Interleukin-13 in asthma pathogenesis
Article first published online: 11 NOV 2004
Volume 202, Issue 1, pages 175–190, December 2004
How to Cite
Wills-Karp, M. (2004), Interleukin-13 in asthma pathogenesis. Immunological Reviews, 202: 175–190. doi: 10.1111/j.0105-2896.2004.00215.x
- Issue published online: 11 NOV 2004
- Article first published online: 11 NOV 2004
Summary: 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.