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

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Title: MAVS-dependent IRF3/7 bypass of interferon p-induction restricts the response to measles infection in CD150Tg mouse bone marrow-derived dendritic cells
Authors: Takaki, Hiromi Browse this author
Honda, Kenya Browse this author
Atarashi, Koji Browse this author
Kobayashi, Fukiko Browse this author
Ebihara, Takashi Browse this author
Oshiumi, Hiroyuki Browse this author →KAKEN DB
Matsumoto, Misako Browse this author →KAKEN DB
Shingai, Masashi Browse this author
Seya, Tsukasa Browse this author →KAKEN DB
Keywords: Innate immunity
Dendritic cells
Type I interferon
Mitochondrial antiviral signaling protein
Measles virus
Issue Date: Feb-2014
Publisher: Pergamon-elsevier science ltd
Journal Title: Molecular immunology
Volume: 57
Issue: 2
Start Page: 100
End Page: 109
Publisher DOI: 10.1016/j.molimm.2013.08.007
PMID: 24096085
Abstract: 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.
Type: article (author version)
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 瀬谷 司

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