心臓のサルコプラズマ網膜のカルシウムATPアゼは,実験的な心筋病の自己免疫抗原である
A R Sharaf1, J Narula, P D Nicol
1Al-Azhar University, Cairo, Egypt.
Circulation
|March 1, 1994
まとめ
自己免疫性心筋炎は,サルコプラズマ網膜のカルシウムATPASE (SR-ATPase) を標的として誘発することができます. SR-ATPaseまたはその抗体による予防接種は,心臓筋細胞のカルシウム調節を妨害することで,心臓の損傷や心筋炎を引き起こす.
科学分野:
- 心臓病学 心臓病学
- 免疫学 免疫学とは
- 病理学 パトロジー
背景:
- 自己免疫性心筋炎は,様々な心筋抗原と関連しています.
- サルコプラズマカルシウム過負荷は,心筋病の既知の要因です.
- サルコプラズマカルシウム調節障害と心筋炎の病原性との間に潜在的な関連がある.
研究 の 目的:
- サルコプラズマ網膜カルシウムATPase (SR-ATPase) またはそれに対する抗体による免疫が心筋病および心筋炎を誘発するかどうかを調査する.
- 細胞内カルシウムと心筋収縮性の調節におけるSR-ATPaseの役割を調査する.
主な方法:
- 犬の心臓型SR-ATPase.に対するモノクローナル抗体 (4C11-20.21) を生成した.
- 精製されたSR-ATPaseタンパク質または抗体を生成するハイブリドオーム細胞をマウスに注入した.
- ヒストロジーと顕微鏡を用いて心筋病変,筋細胞変性,抗体の局所化を評価した.
主要な成果:
- SR-ATPaseタンパク質で免疫を受けたマウスは,時間の経過とともに心筋病変と心筋炎を発症した.
- 4C11-20.21抗体を注射したマウスは,細胞浸透なしに心筋細胞変性を示した.
- アンチボディは,サブサルコレマ・ミオチューブル系と隣接するサルコレマに局所化され,心筋細胞にコンプリメントの堆積がある.
結論:
- 心臓のSR-ATPaseは,自己免疫性心筋炎を誘発できる自己免疫原体として作用する.
- 心臓のSR-ATPaseに対する抗体は,心筋のエネルギーに依存するプロセスを阻害する.
- 観察された筋縮症は,カルシウム調節への干渉による可能性があり,筋縮性に影響を与えます.
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