B cell dysfunction in chronic hepatitis B virus infection

被引:4
作者
Ma, Lijie [1 ]
Sun, Xuehua [1 ]
Kong, Xiaoni [1 ]
Gao, Yueqiu [1 ]
机构
[1] Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Inst Clin Immunol, Dept Liver Dis, Shanghai, Peoples R China
基金
中国国家自然科学基金;
关键词
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); SURFACE-ANTIGEN; CORE ANTIGEN; T-CELLS; IMMUNE-RESPONSE; MOLECULAR-BASIS; ANTIBODIES; HBV; PD-1; RECEPTOR; DISEASE;
D O I
10.1016/j.livres.2020.09.004
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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 amplifi-cation of CD19 thorn CD10-CD27-CD21- atypical memory B cell subsets and CD19 thorn 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.& COPY; 2021 The Third Affiliated Hospital of Sun Yat-sen University. Publishing Services by Elsevier B. V. on behalf of KeAi Communications Co., Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
引用
收藏
页码:11 / 15
页数:5
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