『徳島大学 教育・研究者情報データベース (EDB)』---[学外] /
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EID=333239EID:333239, Map:0, LastModified:2018年5月14日(月) 16:12:23, Operator:[有持 秀喜], Avail:TRUE, Censor:0, Owner:[安友 康二], Read:継承, Write:継承, Delete:継承.
種別 (必須): 学術論文 (審査論文) [継承]
言語 (必須): 英語 [継承]
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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) Zaman Taskia Sultana (日) Taskia Sultana Zaman (読) たすきあ さるたな ざまん
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学籍番号 (推奨): **** [ユーザ]
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2.有持 秀喜 ([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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3. (英) Maruyama Satoshi (日) 丸山 悟史 (読) まるやま さとし
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学籍番号 (推奨): **** [ユーザ]
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4.石舟 智恵子 ([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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5.九十九 伸一 ([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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6.北村 明子
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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 Balances Th17 and Induced Regulatory T Cell Functions in Dendritic Cells by Regulating Aldh1a2 Expression.  (日)    [継承]
副題 (任意):
要約 (任意): (英) Dendritic cells (DCs) are important for adaptive immune responses through the activation of T cells. The molecular interplay between DCs and T cells determines the magnitude of T cell responses or outcomes of functional differentiation of T cells. In this study, we demonstrated that DCs in mice that are Rbpj deficient in CD11c(+) cells (Rbpj(-/-) mice) promoted the differentiation of IL-17A-producing Th17 cells. Rbpj-deficient DCs expressed little Aldh1a2 protein that is required for generating retinoic acid. Those DCs exhibited a reduced ability for differentiating regulatory T cells induced by TGF-. Rbpj protein directly regulated Aldh1a2 transcription by binding to its promoter region. The overexpression of Aldh1a2 in Rbpj-deficient DCs negated their Th17-promoting ability. Transfer of naive CD4(+) T cells into Rag1-deficient Rbpj(-/-) mice enhanced colitis with increased Th17 and reduced induced regulatory T cells (iTreg) compared with control Rag1-deficient mice. The cotransfer of iTreg and naive CD4(+) T cells into Rag1-deficient Rbpj(-/-) mice improved colitis compared with transfer of naive CD4(+) T cell alone. Furthermore, cotransfer of DCs from Rbpj(-/-) mice that overexpressed Aldh1a2 or Notch-stimulated DCs together with naive CD4(+) T cells into Rbpj(-/-)Rag1-deficient mice led to reduced colitis with increased iTreg numbers. Therefore, our studies identify Notch signaling in DCs as a crucial balancer of Th17/iTreg, which depends on the direct regulation of Aldh1a2 transcription in DCs.  (日)    [継承]
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誌名 (必須): The Journal of Immunology ([The American Association of Immunologists])
(pISSN: 0022-1767, eISSN: 1550-6606)

ISSN (任意): 1550-6606
ISSN: 0022-1767 (pISSN: 0022-1767, eISSN: 1550-6606)
Title: Journal of immunology (Baltimore, Md. : 1950)
Title(ISO): J Immunol
Publisher: American Association of Immunologists
 (NLM Catalog  (Scopus  (CrossRef (Scopus information is found. [need login])
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(必須): 199 [継承]
(必須): 6 [継承]
(必須): 1989 1997 [継承]
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年月日 (必須): 西暦 2017年 8月 4日 (平成 29年 8月 4日) [継承]
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DOI (任意): 10.4049/jimmunol.1700645    (→Scopusで検索) [継承]
PMID (任意): 28779023    (→Scopusで検索) [継承]
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備考 (任意): 1.(英) PublicationType: Journal Article  (日)    [継承]

標準的な表示

和文冊子 ● Sultana Taskia Zaman, Hideki Arimochi, Satoshi Maruyama, Chieko Ishifune, Shin-ichi Tsukumo, Akiko Kitamura and Koji Yasutomo : Notch Balances Th17 and Induced Regulatory T Cell Functions in Dendritic Cells by Regulating Aldh1a2 Expression., The Journal of Immunology, Vol.199, No.6, 1989-1997, 2017.
欧文冊子 ● Sultana Taskia Zaman, Hideki Arimochi, Satoshi Maruyama, Chieko Ishifune, Shin-ichi Tsukumo, Akiko Kitamura and Koji Yasutomo : Notch Balances Th17 and Induced Regulatory T Cell Functions in Dendritic Cells by Regulating Aldh1a2 Expression., The Journal of Immunology, Vol.199, No.6, 1989-1997, 2017.

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