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Article: Tumor necrosis factor-mediated survival of CD169+ cells promotes immune activation during vesicular stomatitis virus infection

TitleTumor necrosis factor-mediated survival of CD169<sup>+</sup> cells promotes immune activation during vesicular stomatitis virus infection
Authors
KeywordsTumor necrosis factor
Innate immunity
MALT1
TNF
NF-κB
Interferon
Interferons
Issue Date2018
Citation
Journal of Virology, 2018, v. 92, n. 3, article no. e01637-17 How to Cite?
AbstractInnate immune activation is essential to mount an effective antiviral response and to prime adaptive immunity. Although a crucial role of CD169+ cells during vesicular stomatitis virus (VSV) infections is increasingly recognized, factors regulating CD169+ cells during viral infections remain unclear. Here, we show that tumor necrosis factor is produced by CD11b+ Ly6C+ Ly6G+ cells following infection with VSV. The absence of TNF or TNF receptor 1 (TNFR1) resulted in reduced numbers of CD169+ cells and in reduced type I interferon (IFN-I) production during VSV infection, with a severe disease outcome. Specifically, TNF triggered RelA translocation into the nuclei of CD169+ cells; this translocation was inhibited when the paracaspase MALT-1 was absent. Consequently, MALT1 deficiency resulted in reduced VSV replication, defective innate immune activation, and development of severe disease. These findings indicate that TNF mediates the maintenance of CD169+ cells and innate and adaptive immune activation during VSV infection.
Persistent Identifierhttp://hdl.handle.net/10722/293059
ISSN
2023 Impact Factor: 4.0
2023 SCImago Journal Rankings: 1.378
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorShinde, Prashant V.-
dc.contributor.authorXu, Haifeng C.-
dc.contributor.authorManey, Sathish Kumar-
dc.contributor.authorKloetgen, Andreas-
dc.contributor.authorNamineni, Sukumar-
dc.contributor.authorZhuang, Yuan-
dc.contributor.authorHonke, Nadine-
dc.contributor.authorShaabani, Namir-
dc.contributor.authorBellora, Nicolas-
dc.contributor.authorDoerrenberg, Mareike-
dc.contributor.authorTrilling, Mirko-
dc.contributor.authorPozdeev, Vitaly I.-
dc.contributor.authorvan Rooijen, Nico-
dc.contributor.authorScheu, Stefanie-
dc.contributor.authorPfeffer, Klaus-
dc.contributor.authorCrocker, Paul R.-
dc.contributor.authorTanaka, Masato-
dc.contributor.authorDuggimpudi, Sujitha-
dc.contributor.authorKnolle, Percy-
dc.contributor.authorHeikenwalder, Mathias-
dc.contributor.authorRuland, Jürgen-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorBrenner, Dirk-
dc.contributor.authorPandyra, Aleksandra A.-
dc.contributor.authorHoell, Jessica I.-
dc.contributor.authorBorkhardt, Arndt-
dc.contributor.authorHäussinger, Dieter-
dc.contributor.authorLang, Karl S.-
dc.contributor.authorLang, Philipp A.-
dc.date.accessioned2020-11-17T14:57:47Z-
dc.date.available2020-11-17T14:57:47Z-
dc.date.issued2018-
dc.identifier.citationJournal of Virology, 2018, v. 92, n. 3, article no. e01637-17-
dc.identifier.issn0022-538X-
dc.identifier.urihttp://hdl.handle.net/10722/293059-
dc.description.abstractInnate immune activation is essential to mount an effective antiviral response and to prime adaptive immunity. Although a crucial role of CD169+ cells during vesicular stomatitis virus (VSV) infections is increasingly recognized, factors regulating CD169+ cells during viral infections remain unclear. Here, we show that tumor necrosis factor is produced by CD11b+ Ly6C+ Ly6G+ cells following infection with VSV. The absence of TNF or TNF receptor 1 (TNFR1) resulted in reduced numbers of CD169+ cells and in reduced type I interferon (IFN-I) production during VSV infection, with a severe disease outcome. Specifically, TNF triggered RelA translocation into the nuclei of CD169+ cells; this translocation was inhibited when the paracaspase MALT-1 was absent. Consequently, MALT1 deficiency resulted in reduced VSV replication, defective innate immune activation, and development of severe disease. These findings indicate that TNF mediates the maintenance of CD169+ cells and innate and adaptive immune activation during VSV infection.-
dc.languageeng-
dc.relation.ispartofJournal of Virology-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectTumor necrosis factor-
dc.subjectInnate immunity-
dc.subjectMALT1-
dc.subjectTNF-
dc.subjectNF-κB-
dc.subjectInterferon-
dc.subjectInterferons-
dc.titleTumor necrosis factor-mediated survival of CD169<sup>+</sup> cells promotes immune activation during vesicular stomatitis virus infection-
dc.typeArticle-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1128/JVI.01637-17-
dc.identifier.pmid29142134-
dc.identifier.pmcidPMC5774891-
dc.identifier.scopuseid_2-s2.0-85040672435-
dc.identifier.volume92-
dc.identifier.issue3-
dc.identifier.spagearticle no. e01637-17-
dc.identifier.epagearticle no. e01637-17-
dc.identifier.eissn1098-5514-
dc.identifier.isiWOS:000423571600008-
dc.identifier.issnl0022-538X-

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