髓样细胞触发受体2(triggering receptor expressed on myeloid cells 2,TREM2)是小胶质细胞(microglia)表面特异性表达的受体,可通过调控小胶质细胞增殖、活化与吞噬作用以维持神经免疫微环境稳态。大多数研究发现,在阿尔茨海默病与帕金森病中,TREM2主要通过DAP10/12或PLCγ2通路促进M2型小胶质细胞极化,加强小胶质细胞吞噬功能,缓解氧化应激及神经炎症。在癫痫与脑卒中中,TREM2通过激活PI3K 或Wnt通路调控小胶质细胞向疾病相关小胶质细胞转化,以减轻神经炎症并促进组织修复。这些发现表明TREM2在上述神经退行性疾病的病理变化中发挥重要作用,但其潜在作用机制及临床意义仍有待阐明。本综述通过系统全面地概括TREM2的生物学特性、病理生理功能与潜在机制,旨在为TREM2及其相关信号通路作为中枢神经系统疾病临床诊断与治疗的候选靶点提供可靠的理论依据。

Triggering receptor expressed on myeloid cells 2 (TREM2) is a receptor specifically expressed on the surface of microglia. It maintains the homeostasis of the neuroimmune microenvironment by regulating microglia proliferation, activation, and phagocytosis. Numerous studies have demonstrated that in Alzheimer's disease and Parkinson's disease, TREM2 primarily promotes M2-type microglial polarization via the DAP10/12 or PLCγ2 pathway, enhances microglial phagocytic function and alleviating oxidative stress and neuroinflammation. In epilepsy and stroke, TREM2 regulates the transformation of microglia into disease-associated microglia by activating the PI3K or Wnt pathway, thereby reducing neuroinflammation and facilating tissue repair. These findings suggest that TREM2 plays a crucial role in the pathological progress of the aforementioned neurodegenerative diseases; however, its underlying mechanisms and clinical significance remain inadequately characterized. Therefore, this review systematically and comprehensively summarizes the biological characteristics, pathophysiological functions, and potential mechanisms of TREM2, aiming to provide a reliable theoretical foundation for TREM2 and its associated signaling pathways as candidate targets for the clinical diagnosis and treatment of central nervous system diseases.