重症肌无力（MG）是神经系统典型的自身免疫性疾病,其发病与胸腺内发生的异常免疫反应相关,但在胸腺内如何启动免疫反应及MG病情变化的机制尚不明了。我们前期发现，MG患者胸腺内Foxp3低表达，CXCL13、CD4+CXCR5+、BCL6、ICOS、IL21高表达，且与病情严重程度相关；进一步研究发现胸腺生发中心内TFH、B细胞及致病因子-AChRAb共存，且MG患者外周血同样存在CD4+CXCR5+、ICOS的高表达。因此，我们设想MG患者胸腺内存在辅助性T细胞平衡紊乱，在感染、劳累等因素作用下，加速了Th1/Th17、Tfh/Tfr细胞失衡，诱发MG病情变化。本研究拟用形态学、分子免疫学等方法研究MG患者胸腺内Th细胞亚群发生失衡致MG病情变化、波动的机制；为其防治提供实验证据,具有重要指导意义。

Myasthenia gravis (MG) is a typical nervous system autoimmune disease and its incidence was asscioated with abnormal immune response in the thymus. However,how to triggered the abnormal immune reaction and the mechanism of the MG fluctuation are all unclear. We previously study found that the low Foxp3 exprssion and high expression of CXCL13, CD4 + CXCR5 +, BCL6, ICOS, IL21 in thymus and its correlation with MG disease severity. The further study discovered that in germinal center of thymus, the TFH cells, B cells and pathogenic factors -AChRAb coexistence. The high expression of CD4+CXCR5+ and ICOS were also found in peripheral blood of MG patients. Above all, we assume that the imblanced T helper cells was existed. The factors such infections , fatigue were all accelerated the imbalance of Th1/Th17, Tfh/Tfr and induced the MG fluctuation. This reaseach intends to use the morphology, molecular immunology and others to explain how the Th cells imbalanced induced the MG fluctuation. Our data wound provide experimental evidence for the prevention in MG patients and has an important guiding significance.