We showed that the deletion of CD73 on ERCs weakened its ability to inhibit the CD4+ T cell activation and function in vitro and led to poor therapeutic efficiency of ERCs in Con A-induced hepatitis which was associated with extensive liver necrosis, massive infiltration of effector CD4+ T cells, decreased generation of Tregs, and elevated tissue and serum levels of pro-inflammatory cytokines (IFN-γ, TNF-α). This evidence concerns the gene CD4 and hepatitis A virus infection.