Requirement for IL-13 Independently of IL-4 in Experimental Asthma
Gabriele Grünig(San Francisco General Hospital), Martha L. Warnock(San Francisco General Hospital), Adil E. Wakil(San Francisco General Hospital), Rajeev Venkayya(San Francisco General Hospital), Frank Brombacher(San Francisco General Hospital), D Rennick(San Francisco General Hospital), Dean Sheppard(San Francisco General Hospital), Markus Mohrs(San Francisco General Hospital), Debra D. Donaldson(San Francisco General Hospital), Richard M. Locksley(San Francisco General Hospital), David B. Corry(San Francisco General Hospital)
Cited by 1,860
Abstract
The pathogenesis of asthma reflects, in part, the activity of T cell cytokines. Murine models support participation of interleukin-4 (IL-4) and the IL-4 receptor in asthma. Selective neutralization of IL-13, a cytokine related to IL-4 that also binds to the alpha chain of the IL-4 receptor, ameliorated 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 underlie the genetic associations of asthma with both the human 5q31 locus and the IL-4 receptor.
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