心力衰竭的免疫发病机制与治疗策略

Immune pathogenesis and treatment strategies for heart failure

急性心肌梗死(AMI)和急性病毒性心肌炎(AVMC)患者体内存在Th1/Th2/Th17细胞功能失衡;至慢性心力衰竭阶段,Treg细胞数目下降,抑制炎症反应功能降低。实验研究证明,IL-17促进AVMC小鼠病毒复制和体液免疫应答,加重AMI心肌缺血再灌注损伤;他汀类、β受体阻滞剂和芪苈强心等药物可以改善免疫内环境、升高Treg细胞比例,有利于心肌修复和改善心室重构。以上研究和发现推动我们提出心力衰竭免疫发病机制和治疗策略的全新理念。

The imbalance of Th1/Th2/Th17 cells is important in the pathogenesis of acute myocardial infarction （AMI） and acute myocarditis （AVMC）, which might lead to the inhibition of Treg cells in patients with chronic heart failure （CHF） resulting from those diseases. The experimental studies clarified that IL-17 could promote virus replication and humoral immune response in AVMC mice, and exacerbate myocardial ischemia-reperfusion injuries in AMI animals. Some medicines including statins, β-blocker and Qiliqiangxin were recently found to have the benificial effects in myocardium repair and remolding by improving immune-mediated internal enviroment disorder and elevating Treg cell frequency in CHF. Based on these studies, we now raise a new theory about immune pathogenesis and treatment strategies for heart failure.