リポポリサッカリドに対する宿主耐性が多発性硬化症と膜増殖性グルメロネフライトの病原性において
Lancet (London, England)
|July 24, 1976
まとめ
アリルエステラーゼ (ArE) は,LPSを分解し,コンプリメントを活性化することによって,ヒトにおけるリポポリサハリド (LPS) の解毒を可能にしている. 欠乏したArEは多発性硬化症や腎疾患と関連している可能性があります.
科学分野:
- 免疫学 免疫学とは
- バイオケミストリー バイオケミストリー
- 病理学 パトロジー
背景:
- 細菌のリポポリサッカリド (LPS),特に脂質Aに対する宿主耐性が確立されています.
- 生物学的な測定は,LPSに対する宿主の防衛機構を以前実証しました.
研究 の 目的:
- 人間におけるLPSの解毒に起因する酵素を特定する.
- LPSの解毒のメカニズムと宿主防御と疾患の病原性におけるその役割を解明する.
主な方法:
- アルファ-1-リポプロテインに関連したアリルエステラーゼ (ArE) 活性を特定するための酵素アッセイ.
- LPSによるC3補足の活性化に関する研究.
- ArEとC3レベルと疾患状態 (多発性硬化症,膜増殖性グルメロネフライト) の相関.
主要な成果:
- アルファ-1-リポプロテインと関連したアリルエステラーゼ (ArE) は,ヒトにおけるLPSの解毒に起因する可能性が高いと特定されています.
- LPSは,C3補完成分を活性化する.
- 提案されたメカニズムは,ArEがLPSを分解し,その後にLPS補完複合体の補完活性化とクリアランスが行われる.
結論:
- ArEの欠乏は,ミエリンに欠けているため多発性硬化症を引き起こし,LPS応答を損なう可能性があります.
- LPSと併用された感染症剤は,特にLPSに対する過剰反応性のある個体において,潜在的感染を活性化させる可能性があります.
- 膜増殖性グルメロネフライトスにおける低血清ArEおよびC3レベルは,LPSの解毒が損なわれていることを示唆し,C3腎炎因子の生成に潜在的に寄与します.
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