Miyake Shota, Serizawa Kenichi, Onishi Shinichi, Katsura Yoshichika, Baba Masayuki, Kurasawa Mitsue, Tomizawa-Shinohara Haruna, Yorozu Keigo, Matsumoto Yoshihiro, Noguchi-Sasaki Mariko
Product Research Department, Chugai Pharmaceutical Co., Ltd., Yokohama, Japan.
Front Neurol. 2024 May 1;15:1356300. doi: 10.3389/fneur.2024.1356300. eCollection 2024.
Myasthenia gravis (MG) is a chronic autoimmune disease characterized by muscle weakness and fatigue. It is caused by pathological autoantibodies against components expressed at neuromuscular junctions, such as acetylcholine receptor (AChR). Interleukin-6 (IL-6) has been suggested to play a role in the pathogenesis of MG, and IL-6 receptor (IL-6R) antibody treatment may provide a novel therapeutic option. In this study, we investigated the effects of IL-6R antibody treatment in an experimental autoimmune MG (EAMG) mouse model. We demonstrated that IL-6R antibody treatment improved muscle weakness, reduced IgG deposition at neuromuscular junctions, and the levels of AChR autoantibodies in serum. In addition, follicular helper T cells and Th17, plasma cells in lymph nodes were lower in IL-6R antibody treated mice. Our findings suggest that IL-6R blockade may be a novel and effective therapeutic strategy for the treatment of MG.
重症肌无力(MG)是一种以肌肉无力和疲劳为特征的慢性自身免疫性疾病。它由针对神经肌肉接头处表达的成分(如乙酰胆碱受体(AChR))的病理性自身抗体引起。白细胞介素-6(IL-6)已被认为在MG的发病机制中起作用,并且IL-6受体(IL-6R)抗体治疗可能提供一种新的治疗选择。在本研究中,我们研究了IL-6R抗体治疗在实验性自身免疫性MG(EAMG)小鼠模型中的作用。我们证明,IL-6R抗体治疗改善了肌肉无力,减少了神经肌肉接头处的IgG沉积以及血清中AChR自身抗体的水平。此外,接受IL-6R抗体治疗的小鼠淋巴结中的滤泡辅助性T细胞、Th17和浆细胞数量较少。我们的研究结果表明,阻断IL-6R可能是治疗MG的一种新的有效治疗策略。