MIFは,グルココルチコイド誘発によるサイトカイン生成の調節剤である
T Calandra1, J Bernhagen, C N Metz
1Picower Institute for Medical Research, Manhasset, New York 11030, USA.
Nature
|September 7, 1995
まとめ
低レベルのグルココルチコイドは,予期せぬほどにマクロファージの移動阻害因子 (MIF) 産生を増加させる. MIFは,グルココルチコイドの効果を逆調節し,抗炎症作用を覆し,免疫反応に影響を及ぼします.
科学分野:
- 免疫学 免疫学とは
- エンドクリノロジー エンドクリノロジー
- 分子生物学は分子生物学である.
背景:
- グルココルチコイドホルモンは,免疫および炎症の調節に不可欠です.
- 既存の知識では,グルココルチコイドの作用に直接反対する内生媒介物が欠けている.
- マクロファージ移動阻害因子 (MIF) は,炎症性サイトカインおよびセプティックショックの媒介者として認識されています.
研究 の 目的:
- グルココルチコイドとマクロファージにおけるMIF産生との相互作用を調査する.
- MIFがグルココルチコイドの免疫抑制効果に対抗できるかどうかを判断する.
主な方法:
- グルココルチコイドの濃度が異なるマクロファージの刺激.
- グルココルチコイド治療に対するMIF生成の測定.
- モノサイトにおけるリポポリサッカリド (LPS) 誘発のサイトカイン分泌に対するMIFの効果の評価.
- エンドトキセミアに対するグルココルチコイド介護による保護に対するMIFの影響の評価.
主要な成果:
- 低濃度のグルココルチコイドは,マクロファージからMIFの産生を誘発することが判明しました.
- MIFは,LPS刺激モノサイトによるサイトカイン分泌に対するグルココルチコイドの抑制効果を覆すことが観察されました.
- MIFは,致命的なエンドトキセミアに対するグルココルチコイドの保護効果を低下させた.
結論:
- 免疫反応においてMIFとグルココルチコイドを巻き込む新しい対規制システムが特定されました.
- このシステムは,グルココルチコイドの作用に関する伝統的な見解に異議を唱え,炎症を調節するMIFの役割を強調しています.
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