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  1. Article: Type I IFN modulates innate and specific antiviral immunity.

    Durbin, J E / Fernandez-Sesma, A / Lee, C K / Rao, T D / Frey, A B / Moran, T M / Vukmanovic, S / García-Sastre, A / Levy, D E

    Journal of immunology (Baltimore, Md. : 1950)

    2000  Volume 164, Issue 8, Page(s) 4220–4228

    Abstract: ... the immune response. Using mice deficient in multiple aspects of IFN signaling, we found that type I and type II IFN ... reveal an unexpected role for type I IFN in coordinating the host response to viral infection and ... infiltrates. Responsiveness to type I IFN did not influence the generation of virus-specific cytotoxic ...

    Abstract IFNs protect from virus infection by inducing an antiviral state and by modulating the immune response. Using mice deficient in multiple aspects of IFN signaling, we found that type I and type II IFN play distinct although complementing roles in the resolution of influenza viral disease. Both types of IFN influenced the profile of cytokines produced by T lymphocytes, with a significant bias toward Th2 differentiation occurring in the absence of responsiveness to either IFN. However, although a Th1 bias produced through inhibition of Th2 differentiation by IFN-gamma was not required to resolve infection, loss of type I IFN responsiveness led to exacerbated disease pathology characterized by granulocytic pulmonary inflammatory infiltrates. Responsiveness to type I IFN did not influence the generation of virus-specific cytotoxic lymphocytes or the rate of viral clearance, but induction of IL-10 and IL-15 in infected lungs through a type I IFN-dependent pathway correlated with a protective response to virus. Combined loss of both IFN pathways led to a severely polarized proinflammatory immune response and exacerbated disease. These results reveal an unexpected role for type I IFN in coordinating the host response to viral infection and controlling inflammation in the absence of a direct effect on virus replication.
    MeSH term(s) Adjuvants, Immunologic/physiology ; Animals ; Antibodies, Viral/biosynthesis ; Antiviral Agents/metabolism ; Bone Marrow Cells/immunology ; Bone Marrow Cells/metabolism ; Cells, Cultured ; Cytokines/biosynthesis ; DNA-Binding Proteins/deficiency ; DNA-Binding Proteins/genetics ; Immunity, Innate/genetics ; Immunity, Innate/immunology ; Influenza A virus/immunology ; Interferon Type I/physiology ; Lung/immunology ; Lung/metabolism ; Lung/virology ; Macrophages/immunology ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Orthomyxoviridae Infections/genetics ; Orthomyxoviridae Infections/immunology ; Orthomyxoviridae Infections/pathology ; Orthomyxoviridae Infections/virology ; STAT1 Transcription Factor ; Signal Transduction/genetics ; Signal Transduction/immunology ; Trans-Activators/deficiency ; Trans-Activators/genetics
    Chemical Substances Adjuvants, Immunologic ; Antibodies, Viral ; Antiviral Agents ; Cytokines ; DNA-Binding Proteins ; Interferon Type I ; STAT1 Transcription Factor ; Stat1 protein, mouse ; Trans-Activators
    Language English
    Publishing date 2000-04-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.164.8.4220
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: DDX4 enhances antiviral activity of type I interferon by disrupting interaction of USP7/SOCS1 and promoting degradation of SOCS1.

    Miao, Ying / Zhang, Tingting / Guan, Mingcheng / Zhao, Qian / Zhang, Renxia / Liu, Xuyi / Ma, Tianrun / Ren, Tengfei / Zheng, Zhijin / He, Wei / Tian, Wanying / Cui, Qun / Zhai, Xingyu / Zuo, Yibo / Zhu, Hong / Zheng, Hui / Yuan, Yukang

    mBio

    2024  Volume 15, Issue 3, Page(s) e0321323

    Abstract: ... immune response. However, the physiological roles played by DDX4 in antiviral innate immunity remain unclear ... I)-mediated antiviral activity. Our findings demonstrate that IFN-I upregulates DDX4 protein levels, and ... Nevertheless, the extent of DDX4's involvement in the antiviral innate immune response remains largely unexplored ...

    Abstract DEAD-box helicase (DDX) family members play differential roles in regulating innate antiviral immune response. However, the physiological roles played by DDX4 in antiviral innate immunity remain unclear. In this study, we unveiled that DDX4 acts as a positive regulatory molecule of Type-I interferon (IFN-I)-mediated antiviral activity. Our findings demonstrate that IFN-I upregulates DDX4 protein levels, and subsequently, overexpression of DDX4 enhances the IFN-I-mediated signaling pathway. This creates a positive feedback loop that amplifies the antiviral response. DDX4 was found to bind with deubiquitinase ubiquitin-specific protease 7 (USP7), leading to the disruption of the interaction between USP7 and suppressor of cytokine signaling 1 (SOCS1) and the subsequent degradation of SOCS1. This process enhances the antiviral function of IFN-I. Our findings provide new insights into the regulatory role of DDX4 in the IFN-I response.IMPORTANCEDDX4, identified as a putative RNA helicase that modulates RNA secondary structure through RNA binding, is primarily acknowledged for its role in regulating mRNA translation within the germline. Nevertheless, the extent of DDX4's involvement in the antiviral innate immune response remains largely unexplored. This study presents evidence of a previously unrecognized positive feedback loop between DDX4 and the antiviral response, suggesting that disruption of this loop may serve as a novel mechanism for viral evasion. Furthermore, our findings elucidate a positive regulatory mechanism by which the DDX4/USP7/SOCS1 axis mediates the antiviral activity of Type-I interferon, which provides new insight into strategies for improving the efficacy of IFN-based antiviral therapy.
    MeSH term(s) Interferon Type I ; Ubiquitin-Specific Peptidase 7/genetics ; Ubiquitin-Specific Peptidase 7/metabolism ; Suppressor of Cytokine Signaling 1 Protein/metabolism ; Suppressor of Cytokine Signaling Proteins/genetics ; Suppressor of Cytokine Signaling Proteins/metabolism ; Immunity, Innate ; RNA
    Chemical Substances Interferon Type I ; Ubiquitin-Specific Peptidase 7 (EC 3.4.19.12) ; Suppressor of Cytokine Signaling 1 Protein ; Suppressor of Cytokine Signaling Proteins ; RNA (63231-63-0)
    Language English
    Publishing date 2024-02-20
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2557172-2
    ISSN 2150-7511 ; 2161-2129
    ISSN (online) 2150-7511
    ISSN 2161-2129
    DOI 10.1128/mbio.03213-23
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: The Cross-Regulation Between Autophagy and Type I Interferon Signaling in Host Defense.

    Jin, Shouheng

    Advances in experimental medicine and biology

    2019  Volume 1209, Page(s) 125–144

    Abstract: ... to establish the comprehensive antiviral states. Type I IFN signaling should initiate timely to provoke innate ... program. Typical type I IFN response activates the Janus kinase (JAK)-signal transducer and ... autophagy and type I IFN signaling in host defense. ...

    Abstract The production of type I interferons (IFNs) is one of the hallmarks of intracellular antimicrobial program. Typical type I IFN response activates the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway, which results in the transcription of plentiful IFN-stimulated genes (ISGs) to establish the comprehensive antiviral states. Type I IFN signaling should initiate timely to provoke innate and adaptive immune responses for effective elimination of the invading pathogens. Meanwhile, a precise control must come on the stage to restrain the persistent activation of type I IFN responses to avoid attendant toxicity. Autophagy, a conserved eukaryotic degradation system, mediated by a number of autophagy-related (ATG) proteins, plays an essential role in the clearance of invading microorganism and manipulation of type I responses. Autophagy modulates type I IFN responses through regulatory integration with innate immune signaling pathways, and by removing endogenous ligands of innate immune sensors. Moreover, selective autophagy governs the choice of innate immune factors as specific cargoes for degradation, thus tightly monitoring the type I IFN responses. This review will focus on the cross-regulation between autophagy and type I IFN signaling in host defense.
    MeSH term(s) Animals ; Autophagy/immunology ; Host-Pathogen Interactions/immunology ; Humans ; Immunity, Innate ; Interferon Type I/immunology ; STAT Transcription Factors/immunology ; Signal Transduction/immunology
    Chemical Substances Interferon Type I ; STAT Transcription Factors
    Language English
    Publishing date 2019-11-15
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2214-8019 ; 0065-2598
    ISSN (online) 2214-8019
    ISSN 0065-2598
    DOI 10.1007/978-981-15-0606-2_8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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