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Blood, 15 March 2006, Vol. 107, No. 6, pp. 2364-2372. Prepublished online as a Blood First Edition Paper on November 15, 2005; DOI 10.1182/blood-2005-08-3504. This Article Full Text (PDF) Supplemental Figures All Versions of this Article: 2005-08-3504v1 107/6/2364    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Chiesa, S. Articles by Tomasello, E. Search for Related Content PubMed PubMed Citation Articles by Chiesa, S. Articles by Tomasello, E. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted August 30, 2005 Accepted October 24, 2005 Multiplicity and plasticity of Natural Killer cell signaling pathways Sabrina Chiesa, Michael Mingueneau, Nicolas Fuseri, Bernard Malissen, David H Raulet, Marie Malissen, Eric Vivier*, and Elena Tomasello Centre d'Immunologie de Marseille-Luminy, INSERM - CNRS - Universite de la Mediterranee, Marseille, France Department of Molecular and Cell Biology, University of California, Berkeley, CA, USA * Corresponding author; email: vivier{at}ciml.univ-mrs.fr. Natural Killer (NK) cells express an array of activating receptors that associate with DAP12 (KARAP), CD3 and/or FcR ITAM (Immunoreceptor Tyrosine-based Activation Motif)-bearing signaling subunits. In T and mast cells, ITAM-dependent signals are integrated by critical scaffolding elements such as LAT (linker for activation of T cells) and NTAL (non-T cell activation linker). Using mice that are deficient for ITAM-bearing molecules, LAT or NTAL, we show that NK cell cytotoxicity and interferon- secretion are initiated by ITAM-dependent and -independent as well as LAT/NTAL-dependent and -independent pathways. The role of these various signaling circuits depends on the target cell as well as on the activation status of the NK cell. The multiplicity and the plasticity of the pathways that initiate NK cell effector functions contrast with the situation in T cells and B cells and provide an explanation for the resiliency of NK cell effector functions to various pharmacological inhibitors and genetic mutations in signaling molecules. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: H. Hara, C. Ishihara, A. Takeuchi, L. Xue, S. W. Morris, J. M. Penninger, H. Yoshida, and T. 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[Abstract] [Full Text] [PDF] I. C. Macaulay, M. R. Tijssen, D. C. Thijssen-Timmer, A. Gusnanto, M. Steward, P. Burns, C. F. Langford, P. D. Ellis, F. Dudbridge, J.-J. Zwaginga, et al. Comparative gene expression profiling of in vitro differentiated megakaryocytes and erythroblasts identifies novel activatory and inhibitory platelet membrane proteins Blood, April 15, 2007; 109(8): 3260 - 3269. [Abstract] [Full Text] [PDF] X. Chen, P. P. Trivedi, B. Ge, K. Krzewski, and J. L. Strominger Many NK cell receptors activate ERK2 and JNK1 to trigger microtubule organizing center and granule polarization and cytotoxicity PNAS, April 10, 2007; 104(15): 6329 - 6334. [Abstract] [Full Text] [PDF] M. Rabot, H. El Costa, B. Polgar, A. Marie-Cardine, M. Aguerre-Girr, A. Barakonyi, S. Valitutti, A. Bensussan, and P. Le Bouteiller CD160-activating NK cell effector functions depend on the phosphatidylinositol 3-kinase recruitment Int. Immunol., April 1, 2007; 19(4): 401 - 409. 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