1. Cutting Edge: B Cell-Intrinsic T-bet Expression Is Required To Control Chronic Viral Infection.
- Author
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Barnett BE, Staupe RP, Odorizzi PM, Palko O, Tomov VT, Mahan AE, Gunn B, Chen D, Paley MA, Alter G, Reiner SL, Lauer GM, Teijaro JR, and Wherry EJ
- Subjects
- Animals, Cell Separation, Chronic Disease, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Flow Cytometry, Immunoglobulin G immunology, Lymphocytic choriomeningitis virus, Mice, Mice, Transgenic, Oligonucleotide Array Sequence Analysis, B-Lymphocyte Subsets immunology, B-Lymphocytes immunology, Lymphocytic Choriomeningitis immunology, T-Box Domain Proteins immunology
- Abstract
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 virus-specific IgG2a. Our data support a model in which T-bet is a universal controller of antiviral immunity across multiple immune lineages., (Copyright © 2016 by The American Association of Immunologists, Inc.)
- Published
- 2016
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