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. 2020 Dec 14;11:582292. doi: 10.3389/fimmu.2020.582292

Table 1.

The potential functions of B cells in chronic HBV infection.

Potential function Mediators Mechanism Outcome References
Antigen presentation MHC-I molecular Cross-present HBcAg on MHC-I to specific CD8+ T cells and induce CTL cytotoxicity Increase apoptosis of HBcAg-involved cells (13)
Cross-present HBsAg on MHC-I to specific CD8+ T cells and induce CTL cytotoxcity Increase apoptosis of HBsAg-involved cells (14)
MHC-II molecular Present HBcAg on MHC-II to specific CD4+ T cells Promote anti-HBc CD4+ T cell response (15)
Antibody production Self-antibodies Induce an auto-reaction via self-antibodies Impair liver tissue (16)
Anti-HBc antibodies Prime immune complex formation, complement activation via classic pathway and mediate CDC Increase HBV-infected hepatocyte lysis (1719)
Anti-HBs antibodies Produce anti-HBs antibodies to bind HBsAg, and block HBV entry and replication Reduce HBV spread (20, 21)
Initiate immune complex formation, further recruit NK cells, and mediate ADCC Increase apoptosis of HBV-infected hepatocytes (17, 22)
Initiate immune complex formation, further recruit Kupffer cells, and mediate ADCP Promote HBV clearance (23)
Participate in immune complex formation and DC binding Induce T cell priming (24)
Immune regulation IL-10 Inhibit effector T cells and enhance regulatory T cell function Promote immune tolerance (25, 26)
IL-35 Inhibit the proliferation of effector T cells Interfere with cellular immune responses (27, 28)
IL-6 1. Hinder HBV entry into hepatocytes and promote cccDNA decay to play a non-cytolytic antiviral activity
2. Support effector CD4+ T cell response
1. Reduce HBV infection and decrease HBV persistence
2. Increase effector CD4+ T cell responses
(2931)
(32, 33)
IFN-γ, TNF-α 1. Induce cccDNA decay and then play a non-cytolytic antiviral activity
2. Influence the development and responses of CD4+ T cells
1. Decrease HBV persistence
2. Promote effector CD4+ T cell responses
(34)
(32, 33)

ADCC, antibody-dependent cellular cytotoxicity; ADCP, antibody-dependent cellular phagocytosis; CDC, compliment-dependent cytotoxicity; MHC-I, major histocompatibility complex class I; MHC-II, major histocompatibility complex class II; DCs, dendritic cells.