我们的前期研究证实，Tγδ17细胞反应促进急性心肌梗死（AMI）后不良心室重塑。胸腺基质淋巴细胞生成素（TSLP）在炎症反应中常扮演“策划者”的角色。我们的预实验发现，TSLP在AMI后表达升高和促进不良心室重塑，其作用可能与Tγδ17细胞反应有关，但二者的确切关系和调控机制有待进一步阐明。本项目拟①观察AMI后NF-κB和TSLP的表达及细胞定位，明确NF-κB对TSLP的表达调控，阐明AMI后TSLP的上游调控机制；②观察阻断TSLP或升高TSLP后对AMI后心室重塑的和Tγδ17细胞反应影响，以及去除γδT细胞对TSLP作用的影响，阐明TSLP是否通过调控Tγδ17细胞反应促进不良心室重塑；③从间接通过树突状细胞作用和/或直接作用两个角度阐明TSLP调控AMI后Tγδ17细胞反应的机制。结果有助于揭示TSLP与AMI后免疫炎症的关系，完善AMI后炎症反应理论，为其干预提供新的靶点。

Our previous study confirmed that Tγδ17 cell response aggravated adverse ventricular remodeling after acute myocardial infarction (AMI). Thymic stromal lymphopoietin (TSLP) play a regulator role in the inflammatory responses. Our preliminary experiments found that the myocardial expression of TSLP increased after AMI and TSLP may aggravated adverse ventricular remodeling by regulating Tγδ17 cell response. However, the exact relationship between the two deserves further studies. The project plans to ① observe the expression and cellular localization of NF-κB and TSLP in vivo, and investigate the regulatory effect of NF-κB on TSLP expression in vitro, to clarify the upstream regulatory mechanism of TSLP after AMI; ② observe the effect of blocking TSLP or increasing TSLP on ventricular remodeling and Tγδ17 cell response, and the effect of removing γδT cell on TSLP’ activity on ventricular remodeling, to clarify whether TSLP promotes adverse ventricular remodeling by regulating Tγδ17 cell response; ③ clarify whether TSLP indirectly acts through dendritic cells and/or directly acts on Tγδ17 cell response to aggravate adverse ventricular remodeling. The project helps to reveal the relationship between TSLP and the inflammatory response after AMI and improve immune theory for ventricular remodeling, providing a new target for intervention.