グルココルチコイド受容体は,ヒト中性粒子のL-セレクチンとCD11/CD18の発現を調節する
J G Filep1, A Delalandre, Y Payette
1Maisonneuve-Rosemont Hospital, Department of Medicine, University of Montréal, Québec, Canada.
Circulation
|July 1, 1997
まとめ
グルココルチコイドは,活性化された中性粒子の粘着分子に特異的に影響を及ぼし,白血球の蓄積を減少させます. この抗炎症効果は,グルココルチコイド受容体とタンパク質合成を巻き込み,コルチコステロイド作用の新たなメカニズムを提供する.
科学分野:
- 免疫学 免疫学とは
- 細胞生物学 細胞生物学
- 薬理学 薬理学とは
背景:
- グルココルチコイドは,内皮粘着分子をダウンレギュレーションすることによって,白血球の炎症組織への密輸を阻害する可能性があります.
- 本研究では,ヒト中性粒子のL-セレクチンおよびCD11/CD18インテグリン発現に対するグルココルチコイドの影響を調査しています.
研究 の 目的:
- グルココルチコイドがヒト中性粒子のL-セレクチンおよびCD11/CD18インテグリン発現を調節するかどうかを判断する.
- 中性粒子の粘着分子に対するグルココルチコイド作用のメカニズムを解明する.
主な方法:
- 人間の全血は,血小板活性化因子 (PAF) で刺激されました.
- L-セレクチンとCD11/CD18の中性粒子の発現はフローサイトメトリーで測定した.
- デキサメタゾンの効果は,RU-486とサイクロヘキシミドの存在で評価されました.
主要な成果:
- PAFは,中性粒子のL-セレクチンのダウンレギュレーションとCD11/CD18のアップレギュレーションを誘導した.
- デキサメタゾンは,時間および濃度に依存した方法で,L-セレクチンとCD18におけるPAF誘発の変化を弱めた.
- デキサメタゾンの効果はRU-486とサイクロヘキシミドによって阻害され,受容体媒介およびタンパク質合成に依存するメカニズムを示した.
結論:
- グルココルチコイドは,臨床的に重要な濃度で活性化中性粒子の粘着分子の発現を調節する.
- これらの効果は,グルココルチコイド受容体結合とタンパク質合成誘導によって媒介されます.
- これは,抗炎症性コルチコステロイドによる白血球蓄積の抑制のための新しいメカニズムを示唆しています.
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