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Der p2 rBCG also displayed a potent inhibitory effect on Th17 differentiation, and these findings increase our understanding of the cellular basis of Der p2 BCG-mediated inhibition of asthma. Excessive T helper (Th) 2 cells play a key role in orchestrating chronic airway inflammation in allergic asthma. However, Th2 cytokine inhibition has been [http://en.wikipedia.org/wiki/RVX_208 RVX-208] unsuccessful in treating established asthma in patients.[1] Recently, knowledge of the pathogenesis of asthma has broadened to incorporate the contribution of Th17 cells. Th17 cells have been shown to be effective in upregulating neutrophilic and macrophage inflammation in the lung.[2] Recombinant bacille Calmette-Guerin (rBCG), which expresses the Der p2 of house dust mites (Der p2 rBCG), can suppress asthmatic airway inflammation by inducing more allergen-specific T regulatory [http://www.selleckchem.com/products/Neratinib(HKI-272).html selleckchem] cells, while native BCG cannot.[3] Further studies have shown that these effects are involved in regulating the functions and phenotypes of dendritic cells (DC).[4] There is a close relationship between mycobacterial infection and Th17 differentiation; extended freeze-dried BCG blocked transcriptional regulator signatures of Th17 (retinoic acid-related orphan receptor ��t (ROR��t)) cells.[5] Similarly, the frequency of Th17 cells in patients with active tuberculosis is significantly less than that in healthy donors.[6] The Notch signalling pathway [http://www.selleckchem.com/products/BMS-777607.html BMS-777607 cell line] is an important pathway that regulates development with high conservation between species.[7] Notch receptors and ligands are involved in the interaction between DC and T cells. The effects produced by the different Notch receptors and ligands are different. It has been reported that Delta-like proteins 1 and 4 can promote naive T cells to differentiate into Th1, while in the pro-Th2/Th17 environment, the level of the protein jagged-2 on the DC surface is elevated.[8] Hence, we hypothesized that Der p2 rBCG plays an important role in regulating Th17 differentiation causing inhibition of allergic airway inflammation. In this study, we compared the immunoregulatory role of Der p2 rBCG with native BCG in Th17 differentiation by employing a mouse asthma model. Healthy female C57BL/6 mice (6�C8 weeks of age) were purchased from the Experimental Animal Center of Fourth Military Medical University (Xi'an, China). All research protocols were approved by the Animal Experiment Administration Committee of Fourth Military Medical University. Der p2 rBCG was constructed as previously described.[9] Der p2 rBCG and native BCG were cultured and harvested as previously described.[4] Mouse bone morrow was flushed from femurs and tibias, and a single-cell suspension was prepared, followed by erythrolysis in ammonium chloride-potassium buffer.