TY - JOUR
T1 - Requirement for IL-13 independently of IL-4 in experimental asthma
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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U2 - 10.1126/science.282.5397.2261
DO - 10.1126/science.282.5397.2261
M3 - Article
C2 - 9856950
AN - SCOPUS:0032545433
VL - 282
SP - 2261
EP - 2263
JO - Science (New York, N.Y.)
JF - Science (New York, N.Y.)
SN - 0036-8075
IS - 5397
ER -