哮喘的发病机理极为复杂，也尚未阐明。近年发现：γδT细胞是哮喘发病机制的重要细胞。我们前期研究证实：γδT细胞也存在Th1/Th2细胞免疫模式；雾化吸入灭活分枝杆菌可减轻哮喘小鼠气道炎症，改善Th1/Th2细胞因子失衡,同时肺部Vγ1+γδ/Vγ4+γδT细胞比例明显减少，临床哮喘患者气道高反应性（AHR）明显降低，哮喘症状缓解。据此，我们推测吸入灭活分枝杆菌可通过调控γδT细胞降低AHR。本研究首先观察雾化吸入分枝杆菌对γδT细胞谱系的干预作用及对哮喘小鼠AHR的影响；再探讨经灭活分支杆菌干预后的TCR-β-/-小鼠提供的γδT细胞对哮喘小鼠AHR的影响，以验证假说；继而在机制上观察灭活分枝杆菌是干预Notch信号还是影响转录因子T-bet/STAT3，从而恢复γδ1/γδ2平衡。此研究的进展将进一步认识分枝杆菌类药物免疫调节的机制，为其临床防治哮喘提供新依据。

The pathogenesis of asthma is extremely complicated and has not been elucidated. Recently, it was found that γδT cells are important cells in the mechanism of asthma.Our previous studies have confirmed that γδT cells also exist Th1/Th2 cell immune pattern.Inhalation of inactivated Mycobacterium could attenuate airway inflammation and improve Th1/Th2 imbalance. In the same period,the ratio of Vγ1+γδ/Vγ4+γδT cell subsets was significantly decreased in lungs in the bronchial asthma mice models,and airway hyperresponsiveness（AHR） in asthmatic patients was decreased ,the clinical symptoms were significantly alleviated. Accordingly, we assume that inhalation of inactivated mycobacteria can decrease AHR via regulating γδT cells .In this study we observe the effect of inactivated mycobacterium on γδT cell gene genealogy and AHR, and investigate the regulation of AHR by γδT cell derived from inactivated mycobacterium pretreated TCR-β-/- mice and identify the mdlecular mechanism whereby inactivated mycobacterium restore γδ1/γδ2 balance: intervene the Notch signaling or the transcription factors T-bet/STAT3? This research will further recognize the immunomodulatory mechanisms of inhaled Mycobacterium drugs,which would provide new evidence for the prevention and treatment of asthma.