髓样细胞触发受体2在缺血性脑卒中后神经炎症中的作用

The role of triggering receptor expressed on myeloid cells 2 in neuroinflammation afterischemic stroke

缺血性脑卒中(Ischemic stroke,IS)的发病率逐年增加,尽管及时再通血管能够最大程度减缓脑损伤,但患者仍然面临着缺血/再灌注损伤的风险。其诱发的神经炎症导致脑水肿、细胞凋亡、血脑屏障破坏等严重后果。小胶质细胞作为大脑的常驻免疫细胞,可吞噬损伤的神经元,维持脑内稳态。髓样细胞触发受体2(Triggering receptor expressed on myeloid cells 2,TREM2)因在小胶质细胞上高表达且促进细胞的吞噬功能而受到广泛关注。本文主要讨论TREM2的结构、功能以及与小胶质细胞的关系,并详细阐明其在IS中的抗炎作用,为治疗缺血性脑卒中的药物研发提供重要依据。

The incidence of ischemic stroke(IS)is on the rise.Although timely revascularization can relieve brain injury,patients are still at risk of ischemia/reperfusion injury.The induced neuroinflammation will lead to brain edema,cell apoptosis,blood brain barrier destruction and other serious consequences.Microglia,as the permanent immune cells of the brain,can engulf injured neurons and maintain brain homeostasis.Triggering receptor expressed on myeloid cells 2(TREM2)is highly expressed on microglia and promotes cell phagocytosis,which has attracted widespread attention.This article mainly discusses the structure,function and relationship between TREM2 and microglia,and elucidates its anti-inflammatory effect in IS,so as to provide an important basis for drug research and development in the treatment of ischemic stroke.