Allergic rhinitis (AR) is a high-prevalence disease, affecting 10-15% of the general population. AR is sustained by an IgE-mediated reaction, and by a complex inflammatory network of cells, mediators and cytokines that becomes chronic when exposure to allergen persists. A T helper 2 (TH2)-biased immune response is the basis for the allergic inflammation. The current therapeutic strategy is mainly based on drugs (antihistamines, nasal corticosteroids, cromones, decongestants) and allergen immunotherapy. Drugs are overall effective in controlling symptoms, but do not modify the immune background that leads to allergic inflammation, and safety concerns may be present especially for prolonged treatments. Immunotherapy can modify the allergic response, but there is still space for improvement. Nowadays, several approaches are under investigation to optimise the management of AR. On one hand, new drugs and antimediators are being developed; on the other hand, attempts are made to selectively block relevant signal pathways of allergic reaction. Finally, one of the major goals is to modify the TH2-biased immune response by improving the characteristics and modes of action of allergen immunotherapy.
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Ciprandi et al. (2005) studied this question.
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