The Immunobiology of Regulatory T Cells in Hepatitis B and C

Hepatitis B and C continue to be the world challenging problems. The results of currently available treatments with antiviral medications and interferon-based therapy have not been satisfactory and the numbers of newly acquired infection continue to increase. This situation has prompted investigations into novel approaches to decrease the mortality and morbidity of those suffering from hepatitis B and C. The dynamics of regulatory T cells (Tregs) in various stages of the illness have been reported in previous studies. It has been asserted that Tregs may have important roles in sustaining the viral persistence and preventing liver damage although the comprehensive mechanisms of hepatitis immunity mediated by Tregs are not well understood. To understand the immunobiology of regulatory T cells in hepatitis B and hepatitis C, we reviewed original research articles available from online databases. We found that in hepatitis B, Tregs development is influenced by plasmacytoid dendritic cells, soluble heat shock protein (HSP)-60, and toll-like receptor (TLR) 2/4 signaling. Tumor growth factor (TGF)-beta, indoleamine 2,3-dioxygenase (IDO), Tim-3/Gal-9 interactions, toll-like receptor (TLR)-2 stimulation, Notch signaling, HCV-induced miR146a, and contact with dendritic cells or B cells promote Tregs development and activation in hepatitis C. Tregs inhibit the function of cytotoxic T cells in HBV-infected livers whereas interleukin (IL)-8 produced by intrahepatic Tregs contributes to Tregs' role as the regulator of fibrogenesis in chronic hepatitis C. This present paper reports the significance of Tregs in hepatitis B and C as well as their development and suppression in the context of HBV and HCV infection.