The Expression Pattern and Regulatory Mechanism of the G0/G1 Switch Gene 2 () in the Pathogenesis and Treatment of AChR Myasthenia Gravis (MG).

This study is aimed at exploring the expression pattern and methylation level of in the peripheral blood mononuclear cells (PBMCs) of myasthenia gravis (MG) patients with positive acetylcholine receptor (AChR) autoantibodies and revealing the relationship between the methylation pattern and MG. The relationship between the NFAT family members and was explored to reveal the regulatory mechanism of in the pathogenesis and treatment of AChR MG. Moreover, we attempted to demonstrate the potential therapeutic mechanism of tacrolimus in AChR MG. The relative expression level in the PBMCs of healthy people was compared with that in the PBMCs of AChR MG patients with quantitative real-time PCR (qRT-PCR). The methylation frequency of the promoter was detected by bisulfite sequencing PCR (BSP) and pyrosequencing. A dual-luciferase reporter system was used to reveal the relationship between the promoter and nuclear factor of activated T cells 5 (). The qRT-PCR results showed that expression was significantly upregulated in the B cells and CD8+ T cells of AChR MG patients but not in the CD4+ T cells, and these expression differences were significantly associated with a decrease in methylation. , which was speculated to bind to island 1 (p1) in the promoter, may regulate the lymphocyte balance by regulating gene expression but failed to affect the methylation of the promoter. Tacrolimus therapy-induced methylation and overexpression of could significantly reduce the expression of in AChR MG patients. The gene was remarkably upregulated in the PBMCs of MG patients. may affect transcription initiation and downregulate expression through p1 in the promoter, thus controlling gene expression and regulating the lymphocyte balance. Therefore, could be an immune regulatory factor in both AChR MG occurrence and treatment with tacrolimus.