研究表明急性心肌梗死（AMI）后心室重塑与炎症关系密切。2型固有淋巴细胞（ILC2s）属于固有免疫系统，通过产生IL-13/IL-5/Areg等效应分子在多种炎症相关疾病中发挥重要作用。我们的前期研究发现AMI后心脏中ILC2s增多，过继转输ILC2s明显减轻AMI后的心室重塑并改善心功能。因此我们认为ILC2s在AMI后心室重塑中具有保护作用，其具体机制有待进一步阐明。本项目拟：①观察AMI后ILC2s的表达规律；②应用ILC2s过继转输或ILC2KO小鼠观察增加或去除IL2Cs对AMI后心室重塑的影响；③观察去除或增加不同小鼠来源（WT/IL-13KO/IL-5KO/AregKO）的ILC2s对AMI后单核细胞，巨噬细胞的影响，明确ILC2s调控AMI后心室重塑的靶细胞和效应分子。最终深入地阐明ILC2s在AMI后心室重塑中的保护作用和机制，为AMI后心室重塑的靶向治疗提供理论基础。

Recent studies show that ventricular remodeling after acute myocardial infarction (AMI) is closely related to immune inflammation. Type 2 innate lymphoid cells (ILC2s) belong to the innate immune system and play an important role in a variety of inflammation-related diseases by generating effector molecules such as IL-13/IL-5/Areg. Our previous study found increased ILC2s in the heart after AMI. Besides，adoptive transfer of ILC2s significantly reduced ventricular remodeling and improved cardiac function after AMI. Therefore, we believe that ILC2s play a protective role in ventricular remodeling after AMI, and its specific mechanism needs to be further elucidated. This project intends to: ① observe the expression of ILC2s after AMI; ② observe the effects of ILC2s replenishment or deleption on ventricular remodeling after AMI through adoptive transfer ILC2s or ILC2KO mice; ③ observed deleption or replenishment ILC2s from the source of different mice (WT/IL-13KO/IL-5KO/AregKO) on monocytes and macrophages after AMI, to investigate the target cells and functional mediators of ILC2s. These exploratory studies will lead to a comprehensive understanding of the role of ILC2s in ventricular remodeling after AMI, and provide the theoretical and experimental basis for the development of targeted therapy in ventricular remodeling after AMI.