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

Author:

Grünig Gabriele1,Warnock Martha1,Wakil Adil E.1,Venkayya Rajeev1,Brombacher Frank1,Rennick Donna M.1,Sheppard Dean1,Mohrs Markus1,Donaldson Debra D.1,Locksley Richard M.1,Corry David B.1

Affiliation:

1. G. Grünig, R. Venkayya, D. Sheppard, D. B. Corry, Departments of Medicine and the Lung Biology Center at the San Francisco General Hospital, University of California San Francisco, San Francisco, CA 94143, USA. M. Warnock, Department of Pathology, University of California San Francisco, San Francisco, CA 94143, USA. A. E. Wakil, Department of Transplantation, California Pacific Medical Center, San Francisco, CA 94115, USA. F. Brombacher, Department of Immunology at the Groote Schuur Hospital,...

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 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.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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