TREM and TREM-like receptors in inflammation and disease

Since the discovery of triggering receptor expressed on myeloid cells (TREM)-1 in 2000, evidence documenting the profound ability of the TREM and TREM-like receptors to regulate inflammation has rapidly accumulated. Monocytes, macrophages, myeloid dendritic cells, plasmacytoid dendritic cells, neutr...

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Bibliographic Details
Published in:Current opinion in immunology 2009-02, Vol.21 (1), p.38-46
Main Authors: Ford, Jill W, McVicar, Daniel W
Format: Article
Language:English
Subjects:
Allergy and Immunology
Animals
Antigens, CD - immunology
Autoimmune Diseases - immunology
B7 Antigens
Bacterial Infections - immunology
Cell Adhesion
Dendritic Cells - immunology
Dendritic Cells - metabolism
Feedback, Physiological
Gene Expression Regulation
Humans
Inflammation
Membrane Glycoproteins - immunology
Membrane Glycoproteins - metabolism
Osteogenesis
Receptor Cross-Talk
Receptors, Immunologic - immunology
Receptors, Immunologic - metabolism
Signal Transduction
Triggering Receptor Expressed on Myeloid Cells-1
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Summary:Since the discovery of triggering receptor expressed on myeloid cells (TREM)-1 in 2000, evidence documenting the profound ability of the TREM and TREM-like receptors to regulate inflammation has rapidly accumulated. Monocytes, macrophages, myeloid dendritic cells, plasmacytoid dendritic cells, neutrophils, microglia, osteoclasts, and platelets all express at least one member of the TREM family, underscoring the importance of these proteins in the regulation of innate resistance. Recent work on the TREM family includes: characterization of a new receptor expressed on plasmacytoid dendritic cells; definition of a key role for TREM in inflammatory bowel disease and multiple sclerosis; an expanded list of diseases associated with the release of soluble forms of TREM proteins; and identification of the first well characterized TREM ligand: B7-H3, a ligand for TREM-like Transcript (TLT)-2. Moreover, analysis of TREM signaling has now identified key regulatory components and defined pathways that may be responsible for the complex functional interactions between the TREM and toll-like receptors. In addition, there is expanding evidence of a role for TREM in the regulation of integrin function via Plexin-A1. Together these new findings define the TREM and TREM-like receptors as pluripotent modifiers of disease through the integration of inflammatory signals with those associated with leukocyte adhesion.
ISSN:0952-7915
1879-0372
DOI:10.1016/j.coi.2009.01.009