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Article ; Online: Regulation of mitochondrial antiviral signaling pathways.

Moore, Chris B / Ting, Jenny P-Y

2008 Volume 28, Issue 6, Page(s) 735–739

Abstract: ... other signaling molecules to the outer mitochondrial membrane results in the rapid induction of antiviral ... Mitochondrial antiviral immunity involves the detection of viral RNA by intracellular ... in the regulation of this antiviral response. ...

Abstract	Mitochondrial antiviral immunity involves the detection of viral RNA by intracellular pattern-recognition receptors (PRRs) belonging to the RIG-I-like helicase family. The convergence of these and other signaling molecules to the outer mitochondrial membrane results in the rapid induction of antiviral cytokines including type-1 interferon. Here, we discuss recent studies describing new molecules implicated in the regulation of this antiviral response.
MeSH term(s)	Adaptor Proteins, Signal Transducing/immunology ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Cytokines/metabolism ; Humans ; Interferon Type I/immunology ; Interferon Type I/metabolism ; Mitochondria/immunology ; Mitochondria/metabolism ; RNA Helicases/metabolism ; RNA, Viral/metabolism ; Receptors, Pattern Recognition/metabolism ; Signal Transduction ; Toll-Like Receptors/metabolism ; Viruses/immunology
Chemical Substances	Adaptor Proteins, Signal Transducing ; Cytokines ; Interferon Type I ; MAVS protein, human ; RNA, Viral ; Receptors, Pattern Recognition ; Toll-Like Receptors ; RNA Helicases (EC 3.6.4.13)
Language	English
Publishing date	2008-06-04
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2008.05.005
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Article ; Online: Redox regulation of the immune response.

Morris, Gerwyn / Gevezova, Maria / Sarafian, Victoria / Maes, Michael

Cellular & molecular immunology

2022 Volume 19, Issue 10, Page(s) 1079–1101

Abstract: ... of those antioxidant systems, the tricarboxylic acid cycle, mitochondrial functions, and the metabolism of immune cells ... signaling pathway, mitogen-activated protein kinases, 5' AMP-activated protein kinase, and ... and tolerance, chemotaxis, pathogen sensing, antiviral and antibacterial effects, Toll-like receptor ...

Abstract	The immune-inflammatory response is associated with increased nitro-oxidative stress. The aim of this mechanistic review is to examine: (a) the role of redox-sensitive transcription factors and enzymes, ROS/RNS production, and the activity of cellular antioxidants in the activation and performance of macrophages, dendritic cells, neutrophils, T-cells, B-cells, and natural killer cells; (b) the involvement of high-density lipoprotein (HDL), apolipoprotein A1 (ApoA1), paraoxonase-1 (PON1), and oxidized phospholipids in regulating the immune response; and (c) the detrimental effects of hypernitrosylation and chronic nitro-oxidative stress on the immune response. The redox changes during immune-inflammatory responses are orchestrated by the actions of nuclear factor-κB, HIF1α, the mechanistic target of rapamycin, the phosphatidylinositol 3-kinase/protein kinase B signaling pathway, mitogen-activated protein kinases, 5' AMP-activated protein kinase, and peroxisome proliferator-activated receptor. The performance and survival of individual immune cells is under redox control and depends on intracellular and extracellular levels of ROS/RNS. They are heavily influenced by cellular antioxidants including the glutathione and thioredoxin systems, nuclear factor erythroid 2-related factor 2, and the HDL/ApoA1/PON1 complex. Chronic nitro-oxidative stress and hypernitrosylation inhibit the activity of those antioxidant systems, the tricarboxylic acid cycle, mitochondrial functions, and the metabolism of immune cells. In conclusion, redox-associated mechanisms modulate metabolic reprogramming of immune cells, macrophage and T helper cell polarization, phagocytosis, production of pro- versus anti-inflammatory cytokines, immune training and tolerance, chemotaxis, pathogen sensing, antiviral and antibacterial effects, Toll-like receptor activity, and endotoxin tolerance.
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; Anti-Bacterial Agents ; Anti-Inflammatory Agents ; Antioxidants/metabolism ; Antiviral Agents ; Apolipoprotein A-I/metabolism ; Aryldialkylphosphatase/metabolism ; Cytokines/metabolism ; Glutathione/metabolism ; Immunity ; Lipoproteins, HDL/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; NF-kappa B/metabolism ; Oxidation-Reduction ; Peroxisome Proliferator-Activated Receptors/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Reactive Oxygen Species/metabolism ; Sirolimus ; Thioredoxins/metabolism ; Toll-Like Receptors/metabolism
Chemical Substances	Anti-Bacterial Agents ; Anti-Inflammatory Agents ; Antioxidants ; Antiviral Agents ; Apolipoprotein A-I ; Cytokines ; Lipoproteins, HDL ; NF-kappa B ; Peroxisome Proliferator-Activated Receptors ; Reactive Oxygen Species ; Toll-Like Receptors ; Thioredoxins (52500-60-4) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Aryldialkylphosphatase (EC 3.1.8.1) ; Glutathione (GAN16C9B8O) ; Sirolimus (W36ZG6FT64)
Language	English
Publishing date	2022-09-02
Publishing country	China
Document type	Journal Article ; Review
ZDB-ID	2435097-7
ISSN	2042-0226 ; 1672-7681
ISSN (online)	2042-0226
ISSN	1672-7681
DOI	10.1038/s41423-022-00902-0
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Article: The Dual Regulation of Apoptosis by Flavivirus.

Pan, Yuhong / Cheng, Anchun / Wang, Mingshu / Yin, Zhongqiong / Jia, Renyong

Frontiers in microbiology

2021 Volume 12, Page(s) 654494

Abstract: ... pathogen-infected cells. It contains three signaling pathways: death receptor pathway, mitochondria ... apoptosis by interacting with host proteins, as well as various signaling pathways involved in flaviviruses ... and helps in developing an effective antiviral therapy. ...

Abstract	Apoptosis is a form of programmed cell death, which maintains cellular homeostasis by eliminating pathogen-infected cells. It contains three signaling pathways: death receptor pathway, mitochondria-mediated pathway, and endoplasmic reticulum pathway. Its importance in host defenses is highlighted by the observation that many viruses evade, hinder or destroy apoptosis, thereby weakening the host's immune response. Flaviviruses such as Dengue virus, Japanese encephalitis virus, and West Nile virus utilize various strategies to activate or inhibit cell apoptosis. This article reviews the research progress of apoptosis mechanism during flaviviruses infection, including flaviviruses proteins and subgenomic flaviviral RNA to regulate apoptosis by interacting with host proteins, as well as various signaling pathways involved in flaviviruses-induced apoptosis, which provides a scientific basis for understanding the pathogenesis of flaviviruses and helps in developing an effective antiviral therapy.
Language	English
Publishing date	2021-03-24
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2587354-4
ISSN	1664-302X
ISSN	1664-302X
DOI	10.3389/fmicb.2021.654494
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Article ; Online: Regulation of MAVS Expression and Signaling Function in the Antiviral Innate Immune Response.

Ren, Zhihua / Ding, Ting / Zuo, Zhicai / Xu, Zhiwen / Deng, Junliang / Wei, Zhanyong

Frontiers in immunology

2020 Volume 11, Page(s) 1030

Abstract: ... antiviral response by interfering at multiple points in the MAVS signaling pathways, thereby maintaining ... that culminate in the production of antiviral mediators such as type I interferons. Mitochondrial antiviral ... for viral components. Engagement of these pattern recognition receptors triggers a series of signaling pathways ...

Abstract	Viral infection is controlled by host innate immune cells that express specialized receptors for viral components. Engagement of these pattern recognition receptors triggers a series of signaling pathways that culminate in the production of antiviral mediators such as type I interferons. Mitochondrial antiviral-signaling protein (MAVS) acts as a central hub for signal transduction initiated by RIG-I-like receptors, which predominantly recognize viral RNA. MAVS expression and function are regulated by both post-transcriptional and post-translational mechanisms, of which ubiquitination and phosphorylation play the most important roles in modulating MAVS function. Increasing evidence indicates that viruses can escape the host antiviral response by interfering at multiple points in the MAVS signaling pathways, thereby maintaining viral survival and replication. This review summarizes recent studies on the mechanisms by which MAVS expression and signaling are normally regulated and on the various strategies employed by viruses to antagonize MAVS activity, which may provide new insights into the design of novel antiviral agents.
MeSH term(s)	Adaptor Proteins, Signal Transducing/chemistry ; Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/immunology ; Animals ; Apoptosis/immunology ; Autophagy/immunology ; DEAD Box Protein 58/metabolism ; Host Microbial Interactions/genetics ; Host Microbial Interactions/immunology ; Humans ; Immune Evasion ; Immunity, Innate/genetics ; Models, Immunological ; Protein Processing, Post-Translational ; RNA Processing, Post-Transcriptional ; Receptors, Immunologic/metabolism ; Signal Transduction/immunology ; Viral Proteins/immunology ; Virus Diseases/genetics ; Virus Diseases/immunology
Chemical Substances	Adaptor Proteins, Signal Transducing ; Receptors, Immunologic ; Viral Proteins ; DEAD Box Protein 58 (EC 3.6.4.13)
Keywords	covid19
Language	English
Publishing date	2020-05-27
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.01030
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Article ; Online: Regulation of MDA5-dependent anti-Tembusu virus innate immune responses by LGP2 in ducks.

Li, Tianxu / Zhai, Xinyu / Wang, Wenjie / Lin, Yu / Xing, Bin / Wang, Jinchao / Wang, Xiuyuan / Miao, Runchun / Zhang, Tingting / Wei, Liangmeng

Veterinary microbiology

2021 Volume 263, Page(s) 109281

Abstract: ... to an increase in viral replication. However, the overexpression of duLGP2 promotes expression of mitochondrial ... of innate antiviral signaling in duck, which plays an important role in anti-Tembusu virus (TMUV) infection ... antiviral-signaling protein (MAVS) and duMDA5-mediated proinflammatory cytokines. This study provides a new ...

Abstract	Melanoma differentiation associated factor 5 (MDA5), which belongs to the retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) family, has been proved to be a key pattern recognition receptor of innate antiviral signaling in duck, which plays an important role in anti-Tembusu virus (TMUV) infection. However, laboratory of genetics and physiology 2 (LGP2), the third member of RLRs family, the regulatory function on antiviral innate immunity of MDA5 is currently unclear. In this study, we investigated the subcellular localization of duck LGP2 (duLGP2) and confirmed that it is an important regulator of the duMDA5-mediated host innate antiviral immune response. The present experimental data demonstrate that the overexpression of duLGP2 inhibits duMDA5 downstream transcriptional factor (IRF-7, IFN-β, and NF-κB) promoter activity, and duMDA5-mediated type I IFNs and ISGs expression were significantly suppressed by duLGP2 regardless of viral infection in vitro. The inhibition of duLGP2 on the antiviral activity of duMDA5 ultimately leads to an increase in viral replication. However, the overexpression of duLGP2 promotes expression of mitochondrial antiviral-signaling protein (MAVS) and duMDA5-mediated proinflammatory cytokines. This study provides a new rationale support for the duLGP2 regulates duMDA5-mediated anti-viral immune signaling pathway theory in duck.
MeSH term(s)	Animals ; Antiviral Agents ; Ducks ; Flavivirus/immunology ; Flavivirus Infections/immunology ; Flavivirus Infections/veterinary ; Immunity, Innate/genetics ; Interferon-Induced Helicase, IFIH1/genetics ; Interferon-Induced Helicase, IFIH1/immunology ; RNA Helicases/metabolism
Chemical Substances	Antiviral Agents ; Interferon-Induced Helicase, IFIH1 (EC 3.6.4.13) ; RNA Helicases (EC 3.6.4.13)
Language	English
Publishing date	2021-11-11
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	753154-0
ISSN	1873-2542 ; 0378-1135
ISSN (online)	1873-2542
ISSN	0378-1135
DOI	10.1016/j.vetmic.2021.109281
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Article ; Online: Repression of the expression of proinflammatory genes by mitochondrial transcription factor A is linked to its alternative splicing regulation in human lung epithelial cells.

Luo, Jinsong / Liu, Hong / Li, Daniel K Jun / Song, Bin / Zhang, Yi

BMC immunology

2021 Volume 22, Issue 1, Page(s) 74

Abstract: ... receptor signaling pathway, and also transcription regulation. Further analysis revealed that the promoters ... signaling pathway, type I interferon- and INF-γ-mediated signaling pathways, and viral response pathways. We also ... of neurodegenerative diseases and also with asthma. TFAM deficiency-induced mitochondrial DNA stress primes the antiviral ...

Abstract	Background: Mitochondrial transcription factor A (TFAM) is associated with a number of neurodegenerative diseases and also with asthma. TFAM deficiency-induced mitochondrial DNA stress primes the antiviral innate immune response in mouse embryonic fibroblasts. However, the role of TFAM in asthma related inflammation remains obscure. The purpose of this study was to investigate the regulatory mechanism of TFAM in asthma. Results: In this study, we overexpressed TFAM in human lung epithelial cells (A549), then obtained the TFAM-regulated transcriptome by Illumina sequencing technology. Transcriptome analysis revealed that TFAM overexpression down-regulated and up-regulated the expression of 642 and 169 differentially expressed genes (DEGs), respectively. The TFAM-repressed genes were strongly enriched in cytokine-mediated signaling pathway, type I interferon- and INF-γ-mediated signaling pathways, and viral response pathways. We also revealed that 2563 alternative splicing events in 1796 alternative splicing genes (ASGs) were de-regulated upon TFAM overexpression. These TFAM-responding ASGs were enriched in DNA repair, nerve growth factor receptor signaling pathway, and also transcription regulation. Further analysis revealed that the promoters of TFAM-repressed DEGs were enriched by DNA binding motifs of transcription factors whose alternative splicing was regulated by TFAM. Conclusions: These findings suggest that TFAM regulates not only immune response gene expression in human lung epithelial cells, but also pre-mRNA alternative splicing which may mediate transcriptional regulation; this TFAM-centered gene regulation network could be targeted in developing therapies against various diseases.
MeSH term(s)	A549 Cells ; Alternative Splicing/genetics ; Animals ; Asthma/immunology ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Epithelial Cells/physiology ; Humans ; Inflammation/immunology ; Interferon Type I/metabolism ; Interferon-gamma/metabolism ; Lung/pathology ; Mice ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Signal Transduction/genetics ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transcriptome ; Virus Diseases/immunology
Chemical Substances	DNA-Binding Proteins ; Interferon Type I ; Mitochondrial Proteins ; Transcription Factors ; mitochondrial transcription factor A ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2021-12-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2041500-X
ISSN	1471-2172 ; 1471-2172
ISSN (online)	1471-2172
ISSN	1471-2172
DOI	10.1186/s12865-021-00464-2
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Article ; Online: Regulation of RIG-I-like receptor-mediated signaling: interaction between host and viral factors.

Onomoto, Koji / Onoguchi, Kazuhide / Yoneyama, Mitsutoshi

Cellular & molecular immunology

2021 Volume 18, Issue 3, Page(s) 539–555

Abstract: ... downstream signaling via their interactions with mitochondrial antiviral signaling proteins and activate ... of RLR-mediated signaling pathways. Here, we review the recent advances in the understanding of regulated ... also involved in the regulation of acquired immunity, the deregulation of RLR-mediated signaling is ...

Abstract	Retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) are RNA sensor molecules that play essential roles in innate antiviral immunity. Among the three RLRs encoded by the human genome, RIG-I and melanoma differentiation-associated gene 5, which contain N-terminal caspase recruitment domains, are activated upon the detection of viral RNAs in the cytoplasm of virus-infected cells. Activated RLRs induce downstream signaling via their interactions with mitochondrial antiviral signaling proteins and activate the production of type I and III interferons and inflammatory cytokines. Recent studies have shown that RLR-mediated signaling is regulated by interactions with endogenous RNAs and host proteins, such as those involved in stress responses and posttranslational modifications. Since RLR-mediated cytokine production is also involved in the regulation of acquired immunity, the deregulation of RLR-mediated signaling is associated with autoimmune and autoinflammatory disorders. Moreover, RLR-mediated signaling might be involved in the aberrant cytokine production observed in coronavirus disease 2019. Since the discovery of RLRs in 2004, significant progress has been made in understanding the mechanisms underlying the activation and regulation of RLR-mediated signaling pathways. Here, we review the recent advances in the understanding of regulated RNA recognition and signal activation by RLRs, focusing on the interactions between various host and viral factors.
MeSH term(s)	Animals ; DEAD Box Protein 58/immunology ; Humans ; Immunologic Factors ; Interferon Type I/immunology ; Interferons/immunology ; Mitochondria/immunology ; Receptors, Immunologic/immunology ; Signal Transduction ; Virus Diseases/immunology ; Viruses/immunology ; Interferon Lambda
Chemical Substances	Immunologic Factors ; Interferon Type I ; Receptors, Immunologic ; Interferons (9008-11-1) ; RIGI protein, human (EC 3.6.1.-) ; DEAD Box Protein 58 (EC 3.6.4.13) ; Interferon Lambda
Language	English
Publishing date	2021-01-18
Publishing country	China
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2435097-7
ISSN	2042-0226 ; 1672-7681
ISSN (online)	2042-0226
ISSN	1672-7681
DOI	10.1038/s41423-020-00602-7
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Article ; Online: Negative Regulation of RNF90 on RNA Virus-Triggered Antiviral Immune Responses Targeting MAVS.

Yang, Bo / Zhang, Ge / Qin, Xiao / Huang, Yulu / Ren, Xiaowen / Sun, Jingliang / Ma, Shujun / Liu, Yanzi / Song, Di / Liu, Yue / Cui, Yuhan / Wang, Hui / Wang, Jie

Frontiers in immunology

2021 Volume 12, Page(s) 730483

Abstract: ... Mitochondrial antiviral signaling protein (MAVS, also named Cardif/IPS-1/VISA) is a critical protein ... in RNA virus-induced antiviral signaling pathways. Our previous research suggested that E3 ... The antiviral innate immunity is the first line of host defense against viral infection ...

Abstract	The antiviral innate immunity is the first line of host defense against viral infection. Mitochondrial antiviral signaling protein (MAVS, also named Cardif/IPS-1/VISA) is a critical protein in RNA virus-induced antiviral signaling pathways. Our previous research suggested that E3 ubiquitin-protein ligases RING-finger protein (RNF90) negatively regulate cellular antiviral responses by targeting STING for degradation, though its role in RNA virus infection remains unknown. This study demonstrated that RNF90 negatively regulated RNA virus-triggered antiviral innate immune responses in RNF90-silenced PMA-THP1 cells, RNF90-deficient cells (including HaCaTs, MEFs, and BMDMs), and RNF90-deficient mice. However, RNF90 regulated RNA virus-triggered antiviral innate immune responses independent of STING. RNF90 promoted K48-linked ubiquitination of MAVS and its proteasome-dependent degradation, leading to the inhibition of innate immune responses. Altogether, our findings suggested a novel function and mechanism of RNF90 in antiviral innate immunity.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/immunology ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Chlorocebus aethiops ; Cytokines/genetics ; Cytokines/immunology ; Cytokines/metabolism ; HEK293 Cells ; HaCaT Cells ; Host-Pathogen Interactions ; Humans ; Immunity, Innate ; Mice, Knockout ; Proteasome Endopeptidase Complex/metabolism ; Proteolysis ; Signal Transduction ; THP-1 Cells ; Tripartite Motif Proteins/genetics ; Tripartite Motif Proteins/immunology ; Tripartite Motif Proteins/metabolism ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/immunology ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitination ; Vero Cells ; Vesicular Stomatitis/genetics ; Vesicular Stomatitis/immunology ; Vesicular Stomatitis/metabolism ; Vesicular Stomatitis/virology ; Vesiculovirus/immunology ; Vesiculovirus/pathogenicity ; Mice
Chemical Substances	Adaptor Proteins, Signal Transducing ; Cytokines ; IPS-1 protein, mouse ; MAVS protein, human ; Tripartite Motif Proteins ; TRIM7 protein, human (EC 2.3.2.27) ; Trim7 protein, mouse (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2021-08-27
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.730483
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Article ; Online: Negative regulation of the interferon response by finTRIM82 in the orange spotted grouper.

Lv, Shunyou / Zhang, Ya / Zheng, Jiaying / Huang, Xiaohong / Huang, Youhua / Qin, Qiwei

Fish & shellfish immunology

2019 Volume 88, Page(s) 391–402

Abstract: ... signaling pathways. However, in teleosts, additional TRIM members have been identified and their functions remain ... the melanoma differentiation-associated protein 5 (MDA5), mediator of IRF3 activation (MITA) and mitochondrial ... antiviral-signaling (MAVS) protein-induced IFN response by detecting the transcription of interferon related ...

Abstract	Tripartite motif (TRIM) proteins have been demonstrated to exhibit critical functions in multiple cellular processes, including development, carcinogenesis, and programmed cell death, and are also widely recognized to be important antiviral restriction factors or modulators of immune and inflammatory signaling pathways. However, in teleosts, additional TRIM members have been identified and their functions remain largely unknown. Here, a novel finTRIM gene from orange spotted grouper (EcfinTRIM82) was cloned and characterized. Sequence analysis indicated that EcfinTRIM82 encoded a 575 amino acid peptide which shared 94% and 82% identity with Asian sea bass (Lates calcarifer), and zebrafish (Danio rerio) finTRIM82, respectively. EcfinTRIM82 contained three conserved domains, including a RING, B-Box, and SPRY domain. Using fluorescence microscopy, we found that green fluorescence aggregates were observed in the cytoplasm of EcfinTRIM82-EGFP transfected grouper spleen (GS) cells. As the infection proceeded, EcfinTRIM82 transcription was significantly upregulated in Singapore grouper iridovirus (SGIV) or red-spotted grouper nervous necrosis virus (RGNNV) infected GS cells. This suggests that EcfinTRIM82 might be involved in fish virus infection. The in vitro overexpression of EcfinTRIM82 in GS cells significantly enhanced the replication of SGIV and RGNNV, evidenced by increased expression of viral genes, including the SGIV major capsid protein (MCP), VP19, ICP-18, RGNNV coat protein (CP), and RNA-dependent RNA polymerase (RdRp). Furthermore, the ectopic expression of EcfinTRIM82 significantly decreased the expression of interferon (IFN)-related signaling molecules, including interferon regulatory factor 3 (IRF3), IRF7, interferon stimulated gene 15 (ISG15), ISG56, IFP35, and myxovirus resistance gene (MXI), suggesting that EcfinTRIM82 regulated viral replication via the negative regulation of the host IFN response. In addition, EcfinTRIM82 overexpression substantially decreased the level of proinflammatory cytokine transcription. Furthermore, the ectopic expression of EcfinTRIM82 significantly weakened the melanoma differentiation-associated protein 5 (MDA5), mediator of IRF3 activation (MITA) and mitochondrial antiviral-signaling (MAVS) protein-induced IFN response by detecting the transcription of interferon related cytokines and the promoter activity of IFN. Together, our results demonstrate that finTRIM82 negatively regulates the innate antiviral immune response against grouper virus infection.
MeSH term(s)	Animals ; Bass/immunology ; Bass/virology ; Cloning, Molecular ; DNA Virus Infections/immunology ; DNA Virus Infections/veterinary ; DNA, Complementary ; Fish Diseases/immunology ; Fish Proteins/genetics ; Fish Proteins/immunology ; Gene Expression Regulation ; Immunity, Innate ; Interferon Regulatory Factor-3/genetics ; Interferon Regulatory Factor-3/immunology ; Interferon Regulatory Factors/genetics ; Interferon Regulatory Factors/immunology ; Interferons/immunology ; Iridovirus/immunology ; Phylogeny ; RNA, Messenger ; Sequence Alignment ; Sequence Analysis, DNA ; Spleen/cytology ; Spleen/virology ; Tripartite Motif Proteins/genetics ; Tripartite Motif Proteins/immunology ; Zebrafish/immunology
Chemical Substances	DNA, Complementary ; Fish Proteins ; Interferon Regulatory Factor-3 ; Interferon Regulatory Factors ; RNA, Messenger ; Tripartite Motif Proteins ; Interferons (9008-11-1)
Language	English
Publishing date	2019-03-07
Publishing country	England
Document type	Journal Article
ZDB-ID	1067738-0
ISSN	1095-9947 ; 1050-4648
ISSN (online)	1095-9947
ISSN	1050-4648
DOI	10.1016/j.fsi.2019.03.004
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Article ; Online: Mitochondrial DNA in the regulation of innate immune responses.

Fang, Chunju / Wei, Xiawei / Wei, Yuquan

Protein & cell

2016 Volume 7, Issue 1, Page(s) 11–16

Abstract: ... several innate immune pathways involving TLR9, NLRP3 and STING signaling, which contributes to the signaling ... organelle and considered to be evolved from aerobic prokaryotes more than a billion years ago. Mitochondrial ... regulating antiviral signaling, mounting evidence suggests that mtDNA contributes to inflammatory diseases ...

Abstract	Mitochondrion is known as the energy factory of the cell, which is also a unique mammalian organelle and considered to be evolved from aerobic prokaryotes more than a billion years ago. Mitochondrial DNA, similar to that of its bacterial ancestor’s, consists of a circular loop and contains significant number of unmethylated DNA as CpG islands. The innate immune system plays an important role in the mammalian immune response. Recent research has demonstrated that mitochondrial DNA (mtDNA) activates several innate immune pathways involving TLR9, NLRP3 and STING signaling, which contributes to the signaling platforms and results in effector responses. In addition to facilitating antibacterial immunity and regulating antiviral signaling, mounting evidence suggests that mtDNA contributes to inflammatory diseases following cellular damage and stress. Therefore, in addition to its well-appreciated roles in cellular metabolism and energy production,mtDNA appears to function as a key member in the innate immune system. Here, we highlight the emerging roles of mtDNA in innate immunity.
MeSH term(s)	Animals ; DNA, Mitochondrial/genetics ; Humans ; Immunity, Innate/immunology ; Mitochondria/genetics ; Mitochondria/immunology ; Signal Transduction
Chemical Substances	DNA, Mitochondrial
Language	English
Publishing date	2016-01
Publishing country	Germany
Document type	Journal Article ; Review
ISSN	1674-8018
ISSN (online)	1674-8018
DOI	10.1007/s13238-015-0222-9
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