Abstract
Chronic hepatitis B virus (HBV) infection is one of the main causes of liver diseases, of which the natural history and clinical outcomes are associated with the role of B cells. As humoral immune cells, B cells play a critical role in the process of anti-HBV antibody production. In addition, some studies have also characterized other B cell subsets involved in antigen presentation and regulating the immune response beyond antibody secretion. However, not all B cell subsets play a positive role in the immune response to chronic HBV infection, and various B cell subsets jointly mediate persistent HBV infection, tolerance, and liver damage. Thus, we further sought to elucidate the multiple functions of B cells to gain novel insight into the understanding of chronic hepatitis B (CHB) pathogenesis. We also reviewed the current immunotherapies targeting B cells to explore novel therapeutic interventions for the treatment of chronic HBV infection.
Highlights
Hepatitis B virus (HBV) is a serious global public health problem and major cause of chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC)
It is estimated that more than 250 million people worldwide are chronically infected with HBV [1], and there are approximately one million deaths attributed to HBV-related complications [e.g., cirrhosis and hepatocellular carcinoma (HCC)] each year [2]
The study by Barnaba et al demonstrated that hepatitis B surface antigen (HBsAg)-specific B cells can cross-present HBsAg fragments to cytotoxic T lymphocytes (CTLs) through major histocompatibility complex (MHC)-I molecules [14]; this process of inducing CTL cytotoxicity can cause the death of HBsAg-specific B cells and hinder the production of protective anti-HBs antibodies, which promote persistent HBV infection and long-term transmission
Summary
Hepatitis B virus (HBV) is a serious global public health problem and major cause of chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC). During the HBV vaccine design process, anti-HBs antibodies are utilized to participate in the formation of immune complexes and bind to dendritic cells (DC), which further induce a T cell response [24]. Defects in HBsAg-specific B cells in the secretion of anti-HBs antibodies might promote a persistent HBV infection.
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