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制御性B細胞におけるPI3Kシグナルによる制御機構の解析
https://doi.org/10.24517/00051404
https://doi.org/10.24517/0005140429ca9b01-9272-43b5-8d9a-b7aa48ae2ef8
名前 / ファイル | ライセンス | アクション |
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HO-PR-MATSUSHITA-T-kaken 2013-4p.pdf (478.2 kB)
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Item type | 報告書 / Research Paper(1) | |||||
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公開日 | 2018-07-05 | |||||
タイトル | ||||||
タイトル | 制御性B細胞におけるPI3Kシグナルによる制御機構の解析 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | Analysis of PI3K signaling role in regulatory B cells | |||||
言語 | ||||||
言語 | jpn | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_18ws | |||||
資源タイプ | research report | |||||
ID登録 | ||||||
ID登録 | 10.24517/00051404 | |||||
ID登録タイプ | JaLC | |||||
著者 |
松下, 貴史
× 松下, 貴史 |
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著者別表示 |
Matsushita, Takashi
× Matsushita, Takashi |
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提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 金沢大学附属病院 | |||||
書誌情報 |
平成24(2012)年度 科学研究費補助金 若手研究(B) 研究成果報告書 en : 2012 Fiscal Year Final Research Report 巻 2011-2012, p. 4p., 発行日 2013-04-25 |
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出版者 | ||||||
出版者 | 金沢大学附属病院 | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | 近年、免疫反応を抑制する作用を持つIL-10産生制御性B細胞が発見され、免疫疾患において非常に重要であることが明らかとなった。制御性B細胞の分化・増殖にはB細胞の表面マーカーであるCD19およびそのシグナル伝達(PI3Kシグナル)が重要であることが示唆されている。本研究では、PI3Kシグナルによる制御性B細胞の制御機構を解析した。本研究にてPI3Kの阻害剤が、用量依存性にIL-10産生を阻害しりことを明らかとした。さらにPI3K/AKTのinhibitorであるPTENのB細胞特異的欠損マウスを作成し、同マウスにてIL-10産生制御性B細胞が著増していることを確認した。B細胞特異的PTEN欠損マウスではContact hypersensitivity反応の著明な低下が認められた。以上より、IL-10産生制御性B細胞の制御機構において、PI3K/AKT経路が重要であることが明らかとなった。 | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | IL-10 producing regulatory B (Breg) cells negatively regulates autoimmune disease and inflammation, such as contact hypersensitivity (CHS). CD19 expression is critical for Breg cells development, since CD19 loss results in decreased number of Breg cell and increased reactivity of CHS. However, molecular mechanism of Breg cell development remains poorly understood. CD19 downstream signal is depend on the activation of phosphoinositide 3-kinases (PI3K)-AKT pathways, while phosphatase and tensin homologue (PTEN) attenuates PI3K-AKT pathways. In this study, we investigated the role of PI3K-AKT pathway in the development of Breg cells. The effect of PI3K-AKT pathway inhibitors on Breg cell development was examined in vitro. B cell-specific PTEN deficient mice, which exhibit aberrant activation of PI3K-AKT pathway in B cell, were generated using Cre-loxp system. CHS severity in B cell-specific PTEN deficient mice was investigated. The current studies demonstrate that PI3K-AKT pathway inhibitors reduced Breg cells in vitro in dose-dependent manner. However, PTEN inhibitor had no effect on Breg cells. Breg cell number and frequency were significantly increased in various organs of B cell-specific PTEN deficient mice when compared with wild-type mice. Furthermore, CHS response was significantly diminished in B cell-specific PTEN deficient mice when compared with wild-type mice. Thus, PI3K-AKTpathway positively regulates Breg cell development, while PTEN negatively regulates it. PI3K-AKT pathway in B cell is critical for Breg cell development and could be a potent therapeutical target. | |||||
内容記述 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 研究課題/領域番号:23791260, 研究期間(年度):2011-2012 | |||||
内容記述 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 出典:研究課題「制御性B細胞におけるPI3Kシグナルによる制御機構の解析」課題番号23791260 (KAKEN:科学研究費助成事業データベース(国立情報学研究所)) (https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-23791260/23791260seika/)を加工して作成 |
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著者版フラグ | ||||||
出版タイプ | AM | |||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/search/?qm=60432126 | |||||
関連名称 | https://kaken.nii.ac.jp/search/?qm=60432126 | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23791260/ | |||||
関連名称 | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23791260/ | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-23791260/23791260seika/ | |||||
関連名称 | https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-23791260/23791260seika/ |