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对抗原呈现细胞不变链的缺乏会减少小鼠动脉样硬化
Jiusong Sun1, Karsten Hartvigsen, Meng-Yun Chou
1Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass., USA.
Circulation
|August 11, 2010
概括
在小鼠中,不变链 (CD74) 缺陷通过降低适应性免疫力来减少动脉样硬化. 这一意想不到的发现与与生俱来的类似B-1细胞的增加有关,促进了保护性IgM和IgG3反应.
科学领域:
- 免疫学 免疫学 免疫学
- 心血管研究研究心血管研究
- 动脉样硬化是一种动脉样硬化.
背景情况:
- 适应性和先天性免疫在动脉生成中至关重要.
- 不变链 (CD74) 促进抗原呈现和T细胞激活.
- CD74在动脉样硬化中的作用需要进一步研究.
研究的目的:
- 测试CD74缺乏是否会降低T细胞活化,并防止动脉样硬化.
- 在动脉样硬化模型中研究CD74缺乏对免疫反应的影响.
主要方法:
- 使用低密度脂蛋白受体缺乏 (Ldlr(-/-)) 和CD74缺乏 (Ldlr(-/-) Cd74(-/-)) 的小鼠.
- 用于免疫的Malondialdehyde修饰的LDL (MDA-LDL) 和热冲击蛋白-65 (HSP-65) 的管理.
- 分析了动脉样硬化,免疫细胞种群,细胞因子释放和免疫球蛋白同型水平.
主要成果:
- 缺少CD74显著降低了动脉样硬化,并在病变中激活T细胞.
- 观察到对MDA-LDL和HSP-65的适应性免疫反应受损.
- 发现了自抗体产生B-1细胞的百分比增加和IgM/IgG3 titre的升高.
结论:
- 不变链缺陷保护Ldlr的小鼠免受动脉样硬化.
- 降低动脉样硬化与受损的适应性免疫力和增加与生俱来的类似B-1细胞反应有关.
- CD74在动脉动脉生成过程中调节免疫反应中发挥着重要作用.
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