抗甲状腺药物和炎症媒介的释放由补体攻击的甲状腺细胞
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
概括
在格雷夫斯病和哈希莫托甲状腺炎中,补充对甲状腺细胞的攻击会导致炎症. 抗甲状腺药物减少了这种炎症,这可能解释了治疗自身免疫性甲状腺疾病的疗效.
科学领域:
- 免疫学 免疫学 免疫学
- 内分泌学 在内分泌学.
- 细胞生物学 细胞生物学
背景情况:
- 甲状腺细胞在自身免疫性甲状腺疾病中面临补充剂攻击,如格雷夫斯病和哈西莫托甲状腺炎.
- 尽管暴露,甲状腺细胞表现出对补充介导细胞死亡的抵抗.
研究的目的:
- 在实验室中研究亚致命补充对甲状腺细胞攻击的影响.
- 探索CD59在调解甲状腺细胞对补充剂反应中的作用.
- 为了确定抗甲状腺药物对补充诱导的甲状腺细胞激活的影响.
主要方法:
- 在体外对受到补充攻击的甲状腺细胞进行研究.
- 测量活性氧代谢物和细胞因子的释放 (前列腺素E2,IL-1α,IL-6).
- 评估CD59表达和功能使用干扰素-,介质素-1α和单克隆抗体.
- 评估抗甲状腺药物 (甲基马,甲) 的作用.
主要成果:
- 亚致补剂攻击诱导了甲状腺细胞的活性氧代谢物和细胞因子释放.
- 用干扰素-和介质素-1α进行预治疗,增强了CD59表达和增加了对补充效应的抵抗力.
- CD59阻塞放大了补充介导的氧基生成和炎症介导体释放.
- 甲基马和propylthiouracil降低了补充攻击的甲状腺细胞的氧基生成和细胞因子释放.
结论:
- 亚致命补体攻击通过触发炎症媒介的释放,加剧了自身免疫性甲状腺疾病的甲状腺损伤.
- 细胞因子诱导的CD59上调可能在体内提供对补充介导损伤的保护.
- 抗甲状腺药物通过抑制甲状腺细胞内的炎症分子释放,可能有助于改善甲状腺炎和疾病缓解.
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