Cutting edge: B cell-intrinsic T-bet expression is required to control chronic viral infection

Burton E. Barnett, Ryan P. Staupe, Pamela M. Odorizzi, Olesya Palko, Vesselin T. Tomov, Alison E. Mahan, Bronwyn Gunn, Diana Chen, Michael A. Paley, Galit Alter, Steven L. Reiner, Georg M. Lauer, John R. Teijaro, E. John Wherry

Research output: Contribution to journalArticlepeer-review

125 Scopus citations


The role of Ab and B cells in preventing infection is established. In contrast, the role of B cell responses in containing chronic infections remains poorly understood. IgG2a (IgG1 in humans) can prevent acute infections, and T-bet promotes IgG2a isotype switching. However, whether IgG2a and B cell-expressed T-bet influence the host-pathogen balance during persisting infections is unclear. We demonstrate that B cell-specific loss of T-bet prevents control of persisting viral infection. T-bet in B cells controlled IgG2a production, as well as mucosal localization, proliferation, glycosylation, and a broad transcriptional program. T-bet controlled a broad antiviral program in addition to IgG2a because T-bet in B cells was important, even in the presence of virusspecific IgG2a. Our data support a model in which T-bet is a universal controller of antiviral immunity across multiple immune lineages.

Original languageEnglish
Pages (from-to)1017-1022
Number of pages6
JournalJournal of Immunology
Issue number4
StatePublished - Aug 15 2016


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