局部无菌性炎症反应是放射性心脏损伤的关键，研究表明PD-1/PD-L1在调控炎症稳态中起中心重要作用，但其在放射性心脏炎症反应中的作用尚不清楚。我们前期研究发现，放射线可诱导小鼠心肌细胞表面PD-L1表达；高表达PD-L1小鼠发生放射性心脏损伤的风险比下降40%；PD-L1表达与心脏损伤成显著负相关。阻断PD-1/PD-L1轴，小鼠心肌T淋巴细胞活化更明显，局部炎症反应更严重。据此，我们提出假说：放射线诱导心肌细胞PD-L1表达,进而与T淋巴细胞表面PD-1受体结合抑制其活化，避免局部过度炎症反应，维持心肌微环境免疫稳态，保护放射性心脏损伤。本研究拟从分子、细胞、组织及动物水平等多层次明确PD-1/PD-L1在放射性心脏损伤中的作用；探讨其参与放射性心脏炎症反应的信号通路；揭示其调控心肌微环境免疫稳态保护放射性心脏损伤的分子机制。本研究将从免疫稳态这个新视点探索防治放射性心脏损伤的新方向。

Local aseptic inflammation plays an important role in radiation-induced heart injury. Studies have shown that PD-1/PDL-1 axis plays an important role in regulating inflammation homeostasis. However, whether PD-1/PDL-1 axis participate in radiation-induced heart inflammation is unclear. Previously, we found that radiation can induce programmed PDL-1 protein expression on the surface of mouse myocardial cells. The risk of radiation-induced heart injury decreased by 40% in mice with high expression levels of PDL-1. There was a negative correlation between PDL-1 expression and elevated levels of heart damage. Blocking the PDL-1 receptor increased T cell activation in myocardial cells of mice after irradiation, indicating an increased local inflammatory response. Accordingly, we speculate that radiation-induced PDL-1 protein expression, inhibits T cell activation by interacting with PD-1receptor, avoids local excessive inflammation, maintains the microenvironment in a steady state, and protects against radiation-induced heart injury. This study will clarify the effect of PD-1/PDL-1 axis in radiation-induced heart injury at the levels of molecules, cells, tissues, whole animals, and patient. We will explore the PD-1/PDL-1 axis related signaling pathways that regulating the local inflammatory reaction. The study will explore the molecular mechanisms of PD-1/PDL-1 axis dependent regulation of immune homeostasis of the myocardial microenvironment in radiation induced heart injury. The study will generate new directions for research into the prevention and control of radiation-induced heart injury.