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CD137 (4-1BB) 欠乏症は,高脂血症マウスの動脈硬化症を軽減する

Hyung Jun Jeon¹, Jae-Hoon Choi, In-Hyuk Jung

¹Division of Life and Pharmaceutical Science, Ewha Womans University, Seoul, Korea.

|February 24, 2010

まとめ

CD137 (4-1BB) シグナリングを遮断すると,動脈硬化症の進行を減少させます. この経路は,炎症性分子とサイトカインを促進し,プラーク形成に寄与します. CD137を標的にすることは,動脈硬化症に対する有望な治療戦略を提供します.

科学分野:

免疫学免疫学とは
心血管生物学心血管生物学
分子医学は分子医学である.

背景:

腫瘍死滅因子受容体スーパーファミリーは,動脈硬化症に関与しています.
CD137 (4-1BB) は動脈硬化性病変に存在するが,その具体的な役割は不明である.
CD137の機能を理解することは,動脈硬化症の治療法の開発に不可欠です.

研究の目的:

動脈硬化症の発達におけるCD137の役割を調査する.
病変形成に対するCD137/CD137リガンドシグナル伝達を阻害する効果を決定する.

主な方法:

CD137欠乏のアポリポプロテインEノックアウト (ApoE(-/-) CD137(-/-)) とLDL受容体ノックアウト (Ldlr(-/-) CD137(-/-)) を生成したマウス.
動脈硬化性プラークのサイズと炎症マーカーを分析した.

主要な成果:

CD137欠乏症は,両方のマウスモデルで動脈硬化性プラークの損傷を減少させた.
病変の減少は,インターフェロン-ガンマ,モノサイト化学誘導タンパク質-1,腫瘍死滅因子-アルファのレベル低下と相関する.
CD137は,内皮細胞および活性化されたモノサイト/マクロファージにおける上調の炎症分子 (MCP-1,IL-6,VCAM-1,ICAM-1) をシグナル化する.

結論:

CD137/CD137のリガンドシグナル伝達は,動脈硬化症の進行において重要な役割を果たします.
CD137経路を阻害することは,動脈硬化症の治療における潜在的な治療標的である.

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