Department of Neurology, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan 250014, PR China.
Medical Research Center, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan 250014, PR China.
Mol Immunol. 2018 Feb;94:200-208. doi: 10.1016/j.molimm.2018.01.005. Epub 2018 Jan 12.
Recent studies have demonstrated the important role of toll-like receptor 9 (TLR9) signalling in autoimmune diseases, but its role in myasthenia gravis (MG) has not been fully established. We show herein that blocking TLR9 signalling via the suppressive oligodeoxynucleotide (ODN) H154 alleviated the symptoms of experimental autoimmune myasthenia gravis (EAMG). With the downregulation of dendritic cells (DCs), TLR9 interruption reduced follicular helper T cells (Tfh) and germinal centre (GC) B cells, leading to decreased antibody production. In addition, TLR9 B cells as well as total B cells in the spleen were inhibited by H154. These findings highlight the critical role of TLR9 in EAMG and suggest that the inhibition of the TLR9 pathway might be a potential pharmacological strategy for the treatment of myasthenia gravis.
最近的研究表明，Toll 样受体 9（TLR9）信号在自身免疫性疾病中具有重要作用，但它在重症肌无力（MG）中的作用尚未完全确定。我们在此表明，通过抑制性寡脱氧核苷酸（ODN）H154 阻断 TLR9 信号可缓解实验性自身免疫性重症肌无力（EAMG）的症状。随着树突状细胞（DC）的下调，TLR9 中断减少了滤泡辅助 T 细胞（Tfh）和生发中心（GC）B 细胞，导致抗体产生减少。此外，TLR9 B 细胞和脾脏中的总 B 细胞均受到 H154 的抑制。这些发现强调了 TLR9 在 EAMG 中的关键作用，并表明抑制 TLR9 途径可能是治疗重症肌无力的一种潜在药理学策略。
