Abstract

Abstract Although allergic asthma is a chronic inflammatory disease of the lung mediated by Th2 cells, the pathways leading to this response are not clear. Recent studies have highlighted influence of pulmonary dendritic cells (DCs) on T-cell differentiation. Rapid DC recruitment into the bronchial mucosa has been well documented in animals and humans in response to allergen. Central to early DC recruitment, CCL20 is the only known ligand for CCR6, a receptor preferentially expressed on immature DCs. The potential importance of CCL20/CCR6 in allergic sensitization was demonstrated in a cockroach model of allergic asthma in which Ccr6-/- mice were protected against asthma. At present, the mechanisms by which allergen induces secretion of DC-attractant chemokines are unknown. We previously showed that bronchial epithelial cells release CCL20 relatively rapidly after house dust mite (HDM) (Nathan, 2009). This induction was not prevented by the inhibiting protein synthesis (cycloheximide) suggesting release through a transcriptionally independent mechanism. These data suggested that HDM may induced the release of preformed stores of CCL20

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