Recent research has shown that the triggering receptor expressed on myeloid cells 2 (TREM2) in microglia is closely related to the pathogenesis of Alzheimer’s disease (AD). The mechanism of this relationship, however, remains unclear. TREM2 is part of the TREM family of receptors, which are expressed primarily in myeloid cells, including monocytes, dendritic cells, and microglia. The TREM family members are cell surface glycoproteins with an immunoglobulin-like extracellular domain, a transmembrane region and a short cytoplasmic tail region. The present article reviews the following: (1) the structure, function, and variant site analysis of the Trem2 gene; (2) the metabolism of TREM2 in peripheral blood and cerebrospinal fluid; and (3) the possible underlying mechanism by which TREM2 regulates innate immunity and participates in AD.