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Requirement for IL-13 Independently of IL-4 in Experimental Asthma

Gabriele Grunig, Martha Warnock, Adil E. Wakil, Rajeev Venkayya, Frank Brombacher, Donna M. Rennick, Dean Sheppard, Markus Mohrs, Debra D. Donaldson, Richard M. Locksley and David B. Corry
Science
New Series, Vol. 282, No. 5397 (Dec. 18, 1998), pp. 2261-2263
Stable URL: http://www.jstor.org/stable/2897135
Page Count: 3
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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 α chain of the IL-4 receptor, ameliorated the asthma phenotype, including airway hyperresponsiveness, eosinophil recruitment, and mucus over-production. Administration of either IL-13 or IL-4 conferred an asthma-like phenotype to nonimmunized T cell-deficient mice by an IL-4 receptor α 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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