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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.
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Submitted April 16, 2007
Accepted September 18, 2007
Analysis of mouse LMIR5/CLM-7 as an activating receptor: differential regulation of LMIR5/CLM-7 in mouse versus human cells
Yoshinori Yamanishi, Jiro Kitaura, Kumi Izawa, Takayuki Matsuoka, Toshihiko Oki, Yang Lu, Fumi Shibata, Satoshi Yamazaki, Hidetoshi Kumagai, Hideaki Nakajima, Mari Maeda-Yamamoto, Victor L.J. Tybulewicz, Toshiyuki Takai, and Toshio Kitamura*
The Division of Cellular Therapy, Advanced Clinical Research, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan
Laboratory of Stem Cell Therapy, Center for Experimental Medicine, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan
National Institute of Vegetable and Tea Science, National Agriculture Research Organization, Shizuoka, Japan
Devision of Immune Cell Biology, National Institute for Medical Research, London, United Kingdom
Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan
* Corresponding author; email: kitamura{at}ims.u-tokyo.ac.jp.
We have analyzed leukocyte mono-immunoglobulin (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. Crosslinking of transduced-mLMIR5 in bone marrow-derived mast cell (BMMC) 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 BMMC were strongly inhibited by DAP12 deficiency. Importantly, crosllinking of endogenous mLMIR5 induced Syk-dependent activation of fetal liver-derived mast cells. Unlike mLMIR5, crosslinking of human LMIR5 (hLMIR5) induced cytokine production of BMMC 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 BMMC. In addition, experiments using DAP10/DAP12 double-deficient BMMC 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.
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