Hepatitis B surface antigen impairs TLR4 signaling by upregulating A20 expression in monocytes.

Clearance HBsAg indicates a functional cure of HBV infection, but in chronic hepatitis B (CHB), it is hard to achieve. HBsAg has been found to regulate anti-viral immune responses, such as the activation of TLR. Our previous jobs proved that HBsAg negatively correlates with TLR2/4 activation in monocytes from CHB patients and blocks TLR2 ligand-indcuced IL-12 production in monocytes. However, how TLR4 signaling is affected by HBsAg remains unknown. In this study, we not only observed impaired TLR4 activation after pretreated monocytes with HBsAg but also identified HBsAg-induced A20 play a role in this impairment, which suggests that targeting A20 may be a viable strategy to restore monocyte functions in CHB.