阻塞性睡眠呼吸暂停综合征(OSAS)是以慢性间歇低氧（CIH）为特征的慢性疾病,并被流行病学研究证实是肿瘤重要的危险因素，但机理并不清楚。近年来发现乏氧是髓源性抑制细胞（MDSC）发挥免疫抑制功能、促进肿瘤免疫逃逸的重要前提条件。鉴于MDSC在肿瘤发生发展中的重要作用，本项目推测，OSAS导致的乏氧环境可以增强MDSC免疫抑制功能，这可能是OSAS促进肿瘤发生发展重要机制。为验证上述假设，本项目以肺癌为研究对象，拟通过构建模拟OSAS的慢性间歇低氧的小鼠模型：（1）分析OSAS病理条件对MDSC对T细胞的免疫抑制功能的影响及分子机制；（2）通过体内外实验，分析在CIH小鼠肺癌的发生和发展中是否依赖MDSC？总之，本项目旨在为进一步认识OSAS促进肿瘤发生发展提供新的线索和理论支撑。

Obstructive sleep apnea syndrome(OSAS) characterized by chronic intermittent hypoxia(CIH) is an important risk factor for tumorigenesis,which has been verified by many clinical studies. Previous studies show that this is closely associated with immunologic function. As important immune suppressor cells,it is unclear whether myeloid-derived suppressor cells(MDSC) play an important role in OSAS-related tumor progression. In our previous studies,we found that the number of MDSC in patients with OSAS was higher than that in the control. Since it is well known that MDSC play an important role in tumor immune escape, we hypothesize that MDSC might be a key molecule in promoting carcinogenesis and enhancing tumor progression in OSAS patients. To verify our hypothesis, we will perform the following experiments through structuring CIH in rats : (1) To detect the levels of MDSC in CIH rats and evaluate its effect on T cells and investigate the molecular mechanism of the suppression of T cells by MDSC ; (3) To analyze whether MDSC play a siginificant role in CIH-induced progression of lung cancer. Taken together, we plan to understand the role of immunologic mechanism in OSAS-related tumor mediated by MDSC.