Recombinant Human TREM2 protein

TREM2 (Triggering Receptor Expressed on Myeloid cells 2) is a transmembrane protein predominantly expressed on immune cells of the myeloid lineage, including microglia, macrophages, and dendritic cells. It plays a critical role in modulating innate immune responses, particularly in the central nervous system and peripheral tissues. Structurally, TREM2 consists of an extracellular immunoglobulin-like domain responsible for ligand binding, a transmembrane region, and a short cytoplasmic tail that associates with adaptor proteins like DAP12 to initiate intracellular signaling. This signaling pathway regulates phagocytosis, inflammation, and cell survival, making TREM2 essential for maintaining tissue homeostasis and responding to damage or infection.

Research has linked TREM2 dysfunction to neurodegenerative diseases, notably Alzheimer’s disease (AD). Genetic variants of TREM2. such as the R47H mutation, impair microglial function, reducing clearance of amyloid-beta plaques and exacerbating neuroinflammation. Beyond AD, TREM2 is implicated in Parkinson’s disease, multiple sclerosis, and cancer, where its role in immune regulation varies by context. These discoveries have spurred interest in TREM2 as a therapeutic target.

Recombinant TREM2 protein, produced via heterologous expression systems (e.g., mammalian or insect cells), typically includes the soluble ectodomain to study ligand interactions or receptor activation mechanisms. It enables in vitro and in vivo investigations into TREM2’s biological functions, including ligand screening, structural analysis, and pathway modulation. Recent studies also explore engineered TREM2 agonists to enhance microglial activity in neurodegeneration. However, challenges remain in understanding its ligand specificity and tissue-specific signaling. Recombinant TREM2 tools are pivotal for dissecting its role in disease and developing targeted therapies, reflecting its growing importance in immunology and neuroscience research.