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

Gabriele Grünig; Martha Warnock; Adil E. Wakil; Rajeev Venkayya; Frank Brombacher; Donna M. Rennick; Dean Sheppard; Markus Mohrs; Debra D. Donaldson; Richard M. Locksley; David B. Corry

doi:10.1126/science.282.5397.2261

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

Gabriele Grünig, Martha Warnock, Adil E. Wakil, Rajeev Venkayya, Frank Brombacher, Donna M. Rennick, Dean Sheppard, Markus Mohrs, Debra D. Donaldson, Richard M. Locksley, David B. Corry

Research Institute

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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 airways 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 α chain-dependent pathway. This pathway may underlie the genetic associations of asthma with both the human 5q31 locus and the IL-4 receptor.

Original language	English (US)
Pages (from-to)	2261-2263
Number of pages	3
Journal	Science
Volume	282
Issue number	5397
DOIs	https://doi.org/10.1126/science.282.5397.2261
State	Published - Dec 18 1998

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10.1126/science.282.5397.2261

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title = "Requirement for IL-13 independently of IL-4 in experimental asthma",

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 airways 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 α chain-dependent pathway. This pathway may underlie the genetic associations of asthma with both the human 5q31 locus and the IL-4 receptor.",

author = "Gabriele Gr{\"u}nig and Martha Warnock and Wakil, {Adil E.} and Rajeev Venkayya and Frank Brombacher and Rennick, {Donna M.} and Dean Sheppard and Markus Mohrs and Donaldson, {Debra D.} and Locksley, {Richard M.} and Corry, {David B.}",

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AU - Grünig, Gabriele

AU - Warnock, Martha

AU - Wakil, Adil E.

AU - Venkayya, Rajeev

AU - Brombacher, Frank

AU - Rennick, Donna M.

AU - Sheppard, Dean

AU - Mohrs, Markus

AU - Donaldson, Debra D.

AU - Locksley, Richard M.

AU - Corry, David B.

PY - 1998/12/18

Y1 - 1998/12/18

N2 - 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 airways 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 α chain-dependent pathway. This pathway may underlie the genetic associations of asthma with both the human 5q31 locus and the IL-4 receptor.

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

Abstract

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