Figure 1.

Antibody production by B cells and antibody-mediated immune response in CHB infection. B cells can produce antibodies, such as anti-HBs, anti-HBc and self-antibodies, and subsequently mediate an antiviral immune response or self-reaction via various potential mechanisms in CHB infection. (1) Anti-HBs antibodies bind to HBsAg to block viral entry and replication; (2) anti-HBs antibodies bind HBsAg and induce cellular phagocytosis of Kupffer cells to consume HBV (ADCP); (3) anti-HBs antibodies bind HBsAg and induce the release of perforin/granzyme in NK cells to eliminate HBV-infected hepatocytes (ADCC); (4) anti-HBs antibodies participate in forming immune complexes and bind to dendritic cells to induce a T cell response; (5) anti-HBc IgG binds HBcAg to induce hepatocyte lysis via the classical complement activation pathway initiating from C1 (CDC); (6) self-antibodies participate in an autoimmune reaction to aggravate liver inflammation. ADCC, antibody-dependent cellular cytotoxicity; ADCP, antibody-dependent cellular phagocytosis; CDC, compliment-dependent cytotoxicity.