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Teleost TLR22 recognizes RNA duplex to induce IFN and protect cells from birnaviruses

発表形態:
原著論文
主要業績:
主要業績
単著・共著:
共著
発表年月:
2008年09月
DOI:
10.4049/jimmunol.181.5.3474
会議属性:
指定なし
査読:
有り
リンク情報:

日本語フィールド

著者:
Matsuo, Aya; Oshiumi, Hiroyuki; Tsujita, Tadayuki; Tsujita, Tadayuki; Mitani, Hiroshi; Kasai, Hisae; Yoshimizu, Mamoru; Matsumoto, Misako; Seya, Tsukasa
題名:
Teleost TLR22 recognizes RNA duplex to induce IFN and protect cells from birnaviruses
発表情報:
Journal of Immunology 巻: 181 号: 5 ページ: 3474-3485
キーワード:
概要:
TLR22 occurs exclusively in aquatic animals and its role is unknown. Herein we show that the fugu (Takifugu rubripes) (fg)TLR3 and fgTLR22 link the IFN-inducing pathway via the fg Toll-IL-1R homology domain-containing adaptor protein 1(fgTICAM-1, or TRIF) adaptor in fish cells. fgTLR3 resides in endoplasmic reticulum and recognizes relatively short-sized dsRNA, whereas fgTLR22 recognizes long-sized dsRNA on the cell surface. On poly(I:C)-stimulated fish cells, both recruit fgTICAM-1, which in turn moves from the TLR to a cytoplasmic signalosome region. Thus, fgTICAM-1 acts as a shuttling platform for IFN signaling. When fish cells expressing fgTLR22 are exposed to dsRNA or aquatic dsRNA viruses, cells induce IFN responses to acquire resistance to virus infection. Thus, fish have a novel TICAM-1-coupling TLR that is distinct from the mammalian TLR3 in cellular localization, ligand selection, and tissue distribution. TLR22 may be a functional substitute of human cell-surface TLR3 and serve as a surveillant for infection with dsRNA virus to alert the immune system for antiviral protection in fish. Copyright © 2008 by The American Association of Immunologists, Inc.
抄録:

英語フィールド

Author:
Matsuo, Aya; Oshiumi, Hiroyuki; Tsujita, Tadayuki; Tsujita, Tadayuki; Mitani, Hiroshi; Kasai, Hisae; Yoshimizu, Mamoru; Matsumoto, Misako; Seya, Tsukasa
Title:
Teleost TLR22 recognizes RNA duplex to induce IFN and protect cells from birnaviruses
Announcement information:
Journal of Immunology Vol: 181 Issue: 5 Page: 3474-3485
An abstract:
TLR22 occurs exclusively in aquatic animals and its role is unknown. Herein we show that the fugu (Takifugu rubripes) (fg)TLR3 and fgTLR22 link the IFN-inducing pathway via the fg Toll-IL-1R homology domain-containing adaptor protein 1(fgTICAM-1, or TRIF) adaptor in fish cells. fgTLR3 resides in endoplasmic reticulum and recognizes relatively short-sized dsRNA, whereas fgTLR22 recognizes long-sized dsRNA on the cell surface. On poly(I:C)-stimulated fish cells, both recruit fgTICAM-1, which in turn moves from the TLR to a cytoplasmic signalosome region. Thus, fgTICAM-1 acts as a shuttling platform for IFN signaling. When fish cells expressing fgTLR22 are exposed to dsRNA or aquatic dsRNA viruses, cells induce IFN responses to acquire resistance to virus infection. Thus, fish have a novel TICAM-1-coupling TLR that is distinct from the mammalian TLR3 in cellular localization, ligand selection, and tissue distribution. TLR22 may be a functional substitute of human cell-surface TLR3 and serve as a surveillant for infection with dsRNA virus to alert the immune system for antiviral protection in fish. Copyright © 2008 by The American Association of Immunologists, Inc.


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