CD11c+単細胞の機能的役割は,高コレステロール血症に関連したアテロゲネシスに起因する
Huaizhu Wu1, R Michael Gower, Hong Wang
1Section of Atherosclerosis and Vascular Medicine, Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA.
Circulation
|May 13, 2009
まとめ
高コレステロールは,単細胞のCD11cを増加させ,単細胞の移動に不可欠なタンパク質である. CD11cをブロックすると,マウスモデルでの単細胞の蓄積と動脈硬化が減少し,心臓血管疾患におけるその役割が強調されます.
科学分野:
- 免疫学 免疫学とは
- 心血管生物学 心血管生物学
- 動脈硬化症の研究研究
背景:
- 単細胞の活性化と移動は,高コレステロール血症によって悪化する状態である動脈硬化症の中心にある.
- ベータ2インテグリンCD11c/CD18は単細胞に発現し,その粘着に影響を与えますが,高コレステロール血症による動脈硬化症におけるその役割は不明です.
研究 の 目的:
- 高コレステロール血症におけるCD11c発現の調節を調査する.
- マウスモデルでの単細胞徴募と動脈硬化症の発達におけるCD11cの役割を決定する.
主な方法:
- CD11c欠乏症のマウスを生成し,アポリポプロテインE欠乏症 (apoE-/-) のマウスと交配させた.
- フローサイトメトリを用いて,高コレステロール症のマウスの白血球におけるCD11c発現を分析した.
- CD11c欠乏症のマウスと対照マウスの単細胞粘着,病変の蓄積,動脈硬化症の発症を評価した.
主要な成果:
- 高コレステロールのapoE-/-マウスは,高脂肪食で,対照群と比較してCD11c+単細胞の増加を示した.
- これらのCD11c+単細胞は,脂質蓄積の兆候とCD11bおよびCD29の発現の増加を示した.
- CD11c欠乏症は,内皮結合体への単細胞結合を低下させ,動脈硬化病変の発達を低下させた.
結論:
- 血液単細胞のCD11c発現は,高コレステロール血症の間,増加する.
- CD11cは,動脈壁への単細胞の徴募に重要な役割を果たします.
- CD11cを標的にすることは,高コレステロール血症における動脈硬化症を減らすための治療戦略を提供することができる.
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