D er p2 recombinant bacille C almette‐ G uerin priming of bone marrow‐derived dendritic cells suppresses D er p2‐induced T helper17 function in a mouse model of asthma

Background and objective Previous studies have demonstrated that our recombinant bacille C almette‐ G uerin ( rBCG ), which expresses D er p2 in house dust mite ( D er p2 rBCG ) suppresses asthmatic airway inflammation by regulating the phenotype and function of dendritic cells ( DC ) and reprogramming T helper ( T h) 0 cell differentiation into different T cell ( T h1/ T h2/ T reg) subtypes. However, the exact role of D er p2 rBCG in reprogramming T h17 differentiation and the relevant mechanisms are not known. The aim of this study was to examine whether D er p2 rBCG ‐mediated inhibition of allergic airway inflammation is mediated by regulating T h17 differentiation in a murine asthma model. Methods Primary mouse bone marrow‐derived dendritic cells ( BMDC ) were infected with D er p2 rBCG and adoptively transferred to D er p2‐intranasally sensitized mice. The role of D er p2 rBCG ‐ BMDC on the regulation of airway inflammation and T h17 cell differentiation was assessed. Results Adoptive transfer of D er p2 rBCG ‐ BMDC suppressed airway inflammation and mucin secretion. D er p2 rBCG ‐ BMDC inhibited excessive T h17 immune responses but not BCG ‐ BMDC . Furthermore, D er p2 rBCG decreased jagged‐2 and increased delta‐like‐4 expressions on BMDC to a greater extent than BCG . Conclusions These findings suggest that DC plays a key role in D er p2 rBCG ‐induced immunoregulation. D er p2 rBCG also displayed a potent inhibitory effect on T h17 differentiation, and these findings increase our understanding of the cellular basis of D er p2 BCG ‐mediated inhibition of asthma.