MAVS-dependent IRF3/7 bypass of interferon p-induction restricts the response to measles infection in CD150Tg mouse bone marrow-derived dendritic cells

Takaki, Hiromi; Honda, Kenya; Atarashi, Koji; Kobayashi, Fukiko; Ebihara, Takashi; Oshiumi, Hiroyuki; Matsumoto, Misako; Shingai, Masashi; Seya, Tsukasa

MAVS-dependent IRF3/7 bypass of interferon p-induction restricts the response to measles infection in CD150Tg mouse bone marrow-derived dendritic cells

Takaki, Hiromi; Honda, Kenya; Atarashi, Koji et al.

Molecular immunology, 2014, 57(2), 100-109

Permalink : https://hdl.handle.net/2115/54683

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アクセス権	open access
URI	https://hdl.handle.net/2115/54683
タイトル	MAVS-dependent IRF3/7 bypass of interferon p-induction restricts the response to measles infection in CD150Tg mouse bone marrow-derived dendritic cells
著者	Takaki, Hiromi ; Honda, Kenya ; Atarashi, Koji ; Kobayashi, Fukiko ; Ebihara, Takashi ; Oshiumi, Hiroyuki ; Matsumoto, Misako ; Shingai, Masashi ; Seya, Tsukasa
著者名 Takaki, Hiromi
著者名 Honda, Kenya
著者名 Atarashi, Koji
著者名 Kobayashi, Fukiko
著者名 Ebihara, Takashi
e-Rad_Researcher 50379103 著者名 Oshiumi, Hiroyuki
e-Rad_Researcher 30332456 著者名 Matsumoto, Misako
著者名 Shingai, Masashi
e-Rad_Researcher 10301805 著者名 Seya, Tsukasa
言語	英語
キーワード	Innate immunity
	Dendritic cells
	Type I interferon
	Mitochondrial antiviral signaling protein (MAVS)
	Measles virus
発行日	2014-02
出版者	Pergamon-elsevier science ltd
収録物名	Molecular immunology
巻(号)	57(2)
ページ	100-109
抄録	Measles virus (MV) infects CD150Tg/ifnar (IFN alpha receptor)(-/-) mice but not CD150 (a human MV receptor)-transgenic (Tg) mice. We have shown that bone marrow-derived dendritic cells (BMDCs) from CD150Tg/Ifnar(-/-) mice are permissive to MV in contrast to those from simple CD150Tg mice, which reveals a crucial role of type I interferon (IFN) in natural tropism against MV. Yet, the mechanism whereby BMDCs produce initial type I IFN has not been elucidated in MV infection. RNA virus infection usually allows cells to generate double-stranded RNA and induce activation of IFN regulatory factor (IRF) 3/7 transcription factors, leading to the production of type I IFN through the retinoic acid-inducible gene I (RIG-I)/melanoma differentiation-associated gene 5 (MDA5)-mitochondrial antiviral signaling protein (MAVS) pathway. In mouse experimental BMDCs models, we found CD150Tg/Mavs(-/-)BMDCs, but not CD150Tg/Irf3(-/-)/Irf7-/-BMDCs, permissive to MV. IFN-alpha/beta were not induced in MV-infected CD150Tg/Mavs--/-BMDCs, while IFN-13 was subtly induced in CD150Tg/Irf3(-/-)/Irf7(-/-)BMDCs. In vivo systemic infection was therefore established by transfer of MV-infected CD150Tg/Mavs-/- BMDCs to CD150Tg//fnar-/- mice. These data indicate that MAVS-dependent, IRF3/7-independent IFN-13 induction triggers the activation of the IFNAR pathway so as to restrict the spread of MV by infected BMDCs. Hence, MAVS participates in the initial induction of type I IFN in BMDCs and IFNAR protects against MV spreading. We also showed the importance of IL-10-producing CD4+ T cells induced by MV-infected BMDCs in vitro, which may account for immune modulation due to the functional aberration of DCs. (C) 2013 Elsevier Ltd. All rights reserved.
資源タイプ	学術雑誌論文
出版タイプ	Accepted Manuscript
PISSN	0161-5890
NCID	AA00307483
関連情報	PMID 24096085
関連情報 (isVersionOf)	出版社版DOI https://doi.org/10.1016/j.molimm.2013.08.007