NLRP3炎症小体在MS/EAE发病机制中的作用及其靶向治疗

多发性硬化症(multiple sclerosis,MS)是由免疫细胞攻击中枢神经系统(central nervous system,CNS)而造成的一种自身免疫性疾病,其具有神经元脱髓鞘、神经胶质细胞增生和轴突损伤等病理特征1]。NLRP3炎症小体作为一种能识别病原体和危险信号的传感器,近年来被发现与许多自身免疫性疾病的发病关系密切2]。本文从NLRP3炎症小体激活的主要途径出发,综述了NLRP3炎症小体在MS及其动物模型——实验性自身免疫性脑脊髓炎(experimental autoimmune encephalomyelitis,EAE)发病中的作用以及靶向治疗研究进展。

NLRP3 inflammasome in pathogenesis of MS/EAE and its targeted therapy

Inflammasomes,the important component of innate immune system,play an important role in inflammatory diseases.NLRP3,the most studied inflammasome,is activated after recognizing danger-associated molecular patterns and pathogen-associated molecular patterns.The activated NLRP3 inflammasome promotes inflammation by maturation and release of the pro-inflammatory cytokines interleukin(IL)-1βand IL-18.Involvement of the NLRP3 inflammasome in the development of multiple sclerosis(MS)and experimental autoimmune encephalomyelitis(EAE)was suggested in a number of studies.Therefore,targeting on NLRP3 inflammasome is one of the promising methods for treatment of related diseases.In this review,we summarize the main ways by which the NLRP3 inflammasome is activated in the cytosol.We also discuss the development and treatment of NLRP3 inflammasome in MS and EAE,and expect to provide reference for the treatment of MS.