Cutting Edge: Inflammatory Responses Can Be Triggered by TREM-1, a Novel Receptor Expressed on Neutrophils and Monocytes1

By A. Bouchon, J. Dietrich, M. Colonna. Journal of Immunology, 2000

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Neutrophils, from marrow to microbes. (2010, background): “…cells (TREM-1) (by ligands not yet identified; Ford and McVicar, 2009), which is upregulated (Bouchon et al., 2000, 2001) and signals through DAP12 (presented earlier) (Bouchon et al., 2000; Tessarz and Cerwenka, 2008), may lead to degranulation and transcriptional activity (Bouchon et al., 2000).”
Association of signal‐regulatory proteins β with KARAP/DAP‐12 (2000, background): “Similarly, the expression of KIR activating isoforms in RBL–2H3 and Ba/F3 mouse pre-B cells as well as of TREM-1 receptor in COS cells does not require association with KARAP/ DAP-12 [8, 10, 18].”
Neutrophil cell surface receptors and their intracellular signal transduction pathways (2013, background): “Those include DAP12and FcRγ-associated receptors such as TREM-1 [226,227] and OSCAR [228]; the Neisseria recognition receptor CEACAM3 [229,230]; as well as scavenger receptors, complement receptors and various intracellular lipid-sensing receptors.”
Mutations in two genes encoding different subunits of a receptor signaling complex result in an identical disease phenotype. (2002, background): “2001a), whereas TREM2 is expressed on macrophages and monocyte-derived dendritic cells, suggesting that TREM2 plays a role in chronic, rather than in acute, inflammation (Bouchon et al. 2000).”