B cell dysfunction in chronic hepatitis B virus infection

Abstract

Chronic hepatitis B (CHB) remains a global health problem. The persistence of hepatitis B surface antigen (HBsAg) in the blood for longer than 6 months after the initial infection is a sign of CHB. The therapeutic goal for the functional cure of CHB is the generation of antibodies against HBsAg. However, the adaptive immune response of patients with CHB cannot generate an efficient antiviral response. Many previous studies have evaluated T cell function and T cell therapy specifically designed to counter hepatitis B virus (HBV) infection. As one of the major components of adaptive immunity, B cells also display dysfunctions in anti-HBsAg antibody (HBsAb) production and antigen presentation. Patients with CHB have amplification of CD19+CD10−CD27−CD21− atypical memory B cell subsets and CD19+CD24hiCD38hi regulatory B cells. Currently, no reviews have summarized specific B cell responses during CHB infection. Thus, in this study, we summarized B cell dysfunction during CHB progression and the potential mechanisms behind these dysfunctions to further our understanding of the mechanisms of adaptive immune response of B cells in the process of CHB development and help provide new methods and ideas for the treatment of CHB.

Keywords

• Chronic hepatitis B virus infection
• B cell dysfunction
• Hepatitis B surface antibody
• Atypical memory B cells (atMBCs)
• Antigen-presenting cells (APCs)
• Regulatory B cells (Bregs)