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Blood, 15 August 2005, Vol. 106, No. 4, pp. 1337-1340. Prepublished online as a Blood First Edition Paper on May 3, 2005; DOI 10.1182/blood-2005-01-0357. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-01-0357v1 106/4/1337    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 McNerney, M. E. Articles by Kumar, V. Search for Related Content PubMed PubMed Citation Articles by McNerney, M. E. Articles by Kumar, V. Related Collections Immunobiology Transplantation Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Brief report 2B4 (CD244)-CD48 interactions provide a novel MHC class I-independent system for NK-cell self-tolerance in mice Megan E. McNerney, Dustin Guzior, and Vinay Kumar From the Committee on Immunology, Department of Pathology, University of Chicago, Chicago, IL. Natural killer (NK) cells must be able to eliminate infected and transformed cells while remaining tolerant of normal cells. NK-cell self-tolerance is thought to be maintained by self-major histocompatibility complex (MHC) class I recognition; however, there are examples where NK cells are not regulated by MHC class I and yet remain self-tolerant. Here, we show that 2B4 (CD244) and CD48 represent a second system for murine NK-cell self-recognition. 2B4 and MHC class I receptors act nonredundantly to inhibit NK lysis of syngeneic tumor cells. NK cells from 2 microglobulin (2m)-deficient mice and NK cells that lack expression of self-MHC-binding inhibitory receptors are inhibited by 2B4. Moreover, we provide the first in vivo evidence for MHC-independent NK self-recognition in a bone marrow rejection assay. These data suggest that NK-cell self-tolerance can be mediated by molecules other than MHC. (Blood. 2005;106:1337-1340) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. A. Wahle, K. H. T. Paraiso, R. D. Kendig, H. R. Lawrence, L. Chen, J. Wu, and W. G. Kerr Inappropriate Recruitment and Activity by the Src Homology Region 2 Domain-Containing Phosphatase 1 (SHP1) Is Responsible for Receptor Dominance in the SHIP-Deficient NK Cell J. Immunol., December 15, 2007; 179(12): 8009 - 8015. [Abstract] [Full Text] [PDF] R. T. Taniguchi, D. Guzior, and V. Kumar 2B4 inhibits NK-cell fratricide Blood, September 15, 2007; 110(6): 2020 - 2023. [Abstract] [Full Text] [PDF] S. Cooley, F. Xiao, M. Pitt, M. Gleason, V. McCullar, T. L. Bergemann, K. L. McQueen, L. A. Guethlein, P. Parham, and J. S. Miller A subpopulation of human peripheral blood NK cells that lacks inhibitory receptors for self-MHC is developmentally immature Blood, July 15, 2007; 110(2): 578 - 586. [Abstract] [Full Text] [PDF] S. Nedvetzki, S. Sowinski, R. A. Eagle, J. Harris, F. Vely, D. Pende, J. Trowsdale, E. Vivier, S. Gordon, and D. M. Davis Reciprocal regulation of human natural killer cells and macrophages associated with distinct immune synapses Blood, May 1, 2007; 109(9): 3776 - 3785. [Abstract] [Full Text] [PDF] J. A. Wahle, K. H. T. Paraiso, A. L. Costello, E. L. Goll, C. L. Sentman, and W. G. Kerr Cutting Edge: Dominance by an MHC-Independent Inhibitory Receptor Compromises NK Killing of Complex Targets. J. Immunol., June 15, 2006; 176(12): 7165 - 7169. [Abstract] [Full Text] [PDF] R. Bhat, P. Eissmann, J. Endt, S. Hoffmann, and C. Watzl Fine-tuning of immune responses by SLAM-related receptors J. Leukoc. Biol., March 1, 2006; 79(3): 417 - 424. [Abstract] [Full Text] [PDF]

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