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Abstract：
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.
摘要：
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。它是由针对神经肌肉接头处表达的成分的病理性自身抗体引起的，例如乙酰胆碱受体(AChR)。白细胞介素-6(IL-6)已被认为在MG的发病机制中起作用。和IL-6受体(IL-6R)抗体治疗可提供新的治疗选择。在这项研究中,我们在实验性自身免疫性MG(EAMG)小鼠模型中研究了IL-6R抗体治疗的效果.我们证明IL-6R抗体治疗改善肌肉无力，减少神经肌肉接头处的IgG沉积，以及血清中AChR自身抗体的水平。此外,在IL-6R抗体处理的小鼠中,淋巴结中的滤泡辅助性T细胞和Th17、浆细胞较低。我们的发现表明，IL-6R阻断可能是治疗MG的一种新颖有效的治疗策略。
