In summary, we have shown that CD103 plays an important role in the pathogenesis of experimental allergic airways disease in pro‐allergic BALB/c mice through regulation of airway expression of AHR and eosinophilia, but not in systemic sensitization to allergen or induction of allergen‐specific IgE. The gene discussed is ITGAE; the disease is Increased total eosinophil count.