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dc.contributor.authorVashist, Neha
dc.contributor.authorTrittel, Stephanie
dc.contributor.authorEbensen, Thomas
dc.contributor.authorChambers, Benedict J
dc.contributor.authorGuzmán, Carlos A
dc.contributor.authorRiese, Peggy
dc.date.accessioned2018-11-28T09:53:06Z
dc.date.available2018-11-28T09:53:06Z
dc.date.issued2018-01-01
dc.identifier.issn1664-3224
dc.identifier.pmid29623077
dc.identifier.doi10.3389/fimmu.2018.00505
dc.identifier.urihttp://hdl.handle.net/10033/621588
dc.description.abstractInnate lymphoid cells (ILCs) represent diversified subsets of effector cells as well as immune regulators of mucosal immunity and are classified into group 1 ILCs, group 2 ILCs, and group 3 ILCs. Group 1 ILCs encompass natural killer (NK) cells and non-NK ILCs (ILC1s) and mediate their functionality via the rapid production of IFN-γ and TNF-α. The current knowledge of ILC1s mainly associates them to inflammatory processes. Much less is known about their regulation during infection and their capacity to interact with cells of the adaptive immune system. The present study dissected the role of ILC1s during early influenza A virus infection, thereby revealing their impact on the antiviral response. Exploiting in vitro and in vivo H1N1 infection systems, a cross-talk of ILC1s with cells of the innate and the adaptive immunity was demonstrated, which contributes to anti-influenza immunity. A novel association of ILC1 functionality and the expression of the glucocorticoid-induced TNFR-related protein (GITR) was observed, which hints toward a so far undescribed role of GITR in regulating ILC1 responsiveness. Overexpression of GITR inhibits IFN-γ production by ILC1s, whereas partial reduction of GITR expression can reverse this effect, thereby regulating ILC1 functionality. These new insights into ILC1 biology define potential intervention targets to modulate the functional properties of ILC1s, thus contributing toward the development of new immune interventions against influenza.en_US
dc.publisherFrontiersen_US
dc.rightsAttribution-NonCommercial-ShareAlike 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/us/*
dc.subjectcross-talken_US
dc.subjectglucocorticoid-induced TNFR-related proteinen_US
dc.subjectinfluenzaen_US
dc.subjectinnate lymphoid cell 1en_US
dc.subjectregulationen_US
dc.titleInfluenza-Activated ILC1s Contribute to Antiviral Immunity Partially Influenced by Differential GITR Expression.en_US
dc.typeArticleen_US
dc.contributor.departmentHZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.en_US
refterms.dateFOA2018-11-28T09:53:06Z
dc.source.journaltitleFrontiers in immunology


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