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抗熱ショックタンパク質60の自己抗体は,内皮損傷経由でアポリプロテインE欠乏マウスの動脈硬化を引き起こす

Georgios Foteinos¹, Ali R Afzal, Kaushik Mandal

¹Department of Cardiac and Vascular Sciences, St. George's University of London, Cranmer Terrance, London SW17 0RE, UK.

|August 24, 2005

まとめ

熱ショックタンパク質60 (HSP60) に対する自己抗体が動脈硬化を引き起こす可能性があります. これらの自己抗体をF ((ab)) 2セグメントでブロックすると,マウスの病変発症を防ぐことが可能であり,HSP60の自己免疫が動脈硬化症における因果的な役割を果たしていることを示唆しています.

科学分野:

免疫学免疫学とは
心血管研究循環器科の研究
動脈硬化症の病原性病原性

背景:

抗熱ショックタンパク質60 (HSP60) の自己抗体とヒトの動脈硬化症の間には,正の関連性がある.
動脈硬化症の発症におけるこれらの自己抗体の因果的な役割は不明である.

研究の目的:

動脈硬化症の発達における抗HSP60自己抗体の因果的役割を調査する.
抗HSP60自己抗体が動脈硬化病変を誘発する特定のメカニズムを決定する.

主な方法:

冠動脈性心疾患患者の抗HSP60自己抗体を分離した.
アポリプロテインE欠乏症のマウスに自己抗体と特定のモノクローナル抗体 (II-13) を注射した.
抗体効果を阻害するためにF(ab) 2セグメントを投与.

主要な成果:

抗HSP60自己抗体の注射は,マウスの動脈硬化病変を有意に増加させた.
モノクローナル抗体II-13は,HSP60残基288-366を標的にし,病変,内皮損傷,免疫細胞蓄積を誘発した.
II-13-誘発性動脈硬化症を阻害した抗体から派生したF(ab) 2セグメント.

結論:

HSP60残留288-366を標的とする自己抗体は,動脈内皮細胞に対する自己免疫反応を通じて動脈硬化を引き起こす.
これらの自己抗体から派生したF(ab) 2セグメントは,動脈硬化症の発症を予防することができます.

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