| ○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): | □ | Peer Review
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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. | 前川 洋一
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| 2. | (英) Tsukumo Shin-ichi (日) (読)
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| 3. | (英) Chiba Shigeru (日) (読)
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| 4. | (英) Hirai Hisamaru (日) (読)
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| 5. | (英) Hayashi Yuki (日) (読)
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| 6. | (英) Okada Hiroko (日) (読)
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| 7. | (英) Kishihara Kenji (日) (読)
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| 8. | 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) Deltal-Notch3 interactious bias the functional differentiation of activated CD4+ T-Cells (日)
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| ○要約 (任意): | □ | (英) Following activation by antigen, naive CD4+ T helper precursor cells execute distinct genetic programs that result in their differentiation toward the type 1 or type 2 helper T cell (Th1 or Th2) phenotype. Although the differentiation and function of these Th subsets has been well studied, little is known about the contribution to these differentiation events of cell surface receptors other than those for soluble cytokines, such as IL-12 or IL-4. Here, we provide direct evidence that the Delta1 interaction with Notch3 on CD4+ T cells transduces signals, promoting development toward the Th1 phenotype. The positive role of Notch signaling in effector cell differentiation was dose dependent, with high levels of stimulation resulting in reduced T cell activation. Our data revealed a clear contribution of Notch pathways to Th1 versus Th2 fate decisions, while also providing insight into another mechanism for inhibition of CD4+ T cell activation. (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. | 細胞分化 (cell differentiation)
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| 4. | (英) Interferon-gamma (日) (読)
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| 5. | (英) Intracellular Signaling Peptides and Proteins (日) (読)
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| 6. | (英) Leishmania major (日) (読)
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| 7. | (英) Leishmaniasis, Cutaneous (日) (読)
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| 8. | (英) Membrane Proteins (日) (読)
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| 9. | (英) Mice (日) (読)
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| 10. | (英) Proto-Oncogene Proteins (日) (読)
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| 11. | (英) Receptors, Cell Surface (日) (読)
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| 12. | (英) Receptors, Notch (日) (読)
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| 13. | (英) T-Box Domain Proteins (日) (読)
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| 14. | (英) Transcription Factors (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): | □ | 1074-7613
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]) | [継承] |
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| ○巻 (必須): | □ | 19
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| ○号 (必須): | □ | 4
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| ○頁 (必須): | □ | 549 559
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| ○都市 (任意): |
| ○年月日 (必須): | □ | 西暦 2003年 10月 初日 (平成 15年 10月 初日)
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| ○URL (任意): |
| ○DOI (任意): | □ | 10.1016/S1074-7613(03)00270-X (→Scopusで検索)
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| ○PMID (任意): | □ | 14563319 (→Scopusで検索)
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| ○備考 (任意): | 1. | (英) Article.Affiliation: Department of Immunology & Parasitology, School of Medicine, The University of Tokushima, 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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