2.50
Hdl Handle:
http://hdl.handle.net/10033/621193
Title:
TNF-mediated survival of CD169+ cells promotes immune activation during vesicular stomatitis virus infection.
Authors:
Shinde, Prashant V; Xu, Haifeng C; Maney, Sathish Kumar; Kloetgen, Andreas; Namineni, Sukumar; Zhuang, Yuan; Honke, Nadine; Shaabani, Namir; Bellora, Nicolas; Doerrenberg, Mareike; Trilling, Mirko; Pozdeev, Vitaly I; van Rooijen, Nico; Scheu, Stefanie; Pfeffer, Klaus; Crocker, Paul R; Tanaka, Masato; Duggimpudi, Sujitha; Knolle, Percy; Heikenwalder, Mathias; Ruland, Jürgen; Mak, Tak W; Brenner, Dirk; Pandyra, Aleksandra A; Hoell, Jessica I; Borkhardt, Arndt; Häussinger, Dieter; Lang, Karl S; Lang, Philipp A
Abstract:
Innate 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 IFN-I production during VSV infection, with a severe disease outcome. Specifically, TNF triggered RelA translocation into the nucleus of CD169+ cells; this translocation was inhibited when paracaspase MALT-1 was absent. Consequently, MALT1 deficiency resulted in reduced VSV replication, defective innate immune activation, and severe disease development. These findings indicate that TNF mediates the maintenance of CD169+ cells and innate and adaptive immune activation during VSV infection.IMPORTANCE Over the last decade, strategically placed CD169+ metallophilic macrophages in the marginal zone of the murine spleen and LN have been shown to play a very important role in host defense against viral pathogens. CD169+ macrophages are shown to activate innate and adaptive immunity via "enforced virus replication" a controlled amplification of virus particles. However, factors regulating the CD169+ macrophages remain to be studied. In this paper, we show that after Vesicular stomatitis virus infection, phagocytes produce tumor necrosis factor (TNF) which signals via TNFR1 and promote "enforced virus replication" in CD169+ macrophages. Consequently, lack of TNF or TNFR1 resulted in defective immune activation and VSV clearance.
Affiliation:
Braunschweiger Zentrum für Systembiology, Rebenring 56, 38106 Braunschweig, Germany.
Citation:
TNF-mediated survival of CD169+ cells promotes immune activation during vesicular stomatitis virus infection. 2017 J. Virol.
Journal:
Journal of virology
Issue Date:
15-Nov-2017
URI:
http://hdl.handle.net/10033/621193
DOI:
10.1128/JVI.01637-17
PubMed ID:
29142134
Type:
Article
Language:
en
ISSN:
1098-5514
Appears in Collections:
publications of the research group bioinformatics in infection research ([BRICS] BIFO)

Full metadata record

DC FieldValue Language
dc.contributor.authorShinde, Prashant Ven
dc.contributor.authorXu, Haifeng Cen
dc.contributor.authorManey, Sathish Kumaren
dc.contributor.authorKloetgen, Andreasen
dc.contributor.authorNamineni, Sukumaren
dc.contributor.authorZhuang, Yuanen
dc.contributor.authorHonke, Nadineen
dc.contributor.authorShaabani, Namiren
dc.contributor.authorBellora, Nicolasen
dc.contributor.authorDoerrenberg, Mareikeen
dc.contributor.authorTrilling, Mirkoen
dc.contributor.authorPozdeev, Vitaly Ien
dc.contributor.authorvan Rooijen, Nicoen
dc.contributor.authorScheu, Stefanieen
dc.contributor.authorPfeffer, Klausen
dc.contributor.authorCrocker, Paul Ren
dc.contributor.authorTanaka, Masatoen
dc.contributor.authorDuggimpudi, Sujithaen
dc.contributor.authorKnolle, Percyen
dc.contributor.authorHeikenwalder, Mathiasen
dc.contributor.authorRuland, Jürgenen
dc.contributor.authorMak, Tak Wen
dc.contributor.authorBrenner, Dirken
dc.contributor.authorPandyra, Aleksandra Aen
dc.contributor.authorHoell, Jessica Ien
dc.contributor.authorBorkhardt, Arndten
dc.contributor.authorHäussinger, Dieteren
dc.contributor.authorLang, Karl Sen
dc.contributor.authorLang, Philipp Aen
dc.date.accessioned2017-12-04T15:05:37Z-
dc.date.available2017-12-04T15:05:37Z-
dc.date.issued2017-11-15-
dc.identifier.citationTNF-mediated survival of CD169+ cells promotes immune activation during vesicular stomatitis virus infection. 2017 J. Virol.en
dc.identifier.issn1098-5514-
dc.identifier.pmid29142134-
dc.identifier.doi10.1128/JVI.01637-17-
dc.identifier.urihttp://hdl.handle.net/10033/621193-
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 IFN-I production during VSV infection, with a severe disease outcome. Specifically, TNF triggered RelA translocation into the nucleus of CD169+ cells; this translocation was inhibited when paracaspase MALT-1 was absent. Consequently, MALT1 deficiency resulted in reduced VSV replication, defective innate immune activation, and severe disease development. These findings indicate that TNF mediates the maintenance of CD169+ cells and innate and adaptive immune activation during VSV infection.IMPORTANCE Over the last decade, strategically placed CD169+ metallophilic macrophages in the marginal zone of the murine spleen and LN have been shown to play a very important role in host defense against viral pathogens. CD169+ macrophages are shown to activate innate and adaptive immunity via "enforced virus replication" a controlled amplification of virus particles. However, factors regulating the CD169+ macrophages remain to be studied. In this paper, we show that after Vesicular stomatitis virus infection, phagocytes produce tumor necrosis factor (TNF) which signals via TNFR1 and promote "enforced virus replication" in CD169+ macrophages. Consequently, lack of TNF or TNFR1 resulted in defective immune activation and VSV clearance.en
dc.language.isoenen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.titleTNF-mediated survival of CD169+ cells promotes immune activation during vesicular stomatitis virus infection.en
dc.typeArticleen
dc.contributor.departmentBraunschweiger Zentrum für Systembiology, Rebenring 56, 38106 Braunschweig, Germany.en
dc.identifier.journalJournal of virologyen

Related articles on PubMed

This item is licensed under a Creative Commons License
Creative Commons
All Items in HZI are protected by copyright, with all rights reserved, unless otherwise indicated.