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Interleukin-13 in asthma pathogenesis.
- Source :
- Immunological Reviews; Dec2004, Vol. 202 Issue 1, p175-190, 16p, 2 Diagrams
- Publication Year :
- 2004
-
Abstract
- Bronchial asthma is a complex disorder that is thought to arise as a result of aberrant T-lytnphocyte responses to noninfectious environmental antigens. In particular, the symptoms of astma are dosely associated with the presence of activated T-helper 2 cell (Th2) cytokine-producing cells [interleukin (IL)-4, IL-5. IL-9, and lL-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 level and genetic variants in the IL-13 gene with asthma and related traits. With the preponderance of evidence continuiting 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. [ABSTRACT FROM AUTHOR]
- Subjects :
- ASTHMA
CARCINOGENESIS
ANTIGENS
DISEASE susceptibility
CYTOKINES
Subjects
Details
- Language :
- English
- ISSN :
- 01052896
- Volume :
- 202
- Issue :
- 1
- Database :
- Complementary Index
- Journal :
- Immunological Reviews
- Publication Type :
- Academic Journal
- Accession number :
- 15502651
- Full Text :
- https://doi.org/10.1111/j.0105-2896.2004.00215.x