TREM2

triggering receptor expressed on myeloid cells 2

5 disorders 2 untyped 2 no genetic record 1 causative 6p21.1 gene with protein product

HGNC:17761 Monarch NCBI Gene 54209 ENSG00000095970 UniProt Q9NZC2 OMIM 605086

Aliases: TREM-2, Trem2a, Trem2b, Trem2c.

Normal function · from ai-gene-review (Q9NZC2, commit 79fe13b38970) · AI-generated, not KB evidence

TREM2 is a type I plasma-membrane immunoglobulin-superfamily receptor expressed mainly by microglia and other myeloid-lineage cells. Together with the TYROBP/DAP12 adaptor, TREM2 converts ligand binding at the cell surface into intracellular signaling through kinases and PLCG2-linked pathways that support cell survival, calcium/ERK signaling, phagocytosis, chemotaxis, microglial activation, and lipid handling. TREM2 recognizes lipid-rich and damage-associated ligands, including aminophospholipids exposed on apoptotic cells, lipoprotein particles and apolipoproteins, and amyloid-beta-lipoprotein complexes. Disease-model annotations involving amyloid plaques, synapse pruning, neuroinflammation, osteoclast biology, and dendritic cell maturation are important contexts but are secondary to the core receptor-ligand signaling and phagocytic myeloid-cell functions.

TREM2 is a plasma-membrane myeloid receptor that associates with TYROBP/DAP12 and transduces ligand binding into intracellular kinase, PLCG2, calcium, ERK, and activation programs in microglia and other myeloid cells.

molecular function: transmembrane signaling receptor activity · directly involved in: signal transduction; regulation of innate immune response; positive regulation of intracellular signal transduction; positive regulation of calcium-mediated signaling; positive regulation of ERK1 and ERK2 cascade · locations: plasma membrane

TREM2 recognizes lipid-rich damage and uptake ligands, including aminophospholipids on apoptotic cells, lipoprotein/apolipoprotein particles, sulfatides, and amyloid-beta-lipoprotein complexes, enabling microglial phagocytosis, activation, migration, and lipid handling.

molecular function: lipid binding · directly involved in: positive regulation of phagocytosis, engulfment; apoptotic cell clearance; positive regulation of microglial cell activation; positive regulation of microglial cell migration; lipid homeostasis · locations: plasma membrane

In the knowledge base · computed from kb/ at build time

Disorders

Relationship is the entry's genetic[].relationship_type. untyped means the entry has a genetic record for the gene but does not type it; its free-text association is shown instead.

Disorder	Relationship	Where the gene appears
Nasu-Hakola Disease	causative	mechanism: TREM2-DAP12 Receptor Complex Loss of Function subtype: PLOSL2
Alzheimer Disease	untyped Risk Factor	mechanism: Neuroinflammation scoped to subtype: Late-Onset Alzheimer's Disease
Tuberculosis	untyped Foamy macrophage formation and Mtb persistence
Amyotrophic Lateral Sclerosis	no genetic record	mechanism: Microglial TREM2 Signaling
Triple-Negative Breast Cancer	no genetic record	mechanism: Intratumoral CXCL9 Deficiency

Mechanism modules · computed from kb/

neuroinflammation_glial_activation via Alzheimer Disease

Identity from HGNC (snapshot 2026-10-01). Page layers are described in the gene pages documentation.