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CUTTING EDGE |
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110
The triggering receptor expressed on myeloid cells 2 (TREM-2) delivers intracellular signals through the adaptor DAP12 to regulate myeloid cell function both within and outside the immune system. The role of TREM-2 in immunity has been obscured by the failure to detect expression of the TREM-2 protein in vivo. In this study, we show that TREM-2 is expressed on macrophages infiltrating the tissues from the circulation and that alternative activation with IL-4 can induce TREM-2. TREM-2 expression is abrogated by macrophage maturation with LPS of IFN-
. Using TREM-2–/– mice, we find that TREM-2 functions to inhibit cytokine production by macrophages in response to the TLR ligands LPS, zymosan, and CpG. Furthermore, we find that TREM-2 completely accounts for the increased cytokine production previously reported by DAP12–/– macrophages. Taken together, these data show that TREM-2 is expressed on newly differentiated and alternatively activated macrophages and functions to restrain macrophage activation.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 I.R.T. was supported by National Institutes of Health Institutional Training Grant T32AI007163.
2 Address correspondence and reprint requests to Dr. Marco Colonna, Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110. E-mail address: mcolonna{at}pathology.wustl.edu
3 Abbreviations used in this paper: TREM-2, triggering receptor expressed on myeloid cells-2; BMDM, bone marrow-derived macrophage; MCSF, macrophage CSF; WT, wild type.
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