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dc.contributor.authorRing, Sarah
dc.contributor.authorEggers, Lars
dc.contributor.authorBehrends, Jochen
dc.contributor.authorWutkowski, Adam
dc.contributor.authorSchwudke, Dominik
dc.contributor.authorKröger, Andrea
dc.contributor.authorHierweger, Alexandra Maximiliane
dc.contributor.authorHölscher, Christoph
dc.contributor.authorGabriel, Gülsah
dc.contributor.authorSchneider, Bianca E.
dc.creatorRing, S.
dc.date.accessioned2019-09-06T07:55:22Z
dc.date.available2019-09-06T07:55:22Z
dc.date.issued2019-01-01
dc.identifier.citationJCI Insight. 2019 Apr 18;5. pii: 126533. doi: 10.1172/jci.insight.126533.en_US
dc.identifier.pmid30998505
dc.identifier.doi10.1172/jci.insight.126533
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85070660696&origin=inward
dc.identifier.urihttp://hdl.handle.net/10033/621928
dc.description.abstractEpidemiological findings indicate that coinfection with influenza viruses is associated with an increased risk of death in patients suffering from tuberculosis but the underlying pathomechanisms are not well understood. In this study, we demonstrate that influenza A virus (IAV) coinfection rapidly impairs control of Mycobacterium tuberculosis (Mtb) in C57BL/6 mice. IAV coinfection was associated with significantly increased bacterial loads, reduced survival and a substantial modulation of innate and adaptive immune defenses including an impaired onset and development of Mtb-specific CD4+ T cell responses and the accumulation of macrophages with increased arginase-1 production in the lungs. Our findings strongly indicate that IAV coinfection compromises the host's ability to control Mtb infection via the production of IL-10 which was rapidly induced upon viral infection. The blockade of IL-10 receptor signaling reduced the bacterial load in coinfected mice to a level comparable with that in Mtb-only-infected animals. Taken together, our data suggest that IL-10 signaling constitutes a major pathway that enhances susceptibility to Mtb during concurrent IAV infectionen_US
dc.language.isoenen_US
dc.publisherAmerican Society for Clinical Investigationen_US
dc.relation.ispartofJCI Insight
dc.relation.ispartofseries10en_US
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.titleBlocking IL-10 receptor signaling ameliorates Mycobacterium tuberculosis infection during influenza-induced exacerbationen_US
dc.typeArticleen_US
dc.contributor.departmentHZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.en_US
dc.identifier.journalJCI Insighten_US
dc.identifier.eid2-s2.0-85070660696
dc.identifier.scopusidSCOPUS_ID:85070660696
dc.relation.volume4
refterms.dateFOA2019-09-06T07:55:22Z


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