Author/Authors :
Jiang، نويسنده , , Hongyan and Xiao، نويسنده , , Rong and Lian، نويسنده , , XiaoRi and Kanekura، نويسنده , , Takuro and Luo، نويسنده , , YangYang and Yin، نويسنده , , YongXing and Zhang، نويسنده , , GuiYing and Yang، نويسنده , , Yan and Wang، نويسنده , , Yaoyao and Zhao، نويسنده , , Ming and Lu، نويسنده , , QianJin، نويسنده ,
Abstract :
The pathogenesis of systemic sclerosis (SSc) is still unclear. CD70, a B cell costimulatory molecule that interacts with CD27 during B–T cell contact, is overexpressed due to demethylation of its promoter regulatory elements in CD4+ T cells from patients with the following autoimmune diseases, namely systemic lupus erythematosus (SLE), subacute cutaneous lupus erythematosus (SCLE) and primary Sjögrenʹs syndrome (pSS). However, as an autoimmune disease, it is unknown whether aberrant expression and methylation of CD70 occur in SSc CD4+ T cells.
ed to investigate whether the aberrant expression and methylation status of CD70 occur in CD4+ T cells from patients with SSc. We found that the CD70 is overexpressed and the CD70 promoter region is demethylated in SSc CD4+ T cells.
findings suggest that demethylation of CD70 promoter region contributes to the overexpression of CD70 in CD4+ T cells and may contribute to autoimmune response in SSc.
Keywords :
DNA methylation , systemic sclerosis , CD70 , CD4+ T cells