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Blood, 15 September 2007, Vol. 110, No. 6, pp. 2020-2023. Prepublished online as a Blood First Edition Paper on May 30, 2007; DOI 10.1182/blood-2007-02-076927. This Article Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2007-02-076927v1 110/6/2020    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 Taniguchi, R. T Articles by Kumar, V. Search for Related Content PubMed PubMed Citation Articles by Taniguchi, R. T Articles by Kumar, V. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted February 27, 2007 Accepted May 28, 2007 2B4 inhibits NK cell fratricide Ruth T Taniguchi*, Dustin Guzior, and Vinay Kumar Department of Pathology, Committee on Immunology, University of Chicago, Chicago, IL, United States * Corresponding author; email: rutht{at}uchicago.edu. 2B4 (CD244) and its ligand, CD48, are expressed on all NK cells. In studies using 2B4 deficient, CD48 deficient, or wild type NK cells with blocking antibodies, we found that in the absence of 2B4-CD48 interactions, activated murine NK cells kill each other. We also show that NK-NK fratricide in the absence of 2B4-CD48 interaction is dependent on perforin both in vitro and in vivo. 2B4 has been reported to have activating, costimulatory, and inhibitory functions on murine NK cells. 2B4-mediated inhibition of NK cell fratricide explains some of the paradoxes of 2B4 function reported in studies of murine NK cells. We show that in the absence of 2B4 signaling, activated NK cells have defective cytotoxicity and proliferation because of fratricide, and not due the absence of a 2B4-dependent activation signal. 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]

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