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This study is aimed at exploring the expression pattern and methylation level of  G0S2  in the peripheral blood mononuclear cells (PBMCs) of myasthenia gravis (MG) patients with positive acetylcholine receptor (AChR) autoantibodies and revealing the relationship between the  G0S2  methylation pattern and MG. The relationship between the NFAT family members and  G0S2  was explored to reveal the regulatory mechanism of  G0S2  in the pathogenesis and treatment of AChR MG. Moreover, we attempted to demonstrate the potential therapeutic mechanism of tacrolimus in AChR MG. The relative  G0S2  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  G0S2  promoter was detected by bisulfite sequencing PCR (BSP) and pyrosequencing. A dual-luciferase reporter system was used to reveal the relationship between the  G0S2  promoter and nuclear factor of activated T cells 5 ( NFAT5 ). The qRT-PCR results showed that  G0S2  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  G0S2  methylation.  NFAT5 , which was speculated to bind to island 1 (p1) in the  G0S2  promoter, may regulate the lymphocyte balance by regulating  G0S2  gene expression but failed to affect the methylation of the  G0S2  promoter. Tacrolimus therapy-induced methylation and overexpression of  NFAT5  could significantly reduce the expression of  G0S2  in AChR MG patients. The  G0S2  gene was remarkably upregulated in the PBMCs of MG patients.  NFAT5  may affect transcription initiation and downregulate  G0S2  expression through p1 in the promoter, thus controlling  G0S2  gene expression and regulating the lymphocyte balance. Therefore,  G0S2  could be an immune regulatory factor in both AChR MG occurrence and treatment with tacrolimus.

The Expression Pattern and Regulatory Mechanism of the G0/G1 Switch Gene 2 (G0S2) in the Pathogenesis and Treatment of AChR Myasthenia Gravis (MG)