TRAF3IP3 negatively regulates cytosolic RNA induced anti-viral signaling by promoting TBK1 K48 ubiquitination

Innate immunity to nucleic acids forms the backbone for anti-viral immunity and several inflammatory diseases. Upon sensing cytosolic viral RNA, retinoic acid-inducible gene-I-like receptors (RLRs) interact with the mitochondrial antiviral signaling protein (MAVS) and activate TANK-binding kinase 1...

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Published inNature communications Vol. 11; no. 1; p. 2193
Main Authors Deng, Meng, Tam, Jason W., Wang, Lufei, Liang, Kaixin, Li, Sirui, Zhang, Lu, Guo, Haitao, Luo, Xiaobo, Zhang, Yang, Petrucelli, Alex, Davis, Beckley K., Conti, Brian J., June Brickey, W., Ko, Ching-Chang, Lei, Yu L., Sun, Shaocong, Ting, Jenny P. -Y.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 04.05.2020
Nature Publishing Group
Nature Portfolio
Subjects
13/1
13/106
13/109
13/31
13/89
14
14/19
38
38/39
38/77
42
42/44
45
49
631/250
631/250/255
631/250/262
692/699
692/699/255
Animals
Antiviral agents
Carrier Proteins - genetics
Carrier Proteins - metabolism
Cell Line
Cells, Cultured
Chlorocebus aethiops
Cytosol - metabolism
Cytosol - virology
Double-stranded RNA
Gene deletion
Gene Expression Regulation
HEK293 Cells
HeLa Cells
Humanities and Social Sciences
Humans
Immune system
Immunity
Inflammatory diseases
Innate immunity
Interferon
Interferon regulatory factor 3
Interferon Type I - genetics
Interferon Type I - metabolism
Jurkat Cells
Kinases
Lysine - genetics
Lysine - metabolism
Macrophages
Membrane Proteins - genetics
Membrane Proteins - metabolism
Mice, Inbred C57BL
Mice, Knockout
Mice, Transgenic
Mitochondria
multidisciplinary
Myeloid cells
Myeloid Cells - metabolism
Myeloid Cells - virology
Nucleic acids
Pattern recognition
Pattern recognition receptors
Polyinosinic:polycytidylic acid
Protein Serine-Threonine Kinases - genetics
Protein Serine-Threonine Kinases - metabolism
Proteins
Receptors
Retinoic acid
Ribonucleic acid
RNA
RNA viruses
RNA, Viral - genetics
RNA, Viral - metabolism
Science
Science (multidisciplinary)
Signal transduction
Signaling
Stomatitis
THP-1 Cells
Ubiquitination
Vero Cells
Vesicular stomatitis Indiana virus - genetics
Vesicular stomatitis Indiana virus - physiology
Viruses
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Abstract Innate immunity to nucleic acids forms the backbone for anti-viral immunity and several inflammatory diseases. Upon sensing cytosolic viral RNA, retinoic acid-inducible gene-I-like receptors (RLRs) interact with the mitochondrial antiviral signaling protein (MAVS) and activate TANK-binding kinase 1 (TBK1) to induce type I interferon (IFN-I). TRAF3-interacting protein 3 (TRAF3IP3, T3JAM) is essential for T and B cell development. It is also well-expressed by myeloid cells, where its role is unknown. Here we report that TRAF3IP3 suppresses cytosolic poly(I:C), 5’ppp-dsRNA, and vesicular stomatitis virus (VSV) triggers IFN-I expression in overexpression systems and Traf3ip3 −/− primary myeloid cells. The mechanism of action is through the interaction of TRAF3IP3 with endogenous TRAF3 and TBK1. This leads to the degradative K48 ubiquitination of TBK1 via its K372 residue in a DTX4-dependent fashion. Mice with myeloid-specific gene deletion of Traf3ip3 have increased RNA virus-triggered IFN-I production and reduced susceptibility to virus. These results identify a function of TRAF3IP3 in the regulation of the host response to cytosolic viral RNA in myeloid cells. RNA viruses can be detected by immune cell pattern recognition receptors, such as RLRs, resulting in MAVS-TBK1-IRF3 signalling and production of antiviral type 1 interferons. Here the authors show that macrophage TRAF3-interacting protein 3 regulates this signalling pathway by interacting with TRAF3 and TBK1 to suppress interferon responses.
AbstractList Innate immunity to nucleic acids forms the backbone for anti-viral immunity and several inflammatory diseases. Upon sensing cytosolic viral RNA, retinoic acid-inducible gene-I-like receptors (RLRs) interact with the mitochondrial antiviral signaling protein (MAVS) and activate TANK-binding kinase 1 (TBK1) to induce type I interferon (IFN-I). TRAF3-interacting protein 3 (TRAF3IP3, T3JAM) is essential for T and B cell development. It is also well-expressed by myeloid cells, where its role is unknown. Here we report that TRAF3IP3 suppresses cytosolic poly(I:C), 5’ppp-dsRNA, and vesicular stomatitis virus (VSV) triggers IFN-I expression in overexpression systems and Traf3ip3 −/− primary myeloid cells. The mechanism of action is through the interaction of TRAF3IP3 with endogenous TRAF3 and TBK1. This leads to the degradative K48 ubiquitination of TBK1 via its K372 residue in a DTX4-dependent fashion. Mice with myeloid-specific gene deletion of Traf3ip3 have increased RNA virus-triggered IFN-I production and reduced susceptibility to virus. These results identify a function of TRAF3IP3 in the regulation of the host response to cytosolic viral RNA in myeloid cells. RNA viruses can be detected by immune cell pattern recognition receptors, such as RLRs, resulting in MAVS-TBK1-IRF3 signalling and production of antiviral type 1 interferons. Here the authors show that macrophage TRAF3-interacting protein 3 regulates this signalling pathway by interacting with TRAF3 and TBK1 to suppress interferon responses.
Innate immunity to nucleic acids forms the backbone for anti-viral immunity and several inflammatory diseases. Upon sensing cytosolic viral RNA, retinoic acid-inducible gene-I-like receptors (RLRs) interact with the mitochondrial antiviral signaling protein (MAVS) and activate TANK-binding kinase 1 (TBK1) to induce type I interferon (IFN-I). TRAF3-interacting protein 3 (TRAF3IP3, T3JAM) is essential for T and B cell development. It is also well-expressed by myeloid cells, where its role is unknown. Here we report that TRAF3IP3 suppresses cytosolic poly(I:C), 5'ppp-dsRNA, and vesicular stomatitis virus (VSV) triggers IFN-I expression in overexpression systems and Traf3ip3 primary myeloid cells. The mechanism of action is through the interaction of TRAF3IP3 with endogenous TRAF3 and TBK1. This leads to the degradative K48 ubiquitination of TBK1 via its K372 residue in a DTX4-dependent fashion. Mice with myeloid-specific gene deletion of Traf3ip3 have increased RNA virus-triggered IFN-I production and reduced susceptibility to virus. These results identify a function of TRAF3IP3 in the regulation of the host response to cytosolic viral RNA in myeloid cells.
RNA viruses can be detected by immune cell pattern recognition receptors, such as RLRs, resulting in MAVS-TBK1-IRF3 signalling and production of antiviral type 1 interferons. Here the authors show that macrophage TRAF3-interacting protein 3 regulates this signalling pathway by interacting with TRAF3 and TBK1 to suppress interferon responses.
Innate immunity to nucleic acids forms the backbone for anti-viral immunity and several inflammatory diseases. Upon sensing cytosolic viral RNA, retinoic acid-inducible gene-I-like receptors (RLRs) interact with the mitochondrial antiviral signaling protein (MAVS) and activate TANK-binding kinase 1 (TBK1) to induce type I interferon (IFN-I). TRAF3-interacting protein 3 (TRAF3IP3, T3JAM) is essential for T and B cell development. It is also well-expressed by myeloid cells, where its role is unknown. Here we report that TRAF3IP3 suppresses cytosolic poly(I:C), 5'ppp-dsRNA, and vesicular stomatitis virus (VSV) triggers IFN-I expression in overexpression systems and Traf3ip3-/- primary myeloid cells. The mechanism of action is through the interaction of TRAF3IP3 with endogenous TRAF3 and TBK1. This leads to the degradative K48 ubiquitination of TBK1 via its K372 residue in a DTX4-dependent fashion. Mice with myeloid-specific gene deletion of Traf3ip3 have increased RNA virus-triggered IFN-I production and reduced susceptibility to virus. These results identify a function of TRAF3IP3 in the regulation of the host response to cytosolic viral RNA in myeloid cells.
Innate immunity to nucleic acids forms the backbone for anti-viral immunity and several inflammatory diseases. Upon sensing cytosolic viral RNA, retinoic acid-inducible gene-I-like receptors (RLRs) interact with the mitochondrial antiviral signaling protein (MAVS) and activate TANK-binding kinase 1 (TBK1) to induce type I interferon (IFN-I). TRAF3-interacting protein 3 (TRAF3IP3, T3JAM) is essential for T and B cell development. It is also well-expressed by myeloid cells, where its role is unknown. Here we report that TRAF3IP3 suppresses cytosolic poly(I:C), 5’ppp-dsRNA, and vesicular stomatitis virus (VSV) triggers IFN-I expression in overexpression systems and Traf3ip3 −/− primary myeloid cells. The mechanism of action is through the interaction of TRAF3IP3 with endogenous TRAF3 and TBK1. This leads to the degradative K48 ubiquitination of TBK1 via its K372 residue in a DTX4-dependent fashion. Mice with myeloid-specific gene deletion of Traf3ip3 have increased RNA virus-triggered IFN-I production and reduced susceptibility to virus. These results identify a function of TRAF3IP3 in the regulation of the host response to cytosolic viral RNA in myeloid cells.
Innate immunity to nucleic acids forms the backbone for anti-viral immunity and several inflammatory diseases. Upon sensing cytosolic viral RNA, retinoic acid-inducible gene-I-like receptors (RLRs) interact with the mitochondrial antiviral signaling protein (MAVS) and activate TANK-binding kinase 1 (TBK1) to induce type I interferon (IFN-I). TRAF3-interacting protein 3 (TRAF3IP3, T3JAM) is essential for T and B cell development. It is also well-expressed by myeloid cells, where its role is unknown. Here we report that TRAF3IP3 suppresses cytosolic poly(I:C), 5’ppp-dsRNA, and vesicular stomatitis virus (VSV) triggers IFN-I expression in overexpression systems and Traf3ip3−/− primary myeloid cells. The mechanism of action is through the interaction of TRAF3IP3 with endogenous TRAF3 and TBK1. This leads to the degradative K48 ubiquitination of TBK1 via its K372 residue in a DTX4-dependent fashion. Mice with myeloid-specific gene deletion of Traf3ip3 have increased RNA virus-triggered IFN-I production and reduced susceptibility to virus. These results identify a function of TRAF3IP3 in the regulation of the host response to cytosolic viral RNA in myeloid cells.RNA viruses can be detected by immune cell pattern recognition receptors, such as RLRs, resulting in MAVS-TBK1-IRF3 signalling and production of antiviral type 1 interferons. Here the authors show that macrophage TRAF3-interacting protein 3 regulates this signalling pathway by interacting with TRAF3 and TBK1 to suppress interferon responses.
ArticleNumber 2193
Author Li, Sirui
June Brickey, W.
Tam, Jason W.
Wang, Lufei
Petrucelli, Alex
Davis, Beckley K.
Guo, Haitao
Conti, Brian J.
Sun, Shaocong
Zhang, Yang
Ko, Ching-Chang
Zhang, Lu
Lei, Yu L.
Luo, Xiaobo
Liang, Kaixin
Deng, Meng
Ting, Jenny P. -Y.
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/32366851$$D View this record in MEDLINE/PubMed
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SSID ssj0000391844
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Snippet Innate immunity to nucleic acids forms the backbone for anti-viral immunity and several inflammatory diseases. Upon sensing cytosolic viral RNA, retinoic...
RNA viruses can be detected by immune cell pattern recognition receptors, such as RLRs, resulting in MAVS-TBK1-IRF3 signalling and production of antiviral type...
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proquest
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SourceType Open Website
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Aggregation Database
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Publisher
StartPage 2193
SubjectTerms 13/1
13/106
13/109
13/31
13/89
14
14/19
38
38/39
38/77
42
42/44
45
49
631/250
631/250/255
631/250/262
692/699
692/699/255
Animals
Antiviral agents
Carrier Proteins - genetics
Carrier Proteins - metabolism
Cell Line
Cells, Cultured
Chlorocebus aethiops
Cytosol - metabolism
Cytosol - virology
Double-stranded RNA
Gene deletion
Gene Expression Regulation
HEK293 Cells
HeLa Cells
Humanities and Social Sciences
Humans
Immune system
Immunity
Inflammatory diseases
Innate immunity
Interferon
Interferon regulatory factor 3
Interferon Type I - genetics
Interferon Type I - metabolism
Jurkat Cells
Kinases
Lysine - genetics
Lysine - metabolism
Macrophages
Membrane Proteins - genetics
Membrane Proteins - metabolism
Mice, Inbred C57BL
Mice, Knockout
Mice, Transgenic
Mitochondria
multidisciplinary
Myeloid cells
Myeloid Cells - metabolism
Myeloid Cells - virology
Nucleic acids
Pattern recognition
Pattern recognition receptors
Polyinosinic:polycytidylic acid
Protein Serine-Threonine Kinases - genetics
Protein Serine-Threonine Kinases - metabolism
Proteins
Receptors
Retinoic acid
Ribonucleic acid
RNA
RNA viruses
RNA, Viral - genetics
RNA, Viral - metabolism
Science
Science (multidisciplinary)
Signal transduction
Signaling
Stomatitis
THP-1 Cells
Ubiquitination
Vero Cells
Vesicular stomatitis Indiana virus - genetics
Vesicular stomatitis Indiana virus - physiology
Viruses
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Title TRAF3IP3 negatively regulates cytosolic RNA induced anti-viral signaling by promoting TBK1 K48 ubiquitination
URI https://link.springer.com/article/10.1038/s41467-020-16014-0
https://www.ncbi.nlm.nih.gov/pubmed/32366851
https://www.proquest.com/docview/2398125128
https://search.proquest.com/docview/2398631389
https://pubmed.ncbi.nlm.nih.gov/PMC7198545
https://doaj.org/article/17cacfe2c68542b2a667a747cf1f862c
Volume 11
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