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

Yamada, Taisho; Horimoto, Hiromasa; Kameyama, Takeshi; Hayakawa, Sumio; Yamato, Hiroaki; Dazai, Masayoshi; Takada, Ayato; Kida, Hiroshi; Bott, Debbie; Zhou, Angela C; Hutin, David; Watts, Tania H; Asaka, Masahiro; Matthews, Jason; Takaoka, Akinori

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

Yamada, Taisho; Horimoto, Hiromasa; Kameyama, Takeshi et al.

Nature Immunology, 2016, 17(6), 687-694

Permalink : https://hdl.handle.net/2115/63086

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アクセス権	open access
URI	https://hdl.handle.net/2115/63086
タイトル	Constitutive aryl hydrocarbon receptor signaling constrains type I interferon–mediated antiviral innate defense
著者	Yamada, Taisho ; Horimoto, Hiromasa ; Kameyama, Takeshi ; Hayakawa, Sumio ; Yamato, Hiroaki ; Dazai, Masayoshi ; Takada, Ayato ; Kida, Hiroshi ; Bott, Debbie ; Zhou, Angela C ; Hutin, David ; Watts, Tania H ; Asaka, Masahiro ; Matthews, Jason ; Takaoka, Akinori
著者名 Yamada, Taisho
著者名 Horimoto, Hiromasa
e-Rad_Researcher 40569505 著者名 Kameyama, Takeshi
著者名 Hayakawa, Sumio
著者名 Yamato, Hiroaki
著者名 Dazai, Masayoshi
e-Rad_Researcher 10292062 著者名 Takada, Ayato
e-Rad_Researcher 10109506 著者名 Kida, Hiroshi
著者名 Bott, Debbie
著者名 Zhou, Angela C
著者名 Hutin, David
著者名 Watts, Tania H
e-Rad_Researcher 10113507 著者名 Asaka, Masahiro
著者名 Matthews, Jason
e-Rad_Researcher 30323611 著者名 Takaoka, Akinori
言語	英語
発行日	2016-06
出版者	Nature Publishing Group
収録物名	Nature Immunology
巻(号)	17(6)
ページ	687-694
記述	Supplementary materials are available on the publisher's website.
抄録	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.
資源タイプ	学術雑誌論文
出版タイプ	Accepted Manuscript
PISSN	1529-2908
EISSN	1529-2916
NCID	AA11466707
関連情報	PMID 27089381
関連情報 (isVersionOf)	出版社版DOI https://doi.org/10.1038/ni.3422