HBV induces inhibitory FcRL receptor on B cells and dysregulates B cell-T follicular helper cell axis.

ABSTRACT: Spontaneous or treatment induced seroconversion in chronic HBV infection is rare and generation of anti-HBs antibodies is the current goal of HBV therapeutics. Here we investigated B and follicular T helper (Tfh) cell defects that persist in HBV infection despite long-term nucleos(t)ide analog (NUC) treatment and possible mechanisms behind them. RNA sequencing revealed that patient B cells have upregulated expression of multiple inhibitory receptors including members of FcRL family and downregulation of genes involved in antigen presentation. An expansion of atypical memory CD19⁺CD10^-CD27^-CD21^- subset of B cells, that express high levels of FcRL5, is persistently present in patients. HBs antigen specific IgG response is concentrated in classical

SUBMITTER: Poonia B 

PROVIDER: S-EPMC6193006 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature