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Flow Cytometry Analysis of Immune Cells Within Murine Aortas
Published on: July 1, 2011
由NKG2D/连接体相互作用引起的免疫激活促进了动脉样硬化
Mingcan Xia1, Nadia Guerra, Galina K Sukhova
1Department of Veterinary and Biomedical Sciences, Pennsylvania State University, 115 Henning Bldg, University Park, PA 16802, USA.
Circulation
|November 23, 2011
概括
NKG2D/连接体相互作用将慢性炎症与动脉样硬化中的代谢功能障碍联系在一起. 阻止这种相互作用可以减少斑块的形成,改善代谢条件,提供潜在的治疗点.
科学领域:
- 免疫学 免疫学 免疫学
- 代谢疾病 代谢疾病
- 心血管研究研究心血管研究
背景情况:
- 慢性炎症和代谢功能障碍会产生反循环,导致动脉样硬化.
- 异常的代谢状态,如高血糖症和脂质失调症触发细胞压力和免疫激活,恶化代谢问题.
- 在动脉样硬化中,连接炎症和代谢功能障碍的精确分子机制尚不清楚.
研究的目的:
- 研究NKG2D (自然杀手细胞激活受体) 和其连接体在动脉样硬化的炎症和代谢周期中的作用.
- 为了确定是否准NKG2D/带通路可以减轻动脉样硬化和相关的代谢功能障碍.
主要方法:
- 在受高血糖和高脂血症影响的人类和小鼠组织中检查NKG2D连接体表达.
- 使用NKG2D淘汰赛小鼠和单克隆抗体阻断来抑制NKG2D功能.
- 在动脉样硬化小鼠模型中评估了斑块形成,全身和器官炎症以及代谢参数.
主要成果:
- 在受代谢疾病影响的器官中,NKG2D连接物显著升高调节,特别是在动脉样性大动脉和炎症肝脏中.
- 试验室研究表明异常代谢物诱导NKG2D联体的上调.
- 在无脂蛋白E缺乏的小鼠中抑制NKG2D功能导致动脉样硬化斑块减少,抑制炎症,并改善代谢条件.
结论:
- NKG2D/连接体相互作用在促进动脉样硬化的炎症和代谢功能障碍循环中起着至关重要的分子桥梁作用.
- 向NKG2D/带通路为治疗动脉样硬化和相关代谢疾病提供了一个有希望的治疗策略.
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