Th17細胞をターゲットとした皮膚疾患の治療

Material type: 文書・図像類

Author: 岡本, 芳伸ほか

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Publication date: 2016-05-26

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Note (General)：: 金沢大学附属病院全身性強皮症は原因不明の線維化疾患で、Th17細胞と関連するIL-17Aなどが関与する報告が近年増えている。線維化の機序解明と臨床応用を目指し、皮膚線維化病変におけるIL-17Aの役割を検討した。成長因子投与による皮膚線維化モデルマウスにおいて、野生型と比較してIL-17A欠損マウス...

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https://kaken.nii.ac.jp/ja/search/?kw=90707100

https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-26860872/

https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-26860872/26860872seika/

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Material Type: 文書・図像類
Title: Th17細胞をターゲットとした皮膚疾患の治療
Author/Editor: 岡本, 芳伸
Okmoato, Yoshinobu
Author Heading: 岡本, 芳伸
Okmoato, Yoshinobu
Publication Date: 2016-05-26
Publication Date (W3CDTF): 2016-05-26
Alternative Title: A study of treatment strategy for fibrotic skin disorders, which targets Th17 cells
Periodical title: 平成27(2015)年度科学研究費補助金若手研究(B) 研究成果報告書 = 2015 Fiscal Year Final Research Report
No. or year of volume/issue: 2014-04-01 – 2016-03-31
Volume: 2014-04-01 – 2016-03-31
Pages: 4p.-
Text Language Code: jpn
Subject Heading: サイトカイン
TGF-β
CTGF
IL-17A
Target Audience: 一般
Note (General): 金沢大学附属病院
全身性強皮症は原因不明の線維化疾患で、Th17細胞と関連するIL-17Aなどが関与する報告が近年増えている。線維化の機序解明と臨床応用を目指し、皮膚線維化病変におけるIL-17Aの役割を検討した。成長因子投与による皮膚線維化モデルマウスにおいて、野生型と比較してIL-17A欠損マウスで線維化が改善し、炎症細胞の浸潤が軽減した。IL-17Aは、皮膚への直接投与でも持続的な線維化を誘導し、成長因子CTGFの産生増加に関連して慢性の線維化病変の維持にかかわることが示唆された。また、薬剤開発を目指し、IL-17A抑制物質ウルソール酸の投与を試みたが、理想的な濃度や投与法などの改良を要すると考えられた。
Systemic sclerosis (SSc) is a fibrotic disorder, the etiology of which has not yet been fully elucidated. Recently, growing evidence has demonstrated that Th17cells and IL-17A plays a crucial role in the pathogenesis of SSc. The aim of this study was to examine the role of IL-17A in the progression of skin fibrosis in experimental murine fibrosis model by exogenous injection of growth factors. The loss of IL-17A significantly attenuated the rapid subcutaneous fibrosis and infiltration of inflammatory cells, to compared with wild-type. The daily injections of IL-17A alone induced fibrosis with time, and increased expression levels of TGF-β1 and CTGF mRNA. This findings suggest that IL-17A contributes to production of CTGF, thereby leading to persistent fibrosis.In addition, with the aim of drug development, we attempt to administer IL-17A-inhibitor agent: ursolic acid. we improve such as the ideal concentration and method of administration.
研究課題/領域番号:26860872, 研究期間(年度):2014-04-01 – 2016-03-31
DOI: 10.24517/00059241
Access Restrictions: 限定公開
Related Material: https://kaken.nii.ac.jp/ja/search/?kw=90707100
https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-26860872/
https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-26860872/26860872seika/
Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）
https://irdb.nii.ac.jp
Original Data Provider (Database): 金沢大学 : 金沢大学学術情報リポジトリKURA