Interleukin-13 in asthma pathogenesis

Immunol Rev. 2004 Dec;202:175-90. doi: 10.1111/j.0105-2896.2004.00215.x.

Abstract

Bronchial asthma is a complex disorder that is thought to arise as a result of aberrant T-lymphocyte responses to noninfectious environmental antigens. In particular, the symptoms of asthma are closely associated with the presence of activated T-helper 2 cell (Th2) cytokine-producing cells [interleukin (IL)-4, IL-5, IL-9, and IL-13] in the airway wall. Although each of the Th2 cytokines likely contributes to the overall immune response directed against environmental antigens, a substantial body of evidence points to a singular role for IL-13 in the regulation of the allergic diathesis. Initial studies in animal models of disease provided compelling evidence that IL-13, independently of other Th2 cytokines, was both necessary and sufficient to induce all features of allergic asthma. The importance of IL-13 in allergic disorders in humans is supported by consistent associations between tissue IL-13 levels and genetic variants in the IL-13 gene with asthma and related traits. With the preponderance of evidence continuing to support a pivotal role for IL-13 in allergic disorders, attention is now turned toward understanding the mechanisms by which this cytokine may mediate the pathophysiological features of allergic disease. The emerging paradigm is that IL-13 induces features of the allergic response via a complex array of actions on resident airway cells rather than through traditional effector pathways involving eosinophils and immunoglobulin E-mediated events. In light of these recent developments, this review explores our current understanding of the singular role of IL-13 in the pathogenesis of asthma, with a particular focus on new insights into the mechanisms by which IL-13 mediates various features of asthma.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Asthma / etiology
  • Asthma / metabolism*
  • Humans
  • Hypersensitivity / immunology
  • Hypersensitivity / metabolism
  • Inflammation / immunology
  • Inflammation / metabolism
  • Inflammation / pathology
  • Interleukin-13 / metabolism*
  • Interleukin-13 Receptor alpha1 Subunit
  • Receptors, Interleukin / metabolism
  • Receptors, Interleukin-13
  • Respiratory System / immunology
  • Respiratory System / metabolism
  • Respiratory System / pathology
  • Signal Transduction / physiology
  • T-Lymphocyte Subsets / immunology
  • T-Lymphocyte Subsets / metabolism
  • Th2 Cells / immunology
  • Th2 Cells / metabolism

Substances

  • IL13RA1 protein, human
  • Interleukin-13
  • Interleukin-13 Receptor alpha1 Subunit
  • Receptors, Interleukin
  • Receptors, Interleukin-13