T淋巴细胞亚群免疫功能失衡在重症肌无力（MG）的发病过程中起着重要作用。G0S2是淋巴细胞增殖的重要调控分子，我们发现，G0S2基因在重症肌无力患者外周血T淋巴细胞中的表达高度上调，其启动子区甲基化程度则显著下调。lncRNA调控基因甲基化在多种疾病的发生中具有重要作用，但在MG中的作用尚未报道。本项目拟从表观遗传学的角度，研究lncRNA ecG0S2通过甲基化转移酶干扰启动子区甲基化，从而影响G0S2表达的调控途径，进而阐明lncRNA ecG0S2-G0S2甲基化对T淋巴细胞免疫平衡的作用及MG发病的分子机制，为开发MG的表观治疗方略提供新的思路和理论依据。

The dysregulation of T lymphocytes is of great importance in the pathogenesis of myasthenia gravis. G0S2 is a key regulator during lymphocyte proliferation. Our previous studies showed the increased expression of G0S2 in the peripheral T lymphocytes of MG patients. Meanwhile, DNA methylation level of G0S2 promoter is downregulated. Many evidences already proved how the lncRNA regulates gene expression by changing DNA methylation of target gene. However, it is still unknown if lncRNA is able to play the similar role during MG pathogenesis. Our future study aims to investigate the role of lncRNA ecG0S2 regarding how it can regulate G0S2 methylation through DNA methyltransferases and finally the expression of G0S2 gene, which may play a major role for maintaining the immune balance of T lymphocytes. Better understanding of this regulation process can provide more evidence to explain the molecular pathomechanism of MG, and offer new perspective on the epigenetic therapy of MG.