内皮祖细胞（EPCs）移植有潜力用于缺血性心肌病的治疗。心梗组织局部微环境对移植细胞活性和功能有重要影响。缺血心肌组织内含有大量调节性T细胞（Tregs）。我们发现心肌Tregs在体外可以直接促进EPCs增殖，减少凋亡。Tregs缺失的心梗小鼠EPCs移植后缺血心肌毛细血管密度明显低于对照组小鼠。同时发现心肌Tregs编码amphiregulin(Areg)的基因和蛋白表达明显高于脾组织Tregs。Areg已被证实具有抗细胞凋亡和促增殖作用。故提出假说：心肌Tregs可以通过Areg相关信号途径提高移植EPCs在缺血组织中的活性和功能，改善心肌供血和心室重构。我们拟利用Tregs 特异性Areg缺失小鼠，针对心肌Tregs调控EPCs活性和功能的作用及其机制进行研究。在此基础上进行Tregs联合EPCs移植治疗急性心梗后左心室重构的动物研究，为EPCs移植治疗缺血性心脏提供新的思路。

Endothelial progenitor cells(EPCs) transplantation is a promising therapy for ischemic heart disease. Acute mycardium infarction(AMI) microenvironment plays vital role on transplanted cells viability and function. Acute ischemic mycardium contains abundant of regulatory T cells(Tregs) immigrated from other place. We found that Tregs in ischemiac mycardium(cardiac Tregs) could facilitate EPCs proliferation and attenuate apoptosis. Deficiency of Tregs made the mice which received EPCs transplantation after AMI had less capillary formation in ischemic region than control mice. Further study found that amphiregulin(Areg) expression level is rather high in cardiac tregs than in spleen tregs. While Areg have anti-apoptosis effect and can facilitate cell proliferation confirmed in cancer field. We suppose that cardiac Tregs in ischemic mycardium could promote transplanted EPCs viability and function through Areg related signal pathway. To verify this, we will take advantage of Tregs specific Areg deficency mice to study the regulation and mechanism of cardiac Tregs on the viability and function of transplanted EPCs. Further, we plan to compare two different transplantation protocols combining Tregs and EPCs in mice after AMI. Through this study, we will clarify the regulation mechanism of cardiac tregs on EPCs viability and function, explore new EPCs transplantation strategy for ischemic heart disease.