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高迁移率族蛋白B1参与被动转移型重症肌无力模型的发病机制。

High mobility group box 1 is involved in the pathogenesis of passive transfer myasthenia gravis model.

作者信息

Maimaitiming Bibinu, Uzawa Akiyuki, Ozawa Yukiko, Yasuda Manato, Kojima Yuta, Kanai Tetsuya, Kuwabara Satoshi

机构信息

Department of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan.

出版信息

Neuroreport. 2021 Jun 9;32(9):803-807. doi: 10.1097/WNR.0000000000001665.

DOI:10.1097/WNR.0000000000001665
PMID:33994526
Abstract

Myasthenia gravis (MG) is an autoimmune disease with autoantibodies against the mainly nicotinic acetylcholine receptor (AChR). High mobility group box1 (HMGB1) acts as a danger signal and drives the pathogenesis of autoimmune-mediated diseases. However, the role of HMGB1 in the pathogenesis of MG is not fully understood. Therefore, in this study, we analyzed serum levels of HMGB1 and immunohistochemical HMGB1 staining of muscle tissues in the passive transfer MG model to investigate the role of HMGB1 in MG. As a result, serum HMGB1 levels tended to be higher and the quantitative score of muscle pathology showed greater HMGB1 deposition (P = 0.02) along with sparser AChR staining and more severe inflammation in the passive transfer MG rats (n = 6) than those in control rats (n = 6). These findings indicate that HMGB1 is an important mediator and biomarker for inflammation in the pathogenesis of MG and can be a therapeutic target in MG.

摘要

重症肌无力(MG)是一种自身免疫性疾病,体内存在主要针对烟碱型乙酰胆碱受体(AChR)的自身抗体。高迁移率族蛋白B1(HMGB1)作为一种危险信号,推动自身免疫介导疾病的发病机制。然而,HMGB1在MG发病机制中的作用尚未完全明确。因此,在本研究中,我们分析了被动转移MG模型中血清HMGB1水平以及肌肉组织的HMGB1免疫组化染色情况,以探讨HMGB1在MG中的作用。结果显示,与对照大鼠(n = 6)相比,被动转移MG大鼠(n = 6)的血清HMGB1水平趋于更高,肌肉病理学定量评分显示HMGB1沉积更多(P = 0.02),同时AChR染色更稀疏,炎症更严重。这些发现表明,HMGB1是MG发病机制中炎症的重要介质和生物标志物,可成为MG的治疗靶点。

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