申请人前期研究发现，galectin-9通过诱导机体免疫应答格局的改变有效地缓解CVB3诱导的病毒性心肌炎。Galectin-9除了影响CD4+T细胞亚群的比例变化，还能有效扩增CVB3感染小鼠心脏浸润CD11b+Gr-1+髓系来源抑制细胞MDSCs。然而，这群细胞的亚型和功能及其在病毒性心肌炎中的作用还不清楚。本研究在明确galectin-9对病毒性心肌炎保护作用的基础上开展深入性研究，利用CVB3诱导的病毒性心肌炎模型，观察galectin-9作用前后小鼠心脏浸润MDSCs比例变化，并进一步分析其表型和功能的差异；通过体外混合培养，研究galectin-9诱导的MDSCs对CD4+T细胞增殖、分化及细胞因子分泌的影响；通过体内转输实验，探讨galectin-9诱导的MDSCs在病毒性心肌炎中的作用及其机制，从而为病毒性心肌炎的发病机制研究和生物学防治提供新的理论基础和实验依据。

Our previous study found that galectin-9 administration ameliorates CVB3 induced myocarditis by promoting the proliferation of regulatory T cells and alternatively activated Th2 cells. In addition, galectin-9 remarkably increased the frequencies of CD11b+Gr-1+ myeloid-derived suppressor cells (MDSCs) in the cardiac tissue with myocarditis. However, the functions of the MDSCs and the role of its subsets in CVB3 induced myocarditis are largely unknown. In the present study, we will further identify the phenotypes and functions of MDSCs, exploring the role and mechanism of MDSCs and its subsets in CVB3-induced myocarditis in vitro and in vivo. Our study will help to further understand the mechanism of CVB3-induced myocarditis and provide a novel therapeutic strategy in treating inflammatory cardiac disease.