The incidence of allergic diseases has dramatically increased in recent decades, especially in urban and industrialized areas. It has been reported that, at present, one third of the population in Japan suffers from bronchial asthma, atopic dermatitis, or allergic rhinitis. The medical cost for treating such patients is huge and on the increase. Thus, it is important socially as well as medically to establish more useful strategies to overcome allergic disorders. Bronchial asthma is a complex disease characterized by airway inflammation involving a Th2-cytokine, interleukin (IL)-13. A substantial body of evidence has accumulated pointing to the pivotal role of IL-13 in the pathogenesis of bronchial asthma. Therefore, IL-13 and its signal pathway are thought to be promising targets to develop a therapeutic agent for bronchial asthma. In this article, we summarize the biological properties of IL-13 itself and its signal transduction pathway, the pathological roles of IL-13 in bronchial asthma, and the agents to inhibit the IL-13 signals that are now under development.
Keywords: STAT6, asthma-model mice, Single nucleotide polymorphisms, Periostin, Chitinase, IL-4 mutein
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