This article is part of the Research Topic Biology of NK cells and NK cell receptors

Review ARTICLE

Front. Immunol., 06 March 2013 | doi: 10.3389/fimmu.2013.00047

Role of inositol phospholipid signaling in natural killer cell biology

  • 1Department of Microbiology and Immunology, State University of New York Upstate Medical University, Syracuse, NY, USA
  • 2Department of Pediatrics, State University of New York Upstate Medical University, Syracuse, NY, USA
  • 3Department of Chemistry, Syracuse University, Syracuse, NY, USA

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.

Keywords: inositol phospholipid, PIP5K, SHIP, PTEN, PI3K, IFNγ, natural killer cells, INPP4

Citation: Gumbleton M and Kerr WG (2013) Role of inositol phospholipid signaling in natural killer cell biology. Front. Immunol. 4:47. doi: 10.3389/fimmu.2013.00047

Received: 30 November 2012; Accepted: 08 February 2013;
Published online: 06 March 2013.

Edited by:

Eric Vivier, Centre d'Immunologie de Marseille-Luminy, France

Reviewed by:

Akira Shibuya, University of Tsukuba, Japan
Jacques Zimmer, Centre de Recherche Public de la Santé, Luxembourg

Copyright: © 2013 Gumbleton and Kerr. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.

*Correspondence: William G. Kerr, Department of Microbiology and Immunology, State University of New York Upstate Medical University, 2204 Weiskotten Hall, 750 East Adams Street, Syracuse, NY 13210, USA. e-mail: kerrw@upstate.edu

Back to top