Figure 2.

Antigen presentation function of B cells in CHB infection. The BCR specifically recognizes and binds HBV antigens that exist alone or are presented on the surface of macrophages or dendritic cells. The engagement enables BCR-antigen internalization into endosomes. Concomitant with receptor-mediated endocytosis, MHC-I/MHC-II molecules produced by B cells converge to form complexes with the HBcAg/HBsAg peptides processed in lysosomes and transferred to the plasma membrane. Naive CD4+ T cells are activated by B cells presenting HBcAg-MHC-II complexes, inducing a CD4+ T cell immune response. In addition, CD8+ T cells are activated by B cells presenting HBcAg/HBsAg-MHC-I complexes, inducing CTL cytotoxic reaction. However, the process promotes the apoptosis of HBsAg-infected cells (including HBsAg-infected B cells) and persistent HBV infection. BCRs, B cell antigen receptors; MHC-I, major histocompatibility complex class I; MHC-II, major histocompatibility complex class II.