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Tumor necrosis factormediated survival of CD169+ cells promotes immune activation during vesicular stomatitis virus infection
- Source :
- Shinde, P V, Xu, H C, Maney, S K, Kloetgen, A, Namineni, S, Zhuang, Y, Honke, N, Shaabani, N, Bellora, N, Doerrenberg, M, Trilling, M, Pozdeev, V I, van Rooijen, N, Scheu, S, Pfeffer, K, Crocker, P R, Tanaka, M, Duggimpudi, S, Knolle, P, Heikenwalder, M, Ruland, J R, Mak, T W, Brenner, D, Pandyra, A A, Hoell, J I, Borkhardt, A, Häussinger, D, Lang, K S & Lang, P A 2018, ' Tumor necrosis factormediated survival of CD169+ cells promotes immune activation during vesicular stomatitis virus infection ', Journal of Virology, vol. 92, no. 3, e01637-17 . https://doi.org/10.1128/JVI.01637-17, CONICET Digital (CONICET), Consejo Nacional de Investigaciones Científicas y Técnicas, instacron:CONICET, Shinde, P V, Xu, H C, Maney, S K, Kloetgen, A, Namineni, S, Zhuang, Y, Honke, N, Shaabani, N, Bellora, N, Doerrenberg, M, Trilling, M, Pozdeev, V I, van Rooijen, N, Scheu, S, Pfeffer, K, Crocker, P R, Tanaka, M, Duggimpudi, S, Knolle, P, Heikenwalder, M, Ruland, J, Mak, T W, Brenner, D, Pandyra, A A, Hoell, J I, Borkhardt, A, Häussinger, D, Lang, K S & Lang, P A 2018, ' Tumor Necrosis Factor-Mediated Survival of CD169+ Cells Promotes Immune Activation during Vesicular Stomatitis Virus Infection ', Journal of Virology, vol. 92, no. 3, e01637-17, pp. e01637-17 . https://doi.org/10.1128/JVI.01637-17, Journal of virology, J. Virol. 92, DOI: 10.1128/JVI.01637-17 (2017), Journal of Virology, 92(3):e01637-17. American Society for Microbiology, Journal of Virology
- Publication Year :
- 2018
-
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 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
- Subjects :
- 0301 basic medicine
Interferon Type I/immunology
Sialic Acid Binding Ig-like Lectin 1
animal diseases
Transcription Factor RelA/metabolism
viruses
TNF
Medizin
Cellular Response to Infection
Macrophages/immunology
Adaptive Immunity
Virus Replication
INTERFERONS
NF-κB
purl.org/becyt/ford/1 [https]
Mice
0302 clinical medicine
Interferon
Vesicular Stomatitis/immunology
innate immunity
Vesiculovirus/physiology
biology
interferon
Bioquímica y Biología Molecular
Acquired immune system
3. Good health
ddc
interferons
Receptors, Tumor Necrosis Factor, Type I
Vesicular stomatitis virus
030220 oncology & carcinogenesis
Interferon Type I
Tumor necrosis factor alpha
Vesicular Stomatitis
NF-ΚB
CIENCIAS NATURALES Y EXACTAS
medicine.drug
INTERFERON
tumor necrosis factor
Immunology
chemical and pharmacologic phenomena
Microbiology
Virus
Ciencias Biológicas
03 medical and health sciences
Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein/genetics
Virology
medicine
Animals
purl.org/becyt/ford/1.6 [https]
Innate immune system
Tumor Necrosis Factor-alpha
TUMOR NECROSIS FACTOR
Macrophages
MALT1
Transcription Factor RelA
Vesiculovirus
biochemical phenomena, metabolism, and nutrition
biology.organism_classification
Tumor Necrosis Factor-alpha/immunology
Immunity, Innate
Mice, Inbred C57BL
030104 developmental biology
Viral replication
Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein
Insect Science
INNATE IMMUNITY
bacteria
Tnf
Malt1
Innate Immunity
Nf-kappa B
Interferons
Tumor Necrosis Factor
Virología
Receptors, Tumor Necrosis Factor, Type I/immunology
Subjects
Details
- Language :
- English
- ISSN :
- 0022538X
- Database :
- OpenAIRE
- Journal :
- Shinde, P V, Xu, H C, Maney, S K, Kloetgen, A, Namineni, S, Zhuang, Y, Honke, N, Shaabani, N, Bellora, N, Doerrenberg, M, Trilling, M, Pozdeev, V I, van Rooijen, N, Scheu, S, Pfeffer, K, Crocker, P R, Tanaka, M, Duggimpudi, S, Knolle, P, Heikenwalder, M, Ruland, J R, Mak, T W, Brenner, D, Pandyra, A A, Hoell, J I, Borkhardt, A, Häussinger, D, Lang, K S & Lang, P A 2018, ' Tumor necrosis factormediated survival of CD169+ cells promotes immune activation during vesicular stomatitis virus infection ', Journal of Virology, vol. 92, no. 3, e01637-17 . https://doi.org/10.1128/JVI.01637-17, CONICET Digital (CONICET), Consejo Nacional de Investigaciones Científicas y Técnicas, instacron:CONICET, Shinde, P V, Xu, H C, Maney, S K, Kloetgen, A, Namineni, S, Zhuang, Y, Honke, N, Shaabani, N, Bellora, N, Doerrenberg, M, Trilling, M, Pozdeev, V I, van Rooijen, N, Scheu, S, Pfeffer, K, Crocker, P R, Tanaka, M, Duggimpudi, S, Knolle, P, Heikenwalder, M, Ruland, J, Mak, T W, Brenner, D, Pandyra, A A, Hoell, J I, Borkhardt, A, Häussinger, D, Lang, K S & Lang, P A 2018, ' Tumor Necrosis Factor-Mediated Survival of CD169+ Cells Promotes Immune Activation during Vesicular Stomatitis Virus Infection ', Journal of Virology, vol. 92, no. 3, e01637-17, pp. e01637-17 . https://doi.org/10.1128/JVI.01637-17, Journal of virology, J. Virol. 92, DOI: 10.1128/JVI.01637-17 (2017), Journal of Virology, 92(3):e01637-17. American Society for Microbiology, Journal of Virology
- Accession number :
- edsair.doi.dedup.....cad07de59d567d0c28c95469b650ca30
- Full Text :
- https://doi.org/10.1128/JVI.01637-17