TREMs in the immune system and beyond

By M. Colonna. Nature reviews. Immunology, 2003

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Microglia in Neurological Diseases: A Road Map to Brain-Disease Dependent-Inflammatory Response (2018, background): “…with a reduced risk of AD (Huang et al., 2017), as well as an allelic variant of the TREM2, a cell-surface receptor exclusively of microglial cells (Colonna, 2003) which is associated to increased risk for developing AD up to threefold (Jonsson et al., 2013; Abduljaleel et al., 2014; Ulrich et…”
Alzheimer's disease risk genes and mechanisms of disease pathogenesis (2014, neutral): “The longest transcript encodes a transmembrane protein that is trafficked to the cell surface where it interacts with DAP12 (also known as TYROBP) and binds with several ligands (94).”
TREM2 mutations implicated in neurodegeneration impair cell surface transport and phagocytosis (2014, background): “Coexpression of DAP12, the signaling adaptor for TREM2 (20), which is not expressed in HEK293 Flp-In cells, did not restore transport and shedding of mutant TREM2 (Fig.”
TREM2 deficiency eliminates TREM2+ inflammatory macrophages and ameliorates pathology in Alzheimer’s disease mouse models (2015, background): “In the brain, the TREM2 receptor is expressed exclusively by myeloid cells (Colonna, 2003).”
Costimulatory signals mediated by the ITAM motif cooperate with RANKL for bone homeostasis (2004, background): “In osteoclast precursor cells, FcRγ and DAP12 associate with multiple immunoreceptor”