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Constitutive aryl hydrocarbon receptor signaling constrains type I interferon–mediated antiviral innate defense

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/63086

Title: Constitutive aryl hydrocarbon receptor signaling constrains type I interferon–mediated antiviral innate defense
Authors: Yamada, Taisho Browse this author
Horimoto, Hiromasa Browse this author
Kameyama, Takeshi Browse this author →KAKEN DB
Hayakawa, Sumio Browse this author
Yamato, Hiroaki Browse this author
Dazai, Masayoshi Browse this author
Takada, Ayato Browse this author →KAKEN DB
Kida, Hiroshi Browse this author →KAKEN DB
Bott, Debbie Browse this author
Zhou, Angela C Browse this author
Hutin, David Browse this author
Watts, Tania H Browse this author
Asaka, Masahiro Browse this author →KAKEN DB
Matthews, Jason Browse this author
Takaoka, Akinori Browse this author →KAKEN DB
Issue Date: Jun-2016
Publisher: Nature Publishing Group
Journal Title: Nature Immunology
Volume: 17
Issue: 6
Start Page: 687
End Page: 694
Publisher DOI: 10.1038/ni.3422
PMID: 27089381
Abstract: Aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that mediates the toxic activity of many environmental xenobiotics. However, its role in innate immune responses during viral infection is not fully understood. Here we demonstrate that constitutive AHR signaling negatively regulates the type I interferon (IFN-I) response during infection with various types of virus. Virus-induced IFN-β production was enhanced in AHR-deficient cells and mice and resulted in restricted viral replication. We found that AHR upregulates expression of the ADP-ribosylase TIPARP, which in turn causes downregulation of the IFN-I response. Mechanistically, TIPARP interacted with the kinase TBK1 and suppressed its activity by ADP-ribosylation. Thus, this study reveals the physiological importance of endogenous activation of AHR signaling in shaping the IFN-I-mediated innate response and, further, suggests that the AHR-TIPARP axis is a potential therapeutic target for enhancing antiviral responses.
Description: Supplementary materials are available on the publisher's website.
Type: article (author version)
URI: http://hdl.handle.net/2115/63086
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 高岡 晃教

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