TREM2在阿尔茨海默病中介导免疫调节的研究进展

Research progress on TREM2-mediated immune responses in Alzheimer's disease

老年人阿尔茨海默病(Alzheimer's disease,AD)发病率极高,目前其最为熟知的病理改变为高度磷酸化的tau蛋白缠结及β淀粉样蛋白(amyloidβ-protein,Aβ)沉积。研究发现,免疫炎症反应在AD发病过程中同样起着重要作用,而小胶质细胞是神经免疫应答过程中的主要参与者。在大脑中,髓系细胞触发受体2(triggering receptor expressed on myeloid cells 2,TREM2)主要表达于小胶质细胞中,其除调控小胶质细胞代谢、生存、吞噬和增殖功能,还可调节小胶质细胞由M1型向M2型转变。近年来关于TREM2调控免疫炎症反应改善AD病理的研究越来越多,该文就TREM2和小胶质细胞对中枢神经系统及AD病理变化的影响展开综述。

The incidence of Alzheimer's disease(AD)among the elderly is extremely high.At present,the most well-known pathological changes are hyperphosphorylated tau protein entanglement and amyloidβ-protein(Aβ)deposition.Remarkably,the immune inflammatory response also plays an important role in the pathogenesis of AD,and microglia plays the main role in the process of neuroinflammatory response.In brain,triggering receptor expressed on myeloid cells 2(TREM2)is mainly expressed in microglia,which not only regulates the metabolism,survival,phagocytosis,and proliferation of microglia,but also regulates the polarization of microglia from M1 type to M2.Over the years,growing evidence has demonstrated that TREM2-mediated immure response leads to the improvement of AD pathology.This article reviews the effects of TREM2 and microglia on the central nervous system and AD biogenesis.