抗甲状腺薬と,補完体に攻撃された甲状腺細胞による炎症媒介体の放出
A P Weetman1, N Tandon, B P Morgan
1Department of Medicine, University of Sheffield Clinical Sciences Centre, Northern General Hospital, UK.
Lancet (London, England)
|September 12, 1992
まとめ
グラブス病とハシモトの甲状腺炎では,甲状腺細胞に対する補完攻撃が炎症を引き起こす. 抗甲状腺薬は,この炎症を軽減し,潜在的に自己免疫性甲状腺疾患における治療効果を説明します.
科学分野:
- 免疫学 免疫学とは
- エンドクリノロジー エンドクリノロジー
- 細胞生物学 細胞生物学
背景:
- 甲状腺細胞は,グレイヴス病やハシモトの甲状腺炎のような自己免疫性甲状腺疾患において,補完体の攻撃に直面する.
- 曝露にもかかわらず,甲状腺細胞は,補足媒介による細胞死に対する抵抗を示します.
研究 の 目的:
- 甲状腺細胞に対する亜致死補完体の攻撃の効果を in vitro で調査する.
- 補足に対する甲状腺細胞の反応を媒介するCD59の役割を調査する.
- 補足誘発性甲状腺細胞活性化に対する抗甲状腺薬の影響を決定する.
主な方法:
- 補完攻撃を受けた甲状腺細胞のインビトロ研究.
- 活性酸素代謝産物とサイトカインの放出 (プロスタグランジンE2,IL-1α,IL-6) の測定.
- CD59の発現と機能の評価は,インターフェロン-ガンマ,インタールイキン-1α,およびモノクローナル抗体を用いて行われました.
- 抗甲状腺薬 (メチマゾール,プロピルチオウラシル) の効果の評価.
主要な成果:
- サブレタル・コンプリメント攻撃は,甲状腺細胞から反応性酸素代謝産物とサイトカインの放出を誘発した.
- インターフェロン・ガンマとインターレウキン-1αによる前治療は,CD59発現を高め,補完効果に対する抵抗性を高めました.
- CD59の封鎖は,補足媒介の酸素ラジカル生成と炎症媒介体の放出を拡大した.
- メチマゾールとプロピルチオウラシルは,補完体が攻撃した甲状腺細胞からの酸素根子の生成とサイトカインの放出を減少させた.
結論:
- 副致死的な補完攻撃は,炎症媒介体の放出を誘発することによって,自己免疫性甲状腺疾患における甲状腺損傷を悪化させる.
- サイトカイン誘発によるCD59のアップレギュレーションは,補完介的ダメージからin vivoで保護を提供することがあります.
- 抗甲状腺薬は,甲状腺細胞内の炎症性分子の放出を抑制することによって,甲状腺炎の改善と疾患の寛解に貢献することができます.
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