Social and economic costs of allergic rhinitis (AR) are impressive; AR may also significantly impact school attendance and performance, quality of life, and sleep (1). The AR immunopathology is characterized by T-helper-2 (Th2)-dependent inflammation and Th1-response impairment. This imbalance is sustained by dysfunction of immune system: allergic patients are lacking in allergen-specific T regulatory cells, so T helper 2 cells may polarize the immune response to allergen and produce large quantity of some interleukins, including IL-4, IL-5, and IL-13, that in turn promote IgE synthesis and eosinophil production, recruitment, and activation at nasal level. This article is protected by copyright. All rights reserved.