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dc.contributor.authorFrentzel, Sarah
dc.contributor.authorKatsoulis-Dimitriou, Konstantinos
dc.contributor.authorJeron, Andreas
dc.contributor.authorSchmitz, Ingo
dc.contributor.authorBruder, Dunja
dc.date.accessioned2019-06-05T09:32:03Z
dc.date.available2019-06-05T09:32:03Z
dc.date.issued2019-05-03
dc.identifier.citationEur J Immunol. 2019 May 3. doi: 10.1002/eji.201847961.en_US
dc.identifier.issn1521-4141
dc.identifier.pmid31049948
dc.identifier.doi10.1002/eji.201847961
dc.identifier.urihttp://hdl.handle.net/10033/621800
dc.description.abstractAcquisition of effector functions in T cells is guided by transcription factors including NF-κB that itself is tightly controlled by inhibitory proteins. The atypical NF-κB inhibitor IκBNS is involved in the development of Th1, Th17 and Treg cells. However, it remained unclear to which extend IκBNS contributes to the acquisition of effector function in T cells specifically responding to a pathogen during in vivo infection. Tracking of adoptively transferred T cells in Listeria monocytogenes infected mice uncovered antigen-specific activation of CD4+ T cells following in vivo pathogen encounter to strongly rely on IκBNS . While IκBNS was largely dispensable for the acquisition of cytotoxic effector function in CD8+ T cells, IκBNS -deficient Th1 effector cells exhibited significantly reduced proliferation, marked changes in the pattern of activation marker expression and reduced production of the Th1-cell cytokines IFNγ, IL2 and TNFα. Complementary in vitro analyses using cells from novel reporter and inducible knockout mice revealed that IκBNS predominantly affects the early phase of Th1-cell differentiation while its function in terminally differentiated cells appears to be negligible. Our data suggest IκBNS as a potential target to modulate specifically CD4+ T-cell responses. This article is protected by copyright. All rights reserved.en_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectCD4+ T cellsen_US
dc.subjectIκBNSen_US
dc.subjectListeria monocytogenesen_US
dc.subjectTh1 cell differentiationen_US
dc.subjectin vivo infectionen_US
dc.titleEssential role of IκB for in vivo CD4 T cell activation, proliferation and Th1 cell differentiation during Listeria monocytogenes infection in mice.en_US
dc.typeArticleen_US
dc.contributor.departmentHZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.en_US
dc.identifier.journalEuropean journal of immunologyen_US
refterms.dateFOA2019-06-05T09:32:03Z
dc.source.journaltitleEuropean journal of immunology


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