小胶质细胞在MS/EAE中的作用及研究进展

Role and research progress of microglia in multiple sclerosis /experimental autoimmune encephalomyelitis

摘要:

多发性硬化（multiple sclerosis，MS）是发生在中枢神经系统（central nervous system，CNS）的一种以炎症反应、髓鞘脱失、胶质增生等为主要病理特征的自身免疫性疾病，实验性自身免疫性脑脊髓膜炎（experimental autoimmune encephalomyelitis，EAE）由于与MS具有非常相似的病理特征及临床表现，已被国际公认为是研究MS发病机制和治疗策略的理想动物模型。尽管CD4⁺ T细胞所介导的自身免疫反应在MS/EAE的病理进程中处于核心地位，但小胶质细胞（microglia，MG）作为CNS与免疫系统沟通的“桥梁”，在MS/EAE中所发挥的作用受到越来越多的关注。除经典的抗原呈递、分泌细胞因子等途径，MG近年来还被证实可通过髓磷脂内化、激活胞内含吡啶结构域3的NOD样受体家族（NOD-like receptor family pyrin domain-containing 3，NLRP3）炎性小体等途径参与MS/EAE病理进程。本文针对MG在MS/EAE中的作用及研究进展进行综述。

Abstract:

Multiple sclerosis （MS） is an autoimmune disease that occurs in the central nervous system（CNS），with main pathological features of inflammatory response， myelin degeneration， and gliosis. Experimental autoimmune encephalomyelitis（EAE） has been widely recognized as an ideal animal model for studying the pathogenesis and treatment strategies of MS due to its similar pathological features and clinical manifestations. Although CD4⁺ T cell-mediated autoimmunity plays a central role in the pathological process of MS/EAE， microglia （MG） as a “bridge” between CNS and the immune system has received more and more attention. In addition to the classical pathways of antigen presentation and cytokine secretion， it is proved that MG can participate in the pathological process of MS/EAE through myelin internalization and activation of intracellular NOD-like receptor family pyrin domain-containing 3（NLRP3） inflammasome. This article reviewed the role and progress of MG in MS/EAE.