淋巴细胞中的氧化低密度脂蛋白受体预防动脉样硬化并预测临床下疾病
Katerina Tsilingiri1, Hortensia de la Fuente2,3, Marta Relaño1
1Vascular Pathophysiology Area (K.T., M.R., R.S.-D., V.F., P.M., F.S.-M.), Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid, Spain.
Circulation
|December 28, 2018
概括
CD69受体对T细胞免疫至关重要,通过抑制Th17细胞的发育来预防动脉样硬化. 患者的CD69水平较低与动脉样硬化风险增加相关.
科学领域:
- 免疫学
- 心血管研究
- 分子生物学
背景情况:
- Th17和调节性T细胞与动脉样硬化有关,但它们的分子调节者尚不清楚.
- CD69受体在T细胞免疫中的作用表明与动脉样硬化的发展有联系.
研究的目的:
- 在动物模型和人类亚临床疾病中研究CD69与动脉样硬化之间的关联.
- 阐明涉及CD69,氧化LDL和T细胞分化的分子机制.
主要方法:
- 使用低密度脂蛋白受体缺乏CD69的小鼠,食高脂肪饮食.
- 在PESA研究的305名参与者中进行了体外T细胞测定和分析CD69和NR4A表达.
主要成果:
- 缺乏淋巴细胞CD69的小鼠表现出较大的动脉样斑块和较高的Th17/Treg比率.
- 在T淋巴细胞上的CD69结合氧化LDL,通过NR4A激活抑制Th17细胞.
- 亚临床动脉样硬化患者的白细胞CD69和NR4A1mRNA水平较低.
结论:
- 淋巴细胞中的CD69缺乏通过破坏T细胞平衡而加剧动脉样硬化.
- 通过CD69氧化的LDL相互作用促进抗炎转录因子.
- CD69表达是亚临床动脉样硬化的独立预测因子.
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