近年来，尽管具有抑制神经内分泌系统激活的药物使用使慢性心力衰竭（心衰）患者的死亡率明显降低，但心衰患者的总体预后仍然欠佳。故寻找新的治疗方法是临床亟待解决的问题。有研究提示心衰也是一个多系统免疫紊乱综合征，患者体内存在针对心肌自身的免疫应答，心肌损伤后自身抗原的暴露启动了免疫应答过程，最终参与了心衰的发生发展。本课题拟了解Tregs/Th17免疫自稳失衡在心衰疾患中的作用。从人群的免疫自稳状态失衡改变与疾病预后相关性入手，检测代表免疫应答的相关指标，同时与经典预后评估指标相结合，证实免疫自稳失衡与患者预后的相关性。在此基础上，建立心衰动物模型，并给予PI3K/AKT/mTOR免疫通路抑制剂以及通路激活剂双向干预，从整体、细胞及分子水平探讨免疫信号通路对Tregs/Th17免疫自稳失衡的干预作用，以及在心衰疾患中的作用，进一步对这些变化进行解析，为心衰的治疗提供新的思路和治疗靶点线索。

Recently, the drug of inhibiting activation of neuroendocrine system has made the reduction in mortality among patients with chronic heart failure, but the overall of CHF patients remains poor prognosis. So looking for a new treatment is the clinical important problems need to be solved immediately. At present, it is speculated that CHF is a multiple system immune disorder syndrome. Myocardial own immune response exist in CHF patients. The trigger of myocardial injury after its antigen exposed started the process of immune response. Usually，immune response in a steady state, immunologic homeostasis，but if the immune response imbalance from steady state, Eventually, myocardial own immune response participate in the development of CHF.This experiment was designed to understand Tregs/Th17 immunologic homeostasis imbalance role in CHF. From the crowd of immune response change of correlation with disease prognosis and testing on behalf of the relevant indexes of immune response, at the same time combined with classic prognostic indicators, it maybe confirm that the imbalance of immunologic homeostasis is correlated to the prognosis of CHF patients. On this basis, to establish animal model of heart failure and PI3K/AKT/mTOR immune pathway inhibitors and activators two-way intervention, as a whole, cellular and molecular levels to explore the immune signaling pathways of Tregs/Th17 immunologic homeostasis from the intervention effect of imbalance, and its role in heart disease. It helps to further understand myocardial remodeling, maybe providing a new way for the therapeutic targets of heart failure and changes in the prognosis of CHF.