T辅助细胞表型在轻度高胆固醇血清症的情况下调节小鼠的动脉样硬化
S A Huber1, P Sakkinen, C David
1Department of Pathology, University of Vermont, Burlington, USA.
Circulation
|May 31, 2001
概括
辅助T细胞表型影响动脉样硬化发展. 转向Th2 (IL-4+) 细胞减少脂肪病变,而Th1 (IFN-玛+) 细胞促进脂肪病变,特别是通过巨细胞激活.
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
- 遗传学 是一个遗传学.
背景情况:
- T细胞在动脉样硬化中发挥着作用.
- 遗传控制和分子途径尚不清楚,特别是在轻度高胆固醇血症中.
研究的目的:
- 评估T辅助细胞表型在脂肪条纹形成中的作用.
- 研究T细胞参与动脉样硬化的遗传控制和分子途径.
主要方法:
- 研究的野生型和转基因C57Bl/6小鼠吃高胆固醇饮食.
- 评估大动脉损伤的基因组测量.
- 分析了T辅助细胞表型 (Th1与Th2) 和细胞因子表达 (IFN-玛,IL-4).
- 使用抗体和细胞因子治疗来调节T细胞反应.
- 检查的 BALB/c Stat 6 淘汰赛小鼠 (Th2 缺乏).
主要成果:
- 转基因小鼠与改变的MHCII类和T辅助细胞表型显示大动脉损伤大小显著减少 (54-82%).
- 减少的Th1 (干扰素-马+) 细胞和增加的Th2 (干扰素-4+) 细胞与较小的病变相关.
- 干扰素-与激活的巨细胞结合在一起,而介质素-4没有.
- 缺乏Th2的小鼠的病变与容易发生动脉样硬化的小鼠相似.
结论:
- 在轻度高胆固醇贫血小鼠中,MHCII类抗原调节CD4+ T辅助细胞表型.
- 脂肪病变的发展与IFN-玛+Th1细胞成正比.
- IFN-可能通过巨细胞激活促进动脉样硬化.
- IL-4可能会限制Th1细胞的反应,从而减少病变的发展.
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