Mouse TREM2 Alexa Fluor™ Plus 647‑conjugated Antibody

TREM2 (Triggering Receptor Expressed by Myeloid cells) is an Ig superfamily cell surface receptor that activates a number of myeloid cell types (1). It is a member of a small gene family located on human chromosome 6p21 and mouse chromosome 17 in a region linked to the MHC (2). A single human TREM2 gene has been described, however, two closely related orthologs were reported in mouse (3). The proteins differ by only three amino acids and were designated TREM2a and TREM2b. TREM2 is type I transmembrane protein consisting of a single extracellular immunoglobulin (V-like) domain, a transmembrane domain with a positively charged lysine residue, and a short cytoplasmic tail (1). It associates with the signal adapter protein, DAP12, for signaling and function. DAP12 has a cytoplasmic ITAM that is phosphorylated upon ligand binding leading to the subsequent activation of cytoplasmic tyrosine kinases. TREM2 is expressed by immature monocyte-derived dendritic cells (DC), and expression is down-regulated upon activation of DC by microbial products and costimulatory signals (4). Ligation of TREM2 on immature DC with anti-TREM2 antibodies results in partial DC activation and the up-regulation of CCR7 and some co-stimulatory molecules. A role for TREM2 in the functioning of osteoclasts and microglia is suggested by the discovery that homozygous loss-of-function mutations in either TREM2 or DAP12 result in Nasu-Hakola disease characterized by a combination of presenile demetia and bone cysts (5). In vitro studies indicate that the differentiation of myeloid precursors into osteoclasts is dramatically impaired in TREM2 deficient individuals (6).