TREM2 Recombinant Rabbit mAb (S-5570)

TREM2 (Triggering Receptor Expressed on Myeloid cells-2) is a single-pass type-I membrane glycoprotein expressed on microglia, macrophages, osteoclasts and dendritic cells that functions as a crucial innate immune sensor and signaling hub; its extracellular Ig-like V-type domain binds anionic lipids, apolipoproteins and phospholipids to detect tissue damage and amyloid plaques, while its short cytoplasmic tail associates with the adaptor DAP12 (TYROBP) to transduce intracellular signals via ITAM motifs that regulate phagocytosis, lipid metabolism, cell survival, inflammatory resolution and metabolic reprogramming toward an anti-inflammatory state. Loss-of-function variants such as the R47H missense mutation strongly increase the risk for late-onset Alzheimer’s disease by impairing microglial clustering around β-amyloid deposits, reducing plaque compaction and exacerbating neurodegeneration, whereas TREM2 deficiency also drives pathologic lipid accumulation, synaptic loss and defective debris clearance in other neurodegenerative, metabolic and inflammatory disorders including Nasu–Hakola disease, frontotemporal dementia, Parkinson’s disease, atherosclerosis and obesity, making TREM2 a pivotal immunomodulatory target for therapeutic antibodies, sTREM2 fusion proteins and small-molecule agonists aimed at restoring microglial homeostasis and neuroprotection.