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Cutting edge: TREM-2 attenuates macrophage activation.

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-gamma. 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.

Pubmed ID: 16951310


  • Turnbull IR
  • Gilfillan S
  • Cella M
  • Aoshi T
  • Miller M
  • Piccio L
  • Hernandez M
  • Colonna M


Journal of immunology (Baltimore, Md. : 1950)

Publication Data

September 15, 2006

Associated Grants

  • Agency: NIAID NIH HHS, Id: T32AI007163

Mesh Terms

  • Adaptor Proteins, Signal Transducing
  • Animals
  • Cell Differentiation
  • Cell Movement
  • Humans
  • Inflammation Mediators
  • Jurkat Cells
  • Lung
  • Macrophage Activation
  • Macrophages, Peritoneal
  • Membrane Glycoproteins
  • Membrane Proteins
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Rats
  • Rats, Wistar
  • Receptors, Immunologic