| ○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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| ○カテゴリ (推奨): |
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| ○学究種別 (推奨): |
| ○組織 (推奨): |
| ○著者 (必須): | 1. | (英) Alam Shamsul Muhammad (日) (読)
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| 2. | (英) Maekawa Yoichi (日) (読)
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| 3. | (英) Kitamura Akiko (日) (読)
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| 4. | (英) Tanigaki Kenji (日) (読)
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| 5. | (英) Yoshimoto Takayuki (日) (読)
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| 6. | (英) Kishihara Kenji (日) (読)
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| 7. | 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) Notch signaling drives IL-22 secretion in CD4+ T cells by stimulating the aryl hydrocarbon receptor. (日)
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| ○要約 (任意): | □ | (英) CD4(+) helper T (Th) cells differentiate toward distinct effector cell lineages characterized by their distinct cytokine expression patterns and functions. Multiple Th cell populations secrete IL-22 that contributes to both protective and pathological inflammatory responses. Although the differentiation of IL-22-producing Th cells is controlled by the aryl hydrocarbon receptor (AhR), little is known about the regulatory mechanisms inducing physiological stimulators for AhR. Here, we show that Notch signaling enhances IL-22 production by CD4(+) T cells by a mechanism involving AhR stimulation. Notch-mediated stimulation of CD4(+) T cells increased the production of IL-22 even in the absence of STAT3. CD4(+) T cells from RBP-J-deficient mice had little ability to produce IL-22 through T cell receptor-mediated stimulation. RBP-J-deficient mice were highly susceptible to the detrimental immunopathology associated with ConA-induced hepatitis with little IL-22 production by CD4(+) T cells. Exogenous IL-22 protected RBP-J-deficient mice from ConA-induced hepatitis. Notch signaling promoted production of endogenous stimulators for AhR, which further augmented IL-22 secretion. Our studies identify a Notch-AhR axis that regulates IL-22 expression and fine-tunes immune system control of inflammatory responses. (日)
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| ○キーワード (推奨): | 1. | (英) Animals (日) (読)
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| 2. | (英) CD4-Positive T-Lymphocytes (日) (読)
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| 3. | (英) Cell Differentiation (日) (読)
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| 4. | (英) Female (日) (読)
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| 5. | (英) Hepatitis, Animal (日) (読)
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| 6. | (英) Immunoglobulin J Recombination Signal Sequence-Binding Protein (日) (読)
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| 7. | (英) Interleukins (日) (読)
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| 8. | (英) Mice (日) (読)
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| 9. | (英) Mice, Inbred C57BL (日) (読)
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| 10. | (英) Mice, Knockout (日) (読)
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| 11. | (英) Mice, Transgenic (日) (読)
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| 12. | (英) Protein Structure, Tertiary (日) (読)
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| 13. | (英) Receptors, Aryl Hydrocarbon (日) (読)
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| 14. | (英) Receptors, Notch (日) (読)
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| 15. | (英) Recombinant Proteins (日) (読)
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| 16. | (英) STAT3 Transcription Factor (日) (読)
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| 17. | (英) Signal Transduction (日) (読)
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| ○発行所 (推奨): |
| ○誌名 (必須): | □ | Proceedings of the National Academy of Sciences of the United States of America ([The National Academy of Sciences of the United States of America])
(pISSN: 0027-8424, eISSN: 1091-6490)
| ○ISSN (任意): | □ | 1091-6490
ISSN: 0027-8424
(pISSN: 0027-8424, eISSN: 1091-6490) Title: Proceedings of the National Academy of Sciences of the United States of AmericaTitle(ISO): Proc Natl Acad Sci U S APublisher: National Academy of Sciences (NLM Catalog)
(Scopus)
(CrossRef)
(Scopus information is found. [need login]) | [継承] |
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| ○巻 (必須): | □ | 107
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| ○号 (必須): | □ | 13
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| ○頁 (必須): | □ | 5943 5948
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| ○都市 (任意): |
| ○年月日 (必須): | □ | 西暦 2010年 3月 15日 (平成 22年 3月 15日)
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| ○URL (任意): |
| ○DOI (任意): | □ | 10.1073/pnas.0911755107 (→Scopusで検索)
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| ○PMID (任意): | □ | 20231432 (→Scopusで検索)
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| ○CRID (任意): |
| ○WOS (任意): | □ | 000276159500046
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| ○備考 (任意): | 1. | (英) Article.Affiliation: Department of Immunology and Parasitology, Institute of Health Biosciences, University of Tokushima Graduate School, Tokushima 770-8503, 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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| 4. | (英) OtherID: PMC2851859 (日)
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