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调控性T细胞调节后血性新血管化.
Yasmine Zouggari1, Hafid Ait-Oufella, Ludovic Waeckel
1Paris-Cardiovascular Research Center, INSERM U970, Hôpital Européen Georges Pompidou, Université Paris 5, 75015 Paris, France.
Circulation
|September 23, 2009
概括
调节性T (Treg) 细胞在缺血后影响血管生长. 减少Treg细胞增强了新血管化,而它们的存在则抑制了它,突出显示Treg细胞是缺血损伤修复的关键调节器.
科学领域:
- 免疫学 免疫学 免疫学
- 血管生物学 血管生物学
- 再生医学是一种再生医学.
背景情况:
- 包括 CD4+ 和 CD8+ T 细胞在内的 T 淋巴细胞对于病后新血管化至关重要.
- 像B7/CD28和CD40-CD40连接体等共刺激途径,以及调节性T细胞 (Treg细胞),影响T细胞激活和免疫反应.
- CD28信号传递对于Treg细胞的生成和恒常状态至关重要,这表明Treg细胞在免疫抑制和T细胞平衡中的作用.
研究的目的:
- 调查Treg细胞激活调节对缺血损伤的免疫炎症反应的假设.
- 为了确定Treg细胞调节对后缺血性新血管化和血管生长的影响.
主要方法:
- 在缺乏CD28,B7-1/2或CD40的小鼠中,通过大腿动脉绑定诱导缺血.
- 评估后缺血性炎症反应,血管生长,足部 perfusion 和毛细血管密度.
- 实验性Treg细胞删除使用抗CD25治疗和采用转移实验在Rag1(-/-) 小鼠.
主要成果:
- CD40缺乏减少了炎症和血管生长; CD28缺乏,特征是Treg细胞较少,显著增强了新血管化.
- 破坏B7-1/2信号传递或Treg细胞枯竭明显改善了后缺血性新血管化.
- 相反,在CD28缺乏的小鼠中增加Treg细胞数量减少了炎症和新血管化,证实了Treg细胞的抑制作用.
结论:
- 调节性T (Treg) 细胞活动在调节后缺血性新血管化的过程中起着重要作用.
- 向Treg细胞代表了一种潜在的治疗策略,以加强在缺血事件后的血管修复.
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