| Literature DB >> 34772811 |
Kerstin Narr1, Yusuf I Ertuna1, Benedict Fallet1, Karen Cornille1, Mirela Dimitrova1, Anna-Friederike Marx1, Katrin Martin1, Tiago Abreu Mota1, Marco Künzli2, David Schreiner2, Tobias M Brunner3,4, Mario Kreutzfeldt5,6, Ingrid Wagner6, Florian Geier7, Lukas Bestmann8, Max Löhning3,4, Doron Merkler5,6, Carolyn G King2, Daniel D Pinschewer9.
Abstract
Chronic viral infections subvert protective B cell immunity. An early type I interferon (IFN-I)-driven bias to short-lived plasmablast differentiation leads to clonal deletion, so-called "decimation," of antiviral memory B cells. Therefore, prophylactic countermeasures against decimation remain an unmet need. We show that vaccination-induced CD4 T cells prevented the decimation of naïve and memory B cells in chronically lymphocytic choriomeningitis virus (LCMV)-infected mice. Although these B cell responses were largely T independent when IFN-I was blocked, preexisting T help assured their sustainability under conditions of IFN-I-driven inflammation by instructing a germinal center B cell transcriptional program. Prevention of decimation depended on T cell-intrinsic Bcl6 and Tfh progeny formation. Antigen presentation by B cells, interactions with antigen-specific T helper cells, and costimulation by CD40 and ICOS were also required. Importantly, B cell-mediated virus control averted Th1-driven immunopathology in LCMV-challenged animals with preexisting CD4 T cell immunity. Our findings show that vaccination-induced Tfh cells represent a cornerstone of effective B cell immunity to chronic virus challenge, pointing the way toward more effective B cell-based vaccination against persistent viral diseases.Entities:
Keywords: B cell decimation; T cell help; T follicular helper cells; chronic viral infection; interferon
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Year: 2021 PMID: 34772811 PMCID: PMC8694065 DOI: 10.1073/pnas.2108157118
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN: 0027-8424 Impact factor: 11.205