Requirement for IL-13 independently of IL-4 in experimental asthma

The pathogenesis of asthma reflects, in part, the activity of T cell cytoki nes. Murine models support participation of interleukin-4 (IL-4) and the IL -4 receptor in asthma. Selective neutralization of IL-13, a cytokine relate d to IL-4 that also binds to the alpha chain of the IL-4 receptor, ameliora ted the asthma phenotype, including airway hyperresponsiveness, eosinophil recruitment, and mucus overproduction. Administration of either IL-13 or IL -4 conferred an asthma-like phenotype to nonimmunized T cell-deficient mice by an IL-4 receptor alpha chain-dependent pathway. This pathway may underl ie the genetic associations of asthma with both the human 5q31 Locus and th e IL-4 receptor.