高迁移率族蛋白B1在多发性硬化中的作用机制研究进展

Research progress on mechanism of high mobility group protein B1 in multiple sclerosis

多发性硬化(MS)是一种由免疫系统故障引起的神经系统疾病,导致针对脑白质组织抗原的自身免疫反应。高迁移率族蛋白B1(HMGB1)近年来在炎症反应及自身免疫性疾病中的作用得到广泛关注,但是HMGB1对MS的作用机制的报道相对较少。有研究表明,HMGB1可能成为治疗MS的新靶点。现就HMGB1的结构、来源及信号传导通路,HMGB1在MS中的作用及相关机制的研究进展做一综述,以期为MS的诊疗提供新的靶点,为进一步临床和实验研究提供基础。

Multiple sclerosis(MS)is a neurological disease caused by a failure of the immune system,which leads to an autoimmune response to white matter tissue antigens.In recent years,the role of high mobility group protein B1(HMGB1)in inflammatory response and autoimmune diseases has been widely concerned,but there are relatively few reports on the mechanism of MS by HMGB1.Some studies have shown that HMGB1 may become a new target for the treatment of MS.This article reviews the structure,source and signal transduction pathway of HMGB1,the role of HMGB1 in MS and related mechanisms,in order to provide a new target for the diagnosis and treatment of MS and provide a basis for further clinical and experimental research.