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trim, sting, dna, immune, cells, pubmed, article, ubiquitination, fig, response, hsv, infection, protein, degradation, google, scholar, cas, antiviral, virus, stimulation, dsdna, mice, data, innate, viral, level, cell, induced, cytosolic, signaling, nature, production, pathway, cgamp, antibody, ubiquitin, expression, ifni, cytokine, central, interaction, activation, stimulated, detected, negative, bmdms, ligase, rna, tbk, assay,

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nature portfolio national key research privacy policy pcdh-cmv-mtrim29-ef1-copgfp tnf-α elisa kits advertising granulocyte-macrophage colony-stimulating factor rig-i-mediated antiviral signaling social media thermo fisher scientific yu-quan wei reprints nature 408 nature 458 nature 448 nature 498 nature 455 nature 494 nature open biosystems goat anti-mouse igg af647-anti-rabbit igg full size image trim-endous functional network activate sting–tbk1–irf3 pathway improve vaccine development sting–tbk1–irf3 signaling pathway development program 2016yfa0502203 intracellular double-stranded dna real-time pcr assay dsdna-mediated signaling pathways k48-specific anti-ubiquitin sting-dependent signaling pathway specific pathogen-free facility sds-polyacrylamide gel electrophoresis conjugated anti-ha antibody anti-k48 ubiquitin antibody irf-3-dependent innate immunity conserved n-terminal domains anti-virus infection response dsdna-induced signal pathway dna-dependent protein kinase dsdna-induced immune response 75 μm id × 15 cm length protein n-terminal acetylation dna virus-triggered response hrp-anti-flag antibody interferon-induced isg15 conjugation proteasome-dependent protein degradation site-directed mutagenesis kit

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         description:Innate immune system is armed by several lines of pattern recognition receptors to sense various viral infection and to initiate antiviral immune response. This process is under a tight control and the negative feedback induced by infection and/or inflammation is critical to maintain immune homoeostasis and to prevent autoimmune disorders, however, the molecular mechanism is not fully understood. Here we report TRIM29, a ubiquitin E3 ligase, functions as an inducible negative regulator of innate immune response triggered by DNA virus and cytosolic DNA. DNA virus and cytosolic DNA stimulation induce TRIM29 expression robustly in macrophages and dendritic cells, although the basal level of TRIM29 is undetectable in those cells. TRIM29 deficiency elevates IFN-I and proinflammatory cytokine production upon viral DNA and cytosolic dsDNA stimulation. Consistently, in vivo experiments show that TRIM29-deficient mice are more resistant to HSV-1 infection than WT controls, indicated by better survival rate and reduced viral load in organs. Mechanism studies suggest that STING–TBK1–IRF3 signaling pathway in TRIM29 KO cells is significantly enhanced and the degradation of STING is impaired. Furthermore, we identify that TRIM29 targets STING for K48 ubiquitination and degradation. This study reveals TRIM29 as a crucial negative regulator in immune response to DNA virus and cytosolic DNA, preventing potential damage caused by overcommitted immune responses.
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      description:Innate immune system is armed by several lines of pattern recognition receptors to sense various viral infection and to initiate antiviral immune response. This process is under a tight control and the negative feedback induced by infection and/or inflammation is critical to maintain immune homoeostasis and to prevent autoimmune disorders, however, the molecular mechanism is not fully understood. Here we report TRIM29, a ubiquitin E3 ligase, functions as an inducible negative regulator of innate immune response triggered by DNA virus and cytosolic DNA. DNA virus and cytosolic DNA stimulation induce TRIM29 expression robustly in macrophages and dendritic cells, although the basal level of TRIM29 is undetectable in those cells. TRIM29 deficiency elevates IFN-I and proinflammatory cytokine production upon viral DNA and cytosolic dsDNA stimulation. Consistently, in vivo experiments show that TRIM29-deficient mice are more resistant to HSV-1 infection than WT controls, indicated by better survival rate and reduced viral load in organs. Mechanism studies suggest that STING–TBK1–IRF3 signaling pathway in TRIM29 KO cells is significantly enhanced and the degradation of STING is impaired. Furthermore, we identify that TRIM29 targets STING for K48 ubiquitination and degradation. This study reveals TRIM29 as a crucial negative regulator in immune response to DNA virus and cytosolic DNA, preventing potential damage caused by overcommitted immune responses.
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      affiliation:
            name:Sichuan University
            address:
               name:Department of Rheumatology and Immunology, State Key Laboratory of Biotherapy and Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, China
               type:PostalAddress
            type:Organization
      name:Yi Liu
      affiliation:
            name:Sichuan University
            address:
               name:Department of Rheumatology and Immunology, State Key Laboratory of Biotherapy and Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, China
               type:PostalAddress
            type:Organization
      name:Bo Zhong
      affiliation:
            name:Wuhan University
            address:
               name:School of Life Science, Wuhan University, Wuhan, China
               type:PostalAddress
            type:Organization
      name:Lunzhi Dai
      url:http://orcid.org/0000-0002-3003-8910
      affiliation:
            name:Sichuan University
            address:
               name:Cancer Center, State Key Laboratory of Biotherapy and Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, China
               type:PostalAddress
            type:Organization
      name:Yu-Quan Wei
      affiliation:
            name:Sichuan University
            address:
               name:Department of General Practice and Lab of PTM, State Key Laboratory of Biotherapy and Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, China
               type:PostalAddress
            type:Organization
      name:Huiyuan Zhang
      affiliation:
            name:Sichuan University
            address:
               name:Department of Rheumatology and Immunology, State Key Laboratory of Biotherapy and Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, China
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Hongbo Hu
      url:http://orcid.org/0000-0002-8177-7641
      affiliation:
            name:Sichuan University
            address:
               name:Department of Rheumatology and Immunology, State Key Laboratory of Biotherapy and Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Rheumatology and Immunology, State Key Laboratory of Biotherapy and Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, China
      name:Department of Rheumatology and Immunology, State Key Laboratory of Biotherapy and Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, China
      name:Department of Rheumatology and Immunology, State Key Laboratory of Biotherapy and Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, China
      name:Department of General Practice and Lab of PTM, State Key Laboratory of Biotherapy and Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, China
      name:Department of Rheumatology and Immunology, State Key Laboratory of Biotherapy and Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, China
      name:Department of Rheumatology and Immunology, State Key Laboratory of Biotherapy and Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, China
      name:Cancer Center, State Key Laboratory of Biotherapy and Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, China
      name:Cancer Center, State Key Laboratory of Biotherapy and Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, China
      name:Department of Rheumatology and Immunology, State Key Laboratory of Biotherapy and Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, China
      name:Department of Rheumatology and Immunology, State Key Laboratory of Biotherapy and Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, China
      name:School of Life Science, Wuhan University, Wuhan, China
      name:Cancer Center, State Key Laboratory of Biotherapy and Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, China
      name:Department of General Practice and Lab of PTM, State Key Laboratory of Biotherapy and Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, China
      name:Department of Rheumatology and Immunology, State Key Laboratory of Biotherapy and Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, China
      name:Department of Rheumatology and Immunology, State Key Laboratory of Biotherapy and Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, China

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