Tumor Necrosis Factor-Mediated Survival of CD169 + Cells Promotes Immune Activation during Vesicular Stomatitis Virus Infection

Autores
Shinde, Prashant V.; Xu, Haifeng C.; Maney, Sathish Kumar; Kloetgen, Andreas; Namineni, Sukumar; Zhuang, Yuan; Honke, Nadine; Shaabani, Namir; Bellora, Nicolás; 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.
Año de publicación
2018
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
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 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.
Fil: Shinde, Prashant V.. Heinrich Heine University; Alemania
Fil: Xu, Haifeng C.. Heinrich Heine University; Alemania
Fil: Maney, Sathish Kumar. Heinrich Heine University; Alemania
Fil: Kloetgen, Andreas. Heinrich Heine University; Alemania
Fil: Namineni, Sukumar. Helmholtz Zentrum Munich; Alemania
Fil: Zhuang, Yuan. Heinrich Heine University; Alemania
Fil: Honke, Nadine. Heinrich Heine University; Alemania
Fil: Shaabani, Namir. The Scripps Research Institute; Estados Unidos
Fil: Bellora, Nicolás. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Patagonia Norte. Instituto Andino Patagónico de Tecnologías Biológicas y Geoambientales. Universidad Nacional del Comahue. Instituto Andino Patagónico de Tecnologías Biológicas y Geoambientales.; Argentina
Fil: Doerrenberg, Mareike. Heinrich Heine University; Alemania
Fil: Trilling, Mirko. Universitat Essen; Alemania
Fil: Pozdeev, Vitaly I.. Heinrich Heine University; Alemania
Fil: van Rooijen, Nico. Department Of Cell Biology, Vrije University; Países Bajos
Fil: Scheu, Stefanie. Heinrich Heine University; Alemania
Fil: Pfeffer, Klaus. Heinrich Heine University; Alemania
Fil: Crocker, Paul R.. University of Dundee; Reino Unido
Fil: Tanaka, Masato. Tokyo University. Laboratory Of Immune Regulation; Japón
Fil: Duggimpudi, Sujitha. Heinrich Heine University; Alemania
Fil: Knolle, Percy. Helmholtz Zentrum Munich; Alemania
Fil: Heikenwalder, Mathias. Helmholtz Zentrum Munich; Alemania
Fil: Ruland, Jürgen. Universitat Technical Zu Munich; Alemania
Fil: Mak, Tak W.. University Health Network; Canadá
Fil: Brenner, Dirk. University of Southern Denmark; Dinamarca
Fil: Pandyra, Aleksandra A.. Universitat Essen; Alemania
Fil: Hoell, Jessica I.. Heinrich Heine University; Alemania
Fil: Borkhardt, Arndt. Heinrich Heine University; Alemania
Fil: Häussinger, Dieter. Heinrich Heine University; Alemania
Fil: Lang, Karl S.. Universitat Essen; Alemania
Fil: Lang, Philipp A.. Heinrich Heine University; Alemania
Materia
INNATE IMMUNITY
INNATE IMMUNITY
INTERFERON
INTERFERONS
MALT1
NF-ΚB
TNF
TUMOR NECROSIS FACTOR
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/89307

id CONICETDig_468be1b96258a946738ab52d2da2622e
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network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Tumor Necrosis Factor-Mediated Survival of CD169 + Cells Promotes Immune Activation during Vesicular Stomatitis Virus InfectionShinde, Prashant V.Xu, Haifeng C.Maney, Sathish KumarKloetgen, AndreasNamineni, SukumarZhuang, YuanHonke, NadineShaabani, NamirBellora, NicolásDoerrenberg, MareikeTrilling, MirkoPozdeev, Vitaly I.van Rooijen, NicoScheu, StefaniePfeffer, KlausCrocker, Paul R.Tanaka, MasatoDuggimpudi, SujithaKnolle, PercyHeikenwalder, MathiasRuland, JürgenMak, Tak W.Brenner, DirkPandyra, Aleksandra A.Hoell, Jessica I.Borkhardt, ArndtHäussinger, DieterLang, Karl S.Lang, Philipp A.INNATE IMMUNITYINNATE IMMUNITYINTERFERONINTERFERONSMALT1NF-ΚBTNFTUMOR NECROSIS FACTORhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1https://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Innate 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.Fil: Shinde, Prashant V.. Heinrich Heine University; AlemaniaFil: Xu, Haifeng C.. Heinrich Heine University; AlemaniaFil: Maney, Sathish Kumar. Heinrich Heine University; AlemaniaFil: Kloetgen, Andreas. Heinrich Heine University; AlemaniaFil: Namineni, Sukumar. Helmholtz Zentrum Munich; AlemaniaFil: Zhuang, Yuan. Heinrich Heine University; AlemaniaFil: Honke, Nadine. Heinrich Heine University; AlemaniaFil: Shaabani, Namir. The Scripps Research Institute; Estados UnidosFil: Bellora, Nicolás. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Patagonia Norte. Instituto Andino Patagónico de Tecnologías Biológicas y Geoambientales. Universidad Nacional del Comahue. Instituto Andino Patagónico de Tecnologías Biológicas y Geoambientales.; ArgentinaFil: Doerrenberg, Mareike. Heinrich Heine University; AlemaniaFil: Trilling, Mirko. Universitat Essen; AlemaniaFil: Pozdeev, Vitaly I.. Heinrich Heine University; AlemaniaFil: van Rooijen, Nico. Department Of Cell Biology, Vrije University; Países BajosFil: Scheu, Stefanie. Heinrich Heine University; AlemaniaFil: Pfeffer, Klaus. Heinrich Heine University; AlemaniaFil: Crocker, Paul R.. University of Dundee; Reino UnidoFil: Tanaka, Masato. Tokyo University. Laboratory Of Immune Regulation; JapónFil: Duggimpudi, Sujitha. Heinrich Heine University; AlemaniaFil: Knolle, Percy. Helmholtz Zentrum Munich; AlemaniaFil: Heikenwalder, Mathias. Helmholtz Zentrum Munich; AlemaniaFil: Ruland, Jürgen. Universitat Technical Zu Munich; AlemaniaFil: Mak, Tak W.. University Health Network; CanadáFil: Brenner, Dirk. University of Southern Denmark; DinamarcaFil: Pandyra, Aleksandra A.. Universitat Essen; AlemaniaFil: Hoell, Jessica I.. Heinrich Heine University; AlemaniaFil: Borkhardt, Arndt. Heinrich Heine University; AlemaniaFil: Häussinger, Dieter. Heinrich Heine University; AlemaniaFil: Lang, Karl S.. Universitat Essen; AlemaniaFil: Lang, Philipp A.. Heinrich Heine University; AlemaniaAmerican Society for Microbiology2018-02info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/89307Shinde, Prashant V.; Xu, Haifeng C.; Maney, Sathish Kumar; Kloetgen, Andreas; Namineni, Sukumar; et al.; Tumor Necrosis Factor-Mediated Survival of CD169 + Cells Promotes Immune Activation during Vesicular Stomatitis Virus Infection; American Society for Microbiology; Journal of Virology; 92; 3; 2-2018; 1-180022-538XCONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://jvi.asm.org/lookup/doi/10.1128/JVI.01637-17info:eu-repo/semantics/altIdentifier/doi/10.1128/JVI.01637-17info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:24:14Zoai:ri.conicet.gov.ar:11336/89307instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 10:24:15.122CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Tumor Necrosis Factor-Mediated Survival of CD169 + Cells Promotes Immune Activation during Vesicular Stomatitis Virus Infection
title Tumor Necrosis Factor-Mediated Survival of CD169 + Cells Promotes Immune Activation during Vesicular Stomatitis Virus Infection
spellingShingle Tumor Necrosis Factor-Mediated Survival of CD169 + Cells Promotes Immune Activation during Vesicular Stomatitis Virus Infection
Shinde, Prashant V.
INNATE IMMUNITY
INNATE IMMUNITY
INTERFERON
INTERFERONS
MALT1
NF-ΚB
TNF
TUMOR NECROSIS FACTOR
title_short Tumor Necrosis Factor-Mediated Survival of CD169 + Cells Promotes Immune Activation during Vesicular Stomatitis Virus Infection
title_full Tumor Necrosis Factor-Mediated Survival of CD169 + Cells Promotes Immune Activation during Vesicular Stomatitis Virus Infection
title_fullStr Tumor Necrosis Factor-Mediated Survival of CD169 + Cells Promotes Immune Activation during Vesicular Stomatitis Virus Infection
title_full_unstemmed Tumor Necrosis Factor-Mediated Survival of CD169 + Cells Promotes Immune Activation during Vesicular Stomatitis Virus Infection
title_sort Tumor Necrosis Factor-Mediated Survival of CD169 + Cells Promotes Immune Activation during Vesicular Stomatitis Virus Infection
dc.creator.none.fl_str_mv Shinde, Prashant V.
Xu, Haifeng C.
Maney, Sathish Kumar
Kloetgen, Andreas
Namineni, Sukumar
Zhuang, Yuan
Honke, Nadine
Shaabani, Namir
Bellora, Nicolás
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.
author Shinde, Prashant V.
author_facet Shinde, Prashant V.
Xu, Haifeng C.
Maney, Sathish Kumar
Kloetgen, Andreas
Namineni, Sukumar
Zhuang, Yuan
Honke, Nadine
Shaabani, Namir
Bellora, Nicolás
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.
author_role author
author2 Xu, Haifeng C.
Maney, Sathish Kumar
Kloetgen, Andreas
Namineni, Sukumar
Zhuang, Yuan
Honke, Nadine
Shaabani, Namir
Bellora, Nicolás
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.
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv INNATE IMMUNITY
INNATE IMMUNITY
INTERFERON
INTERFERONS
MALT1
NF-ΚB
TNF
TUMOR NECROSIS FACTOR
topic INNATE IMMUNITY
INNATE IMMUNITY
INTERFERON
INTERFERONS
MALT1
NF-ΚB
TNF
TUMOR NECROSIS FACTOR
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv 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 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.
Fil: Shinde, Prashant V.. Heinrich Heine University; Alemania
Fil: Xu, Haifeng C.. Heinrich Heine University; Alemania
Fil: Maney, Sathish Kumar. Heinrich Heine University; Alemania
Fil: Kloetgen, Andreas. Heinrich Heine University; Alemania
Fil: Namineni, Sukumar. Helmholtz Zentrum Munich; Alemania
Fil: Zhuang, Yuan. Heinrich Heine University; Alemania
Fil: Honke, Nadine. Heinrich Heine University; Alemania
Fil: Shaabani, Namir. The Scripps Research Institute; Estados Unidos
Fil: Bellora, Nicolás. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Patagonia Norte. Instituto Andino Patagónico de Tecnologías Biológicas y Geoambientales. Universidad Nacional del Comahue. Instituto Andino Patagónico de Tecnologías Biológicas y Geoambientales.; Argentina
Fil: Doerrenberg, Mareike. Heinrich Heine University; Alemania
Fil: Trilling, Mirko. Universitat Essen; Alemania
Fil: Pozdeev, Vitaly I.. Heinrich Heine University; Alemania
Fil: van Rooijen, Nico. Department Of Cell Biology, Vrije University; Países Bajos
Fil: Scheu, Stefanie. Heinrich Heine University; Alemania
Fil: Pfeffer, Klaus. Heinrich Heine University; Alemania
Fil: Crocker, Paul R.. University of Dundee; Reino Unido
Fil: Tanaka, Masato. Tokyo University. Laboratory Of Immune Regulation; Japón
Fil: Duggimpudi, Sujitha. Heinrich Heine University; Alemania
Fil: Knolle, Percy. Helmholtz Zentrum Munich; Alemania
Fil: Heikenwalder, Mathias. Helmholtz Zentrum Munich; Alemania
Fil: Ruland, Jürgen. Universitat Technical Zu Munich; Alemania
Fil: Mak, Tak W.. University Health Network; Canadá
Fil: Brenner, Dirk. University of Southern Denmark; Dinamarca
Fil: Pandyra, Aleksandra A.. Universitat Essen; Alemania
Fil: Hoell, Jessica I.. Heinrich Heine University; Alemania
Fil: Borkhardt, Arndt. Heinrich Heine University; Alemania
Fil: Häussinger, Dieter. Heinrich Heine University; Alemania
Fil: Lang, Karl S.. Universitat Essen; Alemania
Fil: Lang, Philipp A.. Heinrich Heine University; Alemania
description 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 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.
publishDate 2018
dc.date.none.fl_str_mv 2018-02
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/89307
Shinde, Prashant V.; Xu, Haifeng C.; Maney, Sathish Kumar; Kloetgen, Andreas; Namineni, Sukumar; et al.; Tumor Necrosis Factor-Mediated Survival of CD169 + Cells Promotes Immune Activation during Vesicular Stomatitis Virus Infection; American Society for Microbiology; Journal of Virology; 92; 3; 2-2018; 1-18
0022-538X
CONICET Digital
CONICET
url http://hdl.handle.net/11336/89307
identifier_str_mv Shinde, Prashant V.; Xu, Haifeng C.; Maney, Sathish Kumar; Kloetgen, Andreas; Namineni, Sukumar; et al.; Tumor Necrosis Factor-Mediated Survival of CD169 + Cells Promotes Immune Activation during Vesicular Stomatitis Virus Infection; American Society for Microbiology; Journal of Virology; 92; 3; 2-2018; 1-18
0022-538X
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://jvi.asm.org/lookup/doi/10.1128/JVI.01637-17
info:eu-repo/semantics/altIdentifier/doi/10.1128/JVI.01637-17
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv American Society for Microbiology
publisher.none.fl_str_mv American Society for Microbiology
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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