Abstract
Allergic diseases are complex disorders involving a combination of genetic and environmental factors. In case of bronchial asthma, these factors result in infiltration of Th-2 lymphocytes, mast cells and eosinophils into asthmatic airways with downstream mediator release and disordered airway function. Cytokines derived from the Th-2 lymphocytes are considered to orchestrate the asthmatic phenotype. Among Th2 cytokines, the significance of IL-13 in the pathogenesis of bronchial asthma has recently emerged. Particularly, the direct action of IL-13 on bronchial epithelial cells is critical for generation of airway hyperresponsiveness. IL-13 signal is regulated by two receptors; one is the heterodimer composed of the IL-13 receptor α1 chain and the IL-4 receptor α chain which transduces IL-13 signal, and the other is the IL-13 receptor α2 chain which blocks the IL-13 signal. In this review article, we present our recent findings about the expression mechanism of the IL-13 receptors on bronchial epithelial cells and the functional role of a single nucleotide polymorphism on IL13 gene as a genetic factor. These findings give us a hint to improve the asthmatic condition by blocking the IL-13 actions.
