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High mobility group box 1 (HMGB1) protein in Multiple Sclerosis (MS): Mechanisms and therapeutic potential

机译：多发性硬化症（MS）中的高迁移率组盒1（HMGB1）蛋白质：机制和治疗潜力

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摘要

Multiple sclerosis (MS) is an autoimmune chronic inflammatory disease with distinctive features of focal demyelination, axonal loss, activation of glial cells, and immune cells infiltration. The precise molecular mechanism underlying the disease progression remains enigmatic despite of the rapid progression on experimental and clinical MS research. The focus of MS therapy relies on the repression of the pathogenic autoimmune response without compromising an adaptive immune response. High mobility group box-1 (HMGB1) protein is a ubiquitous nuclear protein driving pro-inflammatory responses as well as targeting innate immune signaling that initiates and mediates autoimmunity as well as sterile injury. A considerable amount of experimental and human studies suggests the contribution of HMGB1 in the pathogenesis of MS/experimental autoimmune encephalitis (EAE). In this regard, HMGB1 protein has gained increased attention, as an emerging possible therapeutic target against MS. This is more strengthened by the promising therapeutic outcome demonstrated by HMGB1 neutralizing agents in the experimental EAE model. Herein, we attempt to shed more light on the molecular crosstalk of HMGB1 protein in the pathogenesis of MS/EAE suggesting that HMGB1 blockade could impede the pro-inflammatory loop that drives MS autoimmunity.
机译：多发性硬化症（MS）是一种自身免疫性慢性炎症性疾病，具有局灶性脱髓鞘，轴突丧失，神经胶质细胞的激活和免疫细胞浸润的独特特征。尽管对实验和临床MS研究进展迅速进展，但疾病进展的精确分子机制仍然是神秘的。 MS治疗的焦点依赖于抑制致病性自身免疫反应，而不会影响适应性免疫应答。高迁移率组盒-1（HMGB1）蛋白是普遍存在的核蛋白质驱动促炎反应以及靶向先天免疫信号，引发和介导自身免疫以及无菌损伤。相当大量的实验和人类研究表明HMGB1在MS /实验性自身免疫脑炎（EAE）发病机制中的贡献。在这方面，HMGB1蛋白质的注意力增加，作为对MS的出现可能的治疗目标。通过实验EAE模型中的HMGB1中和剂证明的有前途的治疗结果更加强化。在此，我们在MS / EAE的发病机制中试图在HMGB1蛋白的分子串扰上表明HMGB1阻断可能阻碍驱动MS AutoImmunity的促炎环。

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