling in lymphocytes. NK cells from mice with deletion in different members of the inositol phospholipid signaling pathway exhibit defects in development, NK cell repertoire expression and effector function. Here we review the current state of knowledge concerning the function of inositol phospholipid signaling components in NK cell biology.
Highlights
Unlike T and B lymphocytes, natural killer (NK) cells do not rearrange antigen receptor genes in order to detect their cellular targets (Lanier, 1998)
PIP2 and PIP3 can be modified by various phosphatases including inositol polyphosphate 4-phosphatase (INPP4) and SH2 domain-containing inositol5-phosphatase (SHIP) or modified by phosphatase and tensin homologue deleted on chromosome 10 (PTEN) to create PI(3)P, PI(3,4)P2, or PI(4,5)P2, respectively
4-phosphate 5-kinase; PI3K, phosphoinositide 3-kinase; SHIP, SH2 domain-containing inositol-5-phosphatase; PTEN, phosphatase and tensin homologue deleted on chromosome 10; INPP4, inositol polyphosphate 4-phosphatase; PH, pleckstrin homology; ENTH, epsin N-terminal homology; ANTH, AP180 N-terminal homology
Summary
Reviewed by: Akira Shibuya, University of Tsukuba, Japan Jacques Zimmer, Centre de Recherche Public de la Santé, Luxembourg. NK cells utilize an array of activating and inhibitory receptors with the latter largely detecting major histocompatibility complex (MHC) class I ligands, or in the case of 2B4, the signaling lymphocyte activation molecule (SLAM) family ligand CD48. PIP2 and PIP3 can be modified by various phosphatases including inositol polyphosphate 4-phosphatase (INPP4) and SH2 domain-containing inositol5-phosphatase (SHIP) or modified by phosphatase and tensin homologue deleted on chromosome 10 (PTEN) to create PI(3)P, PI(3,4)P2, or PI(4,5)P2, respectively These activities can attenuate signaling pathways or, in the case of the SHIP product PI(3,4)P2, activate them by enabling recruitment of proteins with various PH domain-containing proteins to sites of signaling at the plasma membrane (Kerr, 2011).
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