Biliary atresia (BA) is a pediatric inflammatory disease of the biliary system which leads to cirrhosis and the need for liver transplantation. Various cells types have been reported to participate in the pro-inflammatory response, including Th1, Th2, Th17, CD8⁺ T cells, or NK cells. The suppressive Treg cells, on the contrary, were not functioning properly. The underlying mechanism is largely unknown. Focusing on why the suppressive function of Treg was impaired, we found out methylation status of CpG islands within the Foxp3 promotor of Tregs in BA patients and murine models were both increased. Moreover, when injecting Aza as DNA-methylation inhibitor to RRV infected mice, jaundice rate were decreased and survival of the mice were prolong. Strikingly, Tregs isolated from Aza treated infected mice had better suppressive function than Tregs from the infected mice without Aza treatment. Besides, IL-17+Treg cells and Th17 cells were both elevated in mice when Foxp3 expression was epigenetically down regulated. Thus we concluded that aberrant increased demethylation status of "Foxp3 promoter" in Treg cells leads to impaired Treg suppressive function and participated in inflammatory injury to extrahepatic and intrathepatic bile duct in BA.