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Blood, 15 January 2008, Vol. 111, No. 2, pp. 688-698. Prepublished online as a Blood First Edition Paper on October 10, 2007; DOI 10.1182/blood-2007-04-085787. This Article Full Text Full Text (PDF) Supplemental Figure All Versions of this Article: blood-2007-04-085787v1 111/2/688    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 CrossRef Citing Articles via Google Scholar Google Scholar Articles by Yamanishi, Y. Articles by Kitamura, T. Search for Related Content PubMed PubMed Citation Articles by Yamanishi, Y. Articles by Kitamura, T. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Analysis of mouse LMIR5/CLM-7 as an activating receptor: differential regulation of LMIR5/CLM-7 in mouse versus human cells Yoshinori Yamanishi1, Jiro Kitaura1, Kumi Izawa1, Takayuki Matsuoka1, Toshihiko Oki1, Yang Lu1, Fumi Shibata1, Satoshi Yamazaki2, Hidetoshi Kumagai1, Hideaki Nakajima1, Mari Maeda-Yamamoto3, Victor L. J. Tybulewicz4, Toshiyuki Takai5, and Toshio Kitamura1 1 Division of Cellular Therapy, Advanced Clinical Research Center, Institute of Medical Science, University of Tokyo, Tokyo, Japan; 2 Laboratory of Stem Cell Therapy, Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Tokyo, Japan; 3 National Institute of Vegetable and Tea Science, National Agriculture Research Organization, Shizuoka, Japan; 4 Division of Immune Cell Biology, National Institute for Medical Research, London, United Kingdom; and 5 Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan We have analyzed leukocyte mono-Ig–like receptor 5 (LMIR5) as an activating receptor among paired LMIRs. Mouse LMIR5 (mLMIR5) is expressed in myeloid cells such as mast cells, granulocytes, macrophages, and dendritic cells. Cross-linking of transduced mLMIR5 in bone marrow–derived mast cells (BMMCs) caused activation events, including cytokine production, cell survival, degranulation, and adhesion to the extracellular matrix. mLMIR5 associated with DAP12 and to a lesser extent with DAP10, and mLMIR5-mediated functions of BMMCs were strongly inhibited by DAP12 deficiency. Importantly, cross-linking of endogenous mLMIR5 induced Syk-dependent activation of fetal liver–derived mast cells. Unlike mLMIR5, cross-linking of human LMIR5 (hLMIR5) induced cytokine production of BMMCs even in the absence of both DAP12 and DAP10, suggesting the existence of unidentified adaptors. Interestingly, hLMIR5 possessed a tyrosine residue (Y188) in the cytoplasmic region. Signaling via Y188 phosphorylation played a predominant role in hLMIR5-mediated cytokine production in DAP12-deficient, but not wild-type BMMCs. In addition, experiments using DAP10/DAP12 double-deficient BMMCs suggested the existence of Y188 phoshorylation-dependent and -independent signals from unidentified adaptors. Collectively, although both mouse and human LMIR5 play activatory roles in innate immunity cells, the functions of LMIR5 were differentially regulated in mouse versus human cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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