吸烟引起COPD的炎症导致肺组织降解产生弹性蛋白肽（EP），EP可促进树突状细胞（DCs）诱导T细胞分化为Th17参与COPD炎症发病过程，DCs与T细胞的CD40-CD40L通路和DCs中的 FOXO3是影响DCs诱导T细胞分化为Th17的重要因素，然而EP刺激DCs诱导T细胞向Th17分化是否通过CD40-CD40L通路及FOXO3机制尚无研究。我们前期研究发现Th17细胞在COPD患者及烟草烟雾暴露大鼠肺实质中增多并与炎症相关，故本项目在前期研究的基础上进一步探讨EP刺激下DC对T细胞分化为Th17的CD40-CD40L通路及FOXO3影响。首先探EP刺激下DCs的共刺激分子和FOXO3表达，进而观察在阻断和不阻断CD40-CD40L下EP刺激DC细胞对T细胞分化成Th17的影响。以上研究为本课题的特色与创新点，研究开展将有助于深化认识COPD中免疫炎症的机制以及寻找新的治疗靶点。

The inflammation of COPD caused by Cigarette smoke lead to degradation of lung tissue, which generate elastin pepitedes(EP).EP can promote dendritic cells(DCs) to induce differentiation of Th17 from T cells, which participate the inflammatory process of COPD. The CD40-CD40L pathway of DCs contacted with T cells and the forkhead box o 3(FOXO3) are the important factors which impact DCs polarize T cells to Th17.Whereas whether the EP stimulate DCs polarizing T cells to Th17 by the mechanism of CD40-CD40L pathway and FOXO3 is unclear. We previously demonstrated that Th17 expression had increased in the lung parenchyma of patient with COPD and of rat with emphysema, which associated with inflammation of COPD. So based these researches, we further investigate the effect of EP on pathway of CD40-CD40L and FOXO3 which DC polarize T cells to Th17:Firstly we observe the effect of EP on the co-stimulatory molecules and FOXO3 of DCs. Secondly we investigate the he effect of EP on DCs polarizing T cells to Th17 under the condition of blocking and non-blocking the CD40-CD40L pathway. This research will further recognize the mechanism of immune inflammation in COPD,and provide the new target for treatment of COPD.