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dc.contributor.authorNamineni, Sukumar
dc.contributor.authorO'Connor, Tracy
dc.contributor.authorFaure-Dupuy, Suzanne
dc.contributor.authorJohansen, Pål
dc.contributor.authorRiedl, Tobias
dc.contributor.authorLiu, Kaijing
dc.contributor.authorXu, Haifeng
dc.contributor.authorSingh, Indrabahadur
dc.contributor.authorShinde, Prashant
dc.contributor.authorLi, Fanghui
dc.contributor.authorPandyra, Aleksandra
dc.contributor.authorSharma, Piyush
dc.contributor.authorRingelhan, Marc
dc.contributor.authorMuschaweckh, Andreas
dc.contributor.authorBorst, Katharina
dc.contributor.authorBlank, Patrick
dc.contributor.authorLampl, Sandra
dc.contributor.authorDurantel, David
dc.contributor.authorFarhat, Rayan
dc.contributor.authorWeber, Achim
dc.contributor.authorLenggenhager, Daniela
dc.contributor.authorKündig, Thomas M
dc.contributor.authorStaeheli, Peter
dc.contributor.authorProtzer, Ulrike
dc.contributor.authorWohlleber, Dirk
dc.contributor.authorHolzmann, Bernhard
dc.contributor.authorBinder, Marco
dc.contributor.authorBreuhahn, Kai
dc.contributor.authorAssmus, Lisa Mareike
dc.contributor.authorNattermann, Jacob
dc.contributor.authorAbdullah, Zeinab
dc.contributor.authorRolland, Maude
dc.contributor.authorDejardin, Emmanuel
dc.contributor.authorLang, Philipp A
dc.contributor.authorLang, Karl S
dc.contributor.authorKarin, Michael
dc.contributor.authorLucifora, Julie
dc.contributor.authorKalinke, Ulrich
dc.contributor.authorKnolle, Percy A
dc.contributor.authorHeikenwalder, Mathias
dc.date.accessioned2020-02-10T10:39:39Z
dc.date.available2020-02-10T10:39:39Z
dc.date.issued2020-01-15
dc.identifier.citationJ Hepatol. 2020 Jan 15. pii: S0168-8278(20)30010-6. doi: 10.1016/j.jhep.2019.12.019.en_US
dc.identifier.issn1600-0641
dc.identifier.pmid31954207
dc.identifier.doi10.1016/j.jhep.2019.12.019
dc.identifier.urihttp://hdl.handle.net/10033/622125
dc.description.abstractUsing lymphocytic choriomeningitis virus (LCMV) as a model of liver infection, we first assessed the role of myeloid cells by depletion prior to infection. We investigated the role of hepatocyte-intrinsic innate immune signaling by infecting mice lacking canonical NF-κB signaling (IKKβΔHep) specifically in hepatocytes. In addition, mice lacking hepatocyte-specific interferon-α/β signaling-(IFNARΔHep), or interferon-α/β signaling in myeloid cells-(IFNARΔMyel) were infected.en_US
dc.publisherElsevieren_US
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectCytotoxic T cellsen_US
dc.subjectHepatocytesen_US
dc.subjectInnate Immune responsesen_US
dc.subjectInterferon Stimulated Genesen_US
dc.subjectNF-kB signalingen_US
dc.subjectPRRsen_US
dc.titleA dual role for hepatocyte-intrinsic canonical NF-κB signaling in virus control.en_US
dc.typeArticleen_US
dc.contributor.departmentTWINCORE, Zentrum für experimentelle und klinische Infektionsforschung GmbH,Feodor-Lynen Str. 7, 30625 Hannover, Germany.en_US
dc.identifier.journalJournal of Hepatologyen_US
refterms.dateFOA2020-02-10T10:39:40Z
dc.source.journaltitleJournal of hepatology


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