| ○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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| ○招待 (推奨): |
| ○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. | 北村 明子
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| ○学籍番号 (推奨): |
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| 2. | 佐々木 由紀 ([徳島大学.AWAサポートセンター])
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| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
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| 3. | (英) Abe Takaya (日) (読)
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| 4. | (英) Kano Hirotsugu (日) (読)
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| [継承] |
| 5. | 安友 康二 ([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.病理系.生体防御医学])
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| ○題名 (必須): | □ | (英) An inherited mutation in NLRC4 causes autoinflammation in human and mice. (日)
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| ○副題 (任意): |
| ○要約 (任意): | □ | (英) Autoinflammatory syndromes cause sterile inflammation in the absence of any signs of autoimmune responses. Familial cold autoinflammatory syndrome (FCAS) is characterized by intermittent episodes of rash, arthralgia, and fever after exposure to cold stimuli. We have identified a missense mutation in the NLRC4 gene in patients with FCAS. NLRC4 has been known as a crucial sensor for several Gram-negative intracellular bacteria. The mutation in NLRC4 in FCAS patients promoted the formation of NLRC4-containing inflammasomes that cleave procaspase-1 and increase production of IL-1. Transgenic mice that expressed mutant Nlrc4 under the invariant chain promoter developed dermatitis and arthritis. Inflammation within tissues depended on IL-1-mediated production of IL-17A from neutrophils but not from T cells. Our findings reveal a previously unrecognized link between NLRC4 and a hereditary autoinflammatory disease and highlight the importance of NLRC4 not only in the innate immune response to bacterial infections but also in the genesis of inflammatory diseases. (日)
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| ○キーワード (推奨): | 1. | (英) Amino Acid Sequence (日) (読)
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| 2. | (英) Animals (日) (読)
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| 3. | (英) Apoptosis Regulatory Proteins (日) (読)
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| 4. | (英) Blotting, Western (日) (読)
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| 5. | (英) CARD Signaling Adaptor Proteins (日) (読)
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| 6. | (英) Calcium-Binding Proteins (日) (読)
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| 7. | (英) Caspase 1 (日) (読)
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| 8. | (英) Cells, Cultured (日) (読)
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| 9. | (英) Cryopyrin-Associated Periodic Syndromes (日) (読)
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| 10. | (英) Female (日) (読)
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| 11. | (英) Flow Cytometry (日) (読)
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| 12. | (英) Genetic Predisposition to Disease (日) (読)
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| 13. | (英) Genotype (日) (読)
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| 14. | (英) HEK293 Cells (日) (読)
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| 15. | (英) Humans (日) (読)
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| 16. | (英) Inflammasomes (日) (読)
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| 17. | (英) Interleukin-17 (日) (読)
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| 18. | (英) Interleukin-1beta (日) (読)
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| 19. | (英) Male (日) (読)
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| 20. | (英) Mice, Inbred C57BL (日) (読)
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| 21. | (英) Mice, Transgenic (日) (読)
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| 22. | (英) Molecular Sequence Data (日) (読)
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| 23. | (英) Mutation, Missense (日) (読)
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| 24. | (英) Neutrophils (日) (読)
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| 25. | (英) Pedigree (日) (読)
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| 26. | (英) Sequence Homology, Amino Acid (日) (読)
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| ○発行所 (推奨): |
| ○誌名 (必須): | □ | The Journal of Experimental Medicine ([The Rockefeller University Press])
(pISSN: 0022-1007, eISSN: 1540-9538)
| ○ISSN (任意): | □ | 1540-9538
ISSN: 0022-1007
(pISSN: 0022-1007, eISSN: 1540-9538) Title: The Journal of experimental medicineTitle(ISO): J Exp MedPublisher: Rockefeller University Press (NLM Catalog)
(Scopus)
(CrossRef)
(Scopus information is found. [need login]) | [継承] |
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| ○巻 (必須): | □ | 211
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| ○号 (必須): | □ | 12
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| ○頁 (必須): | □ | 2385 2396
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| ○都市 (任意): |
| ○年月日 (必須): | □ | 西暦 2014年 11月 10日 (平成 26年 11月 10日)
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| ○URL (任意): |
| ○DOI (任意): | □ | 10.1084/jem.20141091 (→Scopusで検索)
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| ○PMID (任意): | □ | 25385754 (→Scopusで検索)
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| ○CRID (任意): |
| ○WOS (任意): |
| ○Scopus (任意): | □ | 2-s2.0-84911922142
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| ○備考 (任意): | 1. | (英) PublicationType: Journal Article (日)
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| 2. | (英) PublicationType: Research Support, Non-U.S. Gov't (日)
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