升高的LDL-C会诱导T细胞代谢功能障碍,并在中年成人中增加炎症和氧化应激
Theodore M DeConne1, Arit Ghosh2, Catherine Awad1
1Department of Kinesiology and Applied Physiology, University of Delaware, Newark, DE, USA.
Journal of applied physiology (Bethesda, Md. : 1985)
|August 4, 2025
概括
极限高的LDL-C激活T细胞,损害线粒体功能,并增加炎症. 这种T细胞功能障碍可能会增加中年成人患年龄相关疾病的风险.
科学领域:
- 免疫学 免疫学 免疫学
- 代谢研究研究 代谢研究
- 衰老研究研究 衰老研究
背景情况:
- T细胞与慢性炎症和与衰老和疾病相关的氧化应激有关.
- T细胞的代谢变化会影响分化,炎症和氧化应激.
- 低密度脂蛋白胆固醇 (LDL-C) 激活T细胞,但其对人类T细胞的直接影响尚不清楚.
研究的目的:
- 研究外源性LDL-C对中年成人CD4+和CD8+T细胞的影响.
- 测试边界高的LDL-C诱导T细胞激活,代谢变化和氧化应激增加的假设.
主要方法:
- 通过细胞外流量分析评估T细胞代谢.
- 通过流细胞计量测量T细胞激活,分化和氧化应激.
主要成果:
- 边界高的LDL-C诱导的CD4+和CD8+T细胞激活.
- 观察到线粒体呼吸功能受损和糖溶性新陈代谢增加.
- 暴露于LDL-C促进了T细胞向效应记忆子集的分化,并增加了炎症性细胞因子和活性氧物种的产生.
结论:
- 极端高的LDL-C诱导T细胞功能障碍,可能增加与年龄有关的疾病的风险.
- 需要进一步研究内源性LDL-C对T细胞功能和疾病风险的体内影响.
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