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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/89307
Ver los metadatos del registro completo
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oai:ri.conicet.gov.ar:11336/89307 |
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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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1844614239044501504 |
score |
13.070432 |