放射性肺炎是胸部肿瘤放射治疗中的常见并发症，且是主要致死原因之一，迄今临床上仍缺乏安全有效的治疗方法。其发生机制尚不明确，目前比较认同的是"细胞因子级联反应"学说，这些因子中研究较热的是TNFa和TGFβ，其调控机制与放射性水解形成的活性氧族有关。最近有研究发现肿瘤细胞经放射线照射后IL-1β的表达水平与放射剂量正相关。我们在前期研究中也发现：大鼠放射性肺炎模型中IL-1β的表达增加，且其上游分子AIM2的表达升高。我们推测在TNFa、TGFβ之外存在一条新的通路促进放射性肺炎的发生和发展，即AIM2炎症小体通路。本研究拟在前期工作基础上进一步深入研究AIM2炎症小体在放射性肺炎发生中的激活和调控机制，从而为放射性肺炎的发病机制研究提供新的理论依据，并为临床上防治放射性肺炎探索新的干预靶点。

Radiation pneumonitis is one of the most common complications in thoracic tumor radiation therapy, and is one of the main causes of death.So far no effective therapy has been found to treat this unique inflammation,with an inexplicable mechanism. Currently, cytokine cascade reaction is widely acclaimed for explaination. Research hotspot has been on TNFa and TGFβ,the regulation mechanism is associated with reactive oxygen species from radioactive hydrolysis. Recent studies have reported that the expression level of IL-1β in radiated tumor cells is positively correlated with radiation dose. Our previous studies also found that IL-1β was up-regulated in rat radiation pneumonitis, accompanied with an increased expression of up-stream AIM2 molecule. We speculate that, in addition to TNFa and TGFβ, a new pathway may promote radiation pneumonitis, which is the AIM2 inflammasome pathway.Based on our previous work,present study aims to further investigate the activation and modulation of AIM2 inflammasome in radiation pneumonitis, in order to provide new evidence for detecting the mechanism of radiation pneumonitis and grope a new target for preventing clinical radiation pneumonitis.