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Review
. 2017 Nov:321:26-34.
doi: 10.1016/j.cellimm.2017.04.012. Epub 2017 Jul 11.

T-bet-expressing B cells during HIV and HCV infections

James J Knox  1 , David E Kaplan  2 , Michael R Betts  3
Affiliations
Review

T-bet-expressing B cells during HIV and HCV infections

James J Knox et al. Cell Immunol. 2017 Nov.

Abstract

T-bet-expressing B cells, first identified as perpetuators of autoimmunity, were recently shown to be critical for murine antiviral responses. While their role in human viral infections remains unclear, B cells expressing T-bet or demonstrating a related phenotype have been described in individuals chronically infected with HIV or HCV, suggesting these cells represent a component of human antiviral responses. In this review, we discuss the induction of T-bet in B cells following both HIV and HCV infections, the factors driving T-bet+ B cell expansions, T-bet's relationship to atypical memory B cells, and the consequences of T-bet induction. We propose potential antiviral roles for T-bet+ B cells and discuss whether this population poses any utility to the HIV and HCV immune responses.

Keywords: B cells; HCV; HIV; Humoral immunology; T-bet.

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Figures

Fig. 1
Fig. 1
T-bet expression by B cell subsets of a healthy human donor. (A) Total B cells, defined by CD19 expression, from the peripheral blood mononuclear cells of an HIV-negative, HCV-negative human donor are depicted. Gates display the identification of naïve (black), resting memory (blue), and CD21-negative (purple) B cell subsets. (B) CD21-negative B cells are separated into CD85j high (red) and CD85j low (grey) subsets. (C) Histogram depicting T-bet expression of the aforementioned B cell subsets.
Fig. 2
Fig. 2
Model proposing the induction and differentiation of T-bet-expressing B cells by viral infections. T-bet is induced in B cells following TLR/cytokine/BCR stimulation during acute viral infection, leading to T-bethighCD21−CD85jhigh subset development. Upon viral clearance (yellow fever virus (YFV) and vaccinia virus (VV) vaccinations), the blood T-bethigh subset contracts in size, potentially due to trafficking of cells into tissues, differentiation into a resting phenotype (T-betlow), or cell death. However, during chronic HIV and HCV infections, persistent viral replication and immune activation induces expansion and maintenance of a large T-bethigh B cell pool. Individuals cured of HCV offer a unique opportunity to assess the fate of HCV-induced T-bet+ B cells following antigen clearance.
See this image and copyright information in PMC

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