This review evaluates the role of IL-5 and IL-5-mediated eosinophil airway infiltration in the development of allergen-driven airway hyperresponsiveness. It discusses the structure and function of IL-5 and its receptor and the mechanisms of IL-5-triggered eosinophil accumulation and inflammation of the airways. New research data from murine models of airway inflammation and hyperresponsiveness utilizing different modes of sensitization to allergen and anti-IL-5 antibody or IL-5-deficient knock-out mice underscore the outstanding role of this cytokine in the pathogenesis of bronchial asthma. This review identifies possible directions for future treatment of airway hyperresponsiveness and concludes that targeting IL-5-driven inflammatory responses may be most beneficial for a novel therapy in bronchial asthma.