近年发现：哮喘并不能完全用Th1/Th2失衡理论解释；IL-17也通过募集中性粒细胞、巨噬细胞浸润及诱导分泌等参与哮喘发病过程；γδT细胞则是合成IL-17的重要细胞。我们前期研究发现：雾化吸入灭活草分枝杆菌可减轻哮喘小鼠气道炎症及IL-17表达，同时肺部Vγ1+γδ/Vγ4+γδT细胞比例明显减少。据此我们假设灭活草分枝杆菌能使γδT细胞分泌IL-17减少。本研究以灭活草分枝杆菌对γδT细胞的影响为切入点，首先观察灭活草分枝杆菌对γδT细胞分泌IL-17的影响，继而在机制上观察灭活草分枝杆菌是干预IL-23-IL-23R信号还是抑制JAK/STAT通路从而减少γδT细胞分泌的IL-17。此研究的进展将进一步认识分枝杆菌类药物免疫调节的具体机制，为临床防治哮喘提供新思路。

Recently, it was found that asthma cannot be comprehensively explained by Th1/Th2 balance theory. IL-17 also takes part in asthmatic pathogenetic progress through recruiting infiltration of neutrophils and macrophages as well as inducting secretion.γδ T cells are principal cells which synthetize IL-17. Our previous researches have proved airway inflammation can be reduced through inhaled inactivated mycobacterium phlei in the bronchial asthma mice model, and Vγ1+γδ/Vγ4+γδT cells ratio can be reduced significantly in lungs. We postulated that inactivated mycobacterium phlei could reduce IL-17 produced by γδT cells via inhibition JAK/STAT and interposing the IL-23-IL-23R signal. The aim of the study was to varify wheather inactivated-Mycobacterium phlei could reduce IL-17 produced by γδT in ovalbumin (OVA)-induced asthma model and to identify the molecular mechanism whereby inactivated mycobacterium phlei reduces IL-17 produced by γδT. This research will further recognize the This research will further recognize the immunomodulatory function of Inhaled inactivated-Mycobacterium phlei,which would provide new clues for asthma treatment.