Triggering receptor expressed on myeloid cells 2 (TREM2) is a key immunomodulatory receptor broadly expressed on myeloid cells such as macrophages and microglia.
First-pass extracted concept
TREM2
Candidate: concept label1 source documents8 linked claims
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Aliases
Triggering receptor expressed on myeloid cells 2
Evidence Snippets
Supporting Sources
Linked Claims
In neurodegenerative disease contexts, TREM2 attenuates neuroinflammation and slows disease progression by promoting amyloid-beta clearance, inhibiting tau hyperphosphorylation, and modulating microglial polarization.
TREM2 is a key immunomodulatory receptor on myeloid cells that orchestrates glucose metabolism and inflammatory responses.
TREM2 enhances glycolysis and suppresses fatty acid oxidation to facilitate macrophage polarization toward a reparative M2 phenotype.
TREM2 signaling includes PI3K/Akt, MAPK, NF-κB, and STAT3 cascades.
In metabolic disorders such as diabetes and obesity, TREM2 exerts protective effects by inhibiting NLRP3 inflammasome activation and maintaining lipid homeostasis.
TREM2-associated macrophage metabolic reprogramming promotes neuroregeneration and remyelination in spinal cord injury and multiple sclerosis contexts.
TREM2 has translational potential as a therapeutic target, including through agonists, gene regulatory strategies, and biomarker use.
Within the tumor microenvironment, TREM2 modulates tumor-associated macrophage metabolic reprogramming through PKM2-dependent glycolysis and promotes an immunosuppressive phenotype linked to tumor progression and therapeutic resistance.