免疫媒介による肌細胞損傷のメカニズム

W H Barry¹

¹Department of Medicine, University of Utah School of Medicine, Salt Lake City.

Circulation

|May 1, 1994

まとめ

免疫系の成分は,移植拒絶,心筋炎,拡張性心筋症候群の間に心臓機能を害します. これらのメカニズムの理解は,免疫媒介性心臓損傷のより良い治療法につながる可能性があります.

科学分野:

心血管疾患の免疫学について
心臓病理学について
移植免疫学移植免疫学

背景:

免疫系の活性化は,様々な状態で心臓の機能不全に寄与する.
血管損傷と筋細胞の変化は,免疫媒介の心臓損傷の重要な特徴です.

研究の目的:

免疫媒介の心臓機能不全のメカニズムを定義する.
免疫媒介性心臓損傷の治療標的を調査する.

主な方法:

免疫システムの構成要素とその心臓機能への影響のレビュー.
心臓損傷におけるユーモラルおよび細胞媒介体の分析.
筋細胞機能における炎症性細胞の役割の調査.

主要な成果:

ユーモラルおよび細胞媒介物質は血管損傷を引き起こし,心室適合性および移植動脈硬化に影響を及ぼします.
細胞毒性Tリンパ球 (CTLs) はミオサイトを in vitro で溶解することができるが, in vivo の有意性は不明である.
炎症性細胞 (中性子,マクロファージ) とサイトカインは,肌細胞の機能と生存に影響を与えます.
ミオサイト抗原を標的にする抗体は,抗体依存メカニズムまたは直接の受容体/チャネル変化を通じて細胞損傷を誘発する.

結論:

免疫媒介の心臓損傷は,血管および筋細胞機能に影響を与える多様なメカニズムを含んでいます.
これらの経路の解明は,免疫媒介性心臓機能不全の標的治療の開発に不可欠です.

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