Published online Jul 21, 2019. doi: 10.3748/wjg.v25.i27.3527
Peer-review started: March 26, 2019
First decision: April 16, 2019
Revised: April 29, 2019
Accepted: May 31, 2019
Article in press: June 1, 2019
Published online: July 21, 2019
Processing time: 116 Days and 8.7 Hours
Hepatitis B virus (HBV) infection is one the leading risk factors for chronic hepatitis, liver fibrosis, cirrhosis and hepatocellular cancer (HCC), which are a major global health problem. A large number of clinical studies have shown that chronic HBV persistent infection causes the dysfunction of innate and adaptive immune response involving monocytes/macrophages, dendritic cells, natural killer (NK) cells, T cells. Among these immune cells, cell subsets with suppressive features have been recognized such as myeloid derived suppressive cells(MDSC), NK-reg, T-reg, which represent a critical regulatory system during liver fibrogenesis or tumourigenesis. However, the mechanisms that link HBV-induced immune dysfunction and HBV-related liver diseases are not understood. In this review we summarize the recent studies on innate and adaptive immune cell dysfunction in chronic HBV infection, liver fibrosis, cirrhosis, and HCC, and further discuss the potential mechanism of HBV-induced immunosuppressive cascade in HBV infection and consequences. It is hoped that this article will help ongoing research about the pathogenesis of HBV-related hepatic fibrosis and HBV-related HCC.
Core tip: We review that hepatitis B virus (HBV) induces suppressive function of the innate and adaptive immune cells in chronic HBV infection, and highlight that immune suppressive cascade contributes to the mechanism of HBV persistent infection. Further, we analyze the potential effects of HBV-induced immunosuppression in HBV-related fibrosis and hepatocellular carcinoma, thus providing underlying research directions for future studies into the pathogenesis of HBV-related disease.