○種別 (必須): | □ | 学術論文 (審査論文)
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○言語 (必須): | □ | 英語
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○審査 (推奨): |
○カテゴリ (推奨): |
○共著種別 (推奨): |
○学究種別 (推奨): |
○組織 (推奨): |
○著者 (必須): | 1. | (英) Fukui Ryutaro (日) (読)
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| 2. | (英) Saitoh Shin-Ichiroh (日) (読)
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| 3. | (英) Kanno Atsuo (日) (読)
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| 4. | (英) Onji Masahiro (日) (読)
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| 5. | (英) Shibata Takuma (日) (読)
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| 6. | (英) Ito Akihiko (日) (読)
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| 7. | (英) Onji Morikazu (日) (読)
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| 8. | 松本 満 ([徳島大学.先端酵素学研究所.重点研究部門])
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| 9. | (英) Akira Shizuo (日) (読)
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| 10. | (英) Yoshida Nobuaki (日) (読)
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| 11. | (英) Miyake Kensuke (日) (読)
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○題名 (必須): | □ | (英) Unc93B1 restricts systemic lethal inflammation by orchestrating Toll-like receptor 7 and 9 trafficking (日)
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○副題 (任意): |
○要約 (任意): | □ | (英) Toll-like receptor-7 (TLR7) and 9, innate immune sensors for microbial RNA or DNA, have been implicated in autoimmunity. Upon activation, TLR7 and 9 are transported from the endoplasmic reticulum (ER) to endolysosomes for nucleic acid sensing by an ER-resident protein, Unc93B1. Little is known, however, about a role for sensor transportation in controlling autoimmunity. TLR9 competes with TLR7 for Unc93B1-dependent trafficking and predominates over TLR7. TLR9 skewing is actively maintained by Unc93B1 and reversed to TLR7 if Unc93B1 loses preferential binding via a D34A mutation. We here demonstrate that mice harboring a D34A mutation showed TLR7-dependent, systemic lethal inflammation. CD4(+) T cells showed marked differentiation toward T helper 1 (Th1) or Th17 cell subsets. B cell depletion abolished T cell differentiation and systemic inflammation. Thus, Unc93B1 controls homeostatic TLR7 activation by balancing TLR9 to TLR7 trafficking. (日)
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○キーワード (推奨): | 1. | (英) Animals (日) (読)
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| 2. | (英) B-Lymphocytes (日) (読)
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| 3. | (英) Cell Differentiation (日) (読)
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| 4. | (英) Cells, Cultured (日) (読)
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| 5. | (英) Inflammation (日) (読)
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| 6. | (英) Lymphocyte Depletion (日) (読)
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| 7. | (英) Membrane Glycoproteins (日) (読)
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| 8. | (英) Membrane Transport Proteins (日) (読)
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| 9. | (英) Mice (日) (読)
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| 10. | (英) Mice, Inbred C57BL (日) (読)
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| 11. | (英) Mice, Knockout (日) (読)
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| 12. | (英) Mice, Transgenic (日) (読)
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| 13. | (英) Mutation (日) (読)
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| 14. | (英) Protein Binding (日) (読)
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| 15. | (英) Protein Transport (日) (読)
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| 16. | (英) Th1 Cells (日) (読)
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| 17. | (英) Th17 Cells (日) (読)
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| 18. | (英) Toll-Like Receptor 7 (日) (読)
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| 19. | (英) Toll-Like Receptor 9 (日) (読)
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○発行所 (推奨): |
○誌名 (必須): | □ | Immunity (Cell Press)
(pISSN: 1074-7613, eISSN: 1097-4180)
○ISSN (任意): | □ | 1097-4180
ISSN: 1074-7613
(pISSN: 1074-7613, eISSN: 1097-4180) Title: ImmunityTitle(ISO): ImmunityPublisher: Cell Press (NLM Catalog)
(Scopus)
(CrossRef)
(Scopus information is found. [need login])
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○巻 (必須): | □ | 35
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○号 (必須): | □ | 1
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○頁 (必須): | □ | 69 81
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○年月日 (必須): | □ | 西暦 2011年 7月 初日 (平成 23年 7月 初日)
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○URL (任意): |
○DOI (任意): | □ | 10.1016/j.immuni.2011.05.010 (→Scopusで検索)
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○PMID (任意): | □ | 21683627 (→Scopusで検索)
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○備考 (任意): | 1. | (英) Article.Affiliation: Division of Infectious Genetics, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minatoku, Tokyo 108-8639, Japan. (日)
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| 2. | (英) Article.PublicationTypeList.PublicationType: Journal Article (日)
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| 3. | (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't (日)
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