Increased production of interleukin (IL)–4 and IL–5 by T–helper cells may be pivotal for the induction and regulation of allergic diseases. We have studied the role of IL–4 and IL–5 in the development of eosinophilic airway inflammation (AI) and airway hyperresponsiveness (AHR) in a mouse model of allergen–induced bronchial asthma. Utilizing different modes of sensitization, we delineated the importance of IL–5–mediated eosinophilic airway infiltration for the development of in vitro and in vivo AHR and demonstrated the inhibition of airway inflammation and AHR by anti–IL–5 antibody treatment. Studies in IL–4– and IL–5 deficient mice revealed the importance of both cytokines for the induction of AI and AHR independently from the production of allergen–specific IgE, and indicated these cytokines as potential targets in novel approaches in the treatment of asthma.

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