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化基因受体7淘汰赛减弱了动脉样硬化斑块的发展

Maren Luchtefeld¹, Christina Grothusen, Andreas Gagalick

¹Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.

|October 6, 2010

概括

化学因子受体7 (CCR7) 的全身缺陷通过损害T细胞迁移和原始化来减少动脉样硬化发展. 这突出了CCR7的作用.

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
炎症性疾病炎症性疾病

背景情况:

动脉样硬化是一种系统性炎症性疾病,涉及斑块形成.
天生的免疫和适应性免疫都在动脉生成中发挥作用,具有复杂的相互作用.
化学因子受体7 (CCR7) 对于免疫细胞在淋巴体器官和炎症组织中的贩运至关重要.

研究的目的:

为了研究系统化基因受体7 (CCR7) 缺乏在动脉生成中的作用.
确定CCR7对T细胞迁移的影响及其对LDLR淘汰小鼠动脉样硬化斑块发育的影响.

主要方法:

使用患有动脉样硬化倾向的低密度脂蛋白受体 (ldlr) 淘汰系统性CCR7缺乏的小鼠.
在CCR7缺乏的小鼠中评估了动脉样硬化斑块的发展.
在动脉样硬化病变中研究T细胞行为 (入/出) 使用活体T细胞和采用氧化低密度脂蛋白 (oxLDL) 的采用转移实验.

主要成果:

缺乏CCR7显著降低了动脉样硬化斑块的发展.
缺乏CCR7的T细胞表现出动脉样硬化病变的进出迁移受损.
收养转移oxLDL原型野生型T细胞,但不是CCR7缺乏的T细胞,在接受者小鼠中复制动脉生成.

结论:

在二次淋巴体器官内,CCR7依赖的T细胞原始化和CCR7介导的T细胞再循环都对动脉样硬化斑块的进展至关重要.
CCR7在调节驱动动动脉硬化的自适应性免疫反应方面发挥着至关重要的作用.

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