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

ABSTRACT: Toll-like receptors (TLRs) play a crucial role in eliminating viral infection. Conversely, viruses have evolved various strategies to disrupt TLR signaling during chronic infection. In the case of hepatitis B virus (HBV), we previously reported that plasma hepatitis B surface antigen (HBsAg) is closely associated with impaired TLR responses in peripheral blood mononuclear cells from chronic hepatitis B (CHB) patients, but the reasons remain unclear. In this study, we investigated the mechanism by which HBsAg suppresses TLR4 signaling in monocyte cell lines. The monocyte cell line THP-1 was pretreated with HBsAg, followed by lipopolysaccharide (LPS) stimulation. Levels of proinflammatory cytokines and the activation of NF-κB, c-JNK, and ERK were examined. We found that HBsAg did not influen

SUBMITTER: Wang C 

PROVIDER: S-EPMC11448406 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature