Interleukin‐13 in asthma pathogenesis
Abstract
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.
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T cells in the lung secrete cytokines, such as IL-13, that promote chemokine production from resident lung cells including epithelial cells, smooth muscle cells and fibroblasts.
“T cells in the lung secrete cytokines, such as IL-13, that promote chemokine production from resident lung cells including epithelial cells, smooth muscle cells and fibroblasts41.”
From The transcription factor PU.1 is required for the development of IL-9-producing T cells and allergic inflammation (2010) · cites this paper as [41]
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- Authors
- Wills‐Karp, M.
- Venue
- Immunological Reviews
- Publisher
- Wiley
- Published
- 2004-11-11
- Volume
- 202
- Issue
- 1
- Pages
- 175-190
- ISSN
- 0105-2896 (ISSN-L)
- 1600-065X
- OpenAlex
- W2065801967
- Cited by
- 683
- References
- 5
- Citations by year
- 2026: 4 · 2025: 14 · 2024: 12 · 2023: 7 · 2022: 15 · 2021: 14 · 2020: 15 · 2019: 26 · 2018: 27 · 2017: 13 · 2016: 36 · 2015: 46 · 2014: 37 · 2013: 49 · 2012: 45
- FWCI
- 4.70
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Immunological Reviews (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (P01HL076383, R01 HL72987, R01HL072987, P01 HL-10342, R01-HL67736, R01HL067736, P01HL010342)
- Topics
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Health Sciences › Medicine › Immunology and Allergy › Allergic Rhinitis and Sensitization
- Keywords
- IL-13, allergic asthma, asthma pathogenesis, Th2 cytokines, airway inflammation, eosinophils, immunoglobulin E, airway epithelial cells, allergic diathesis, animal models of asthma
- MeSH terms
- Asthma, Humans, Hypersensitivity, Inflammation, Respiratory System, Signal Transduction, T-Lymphocyte Subsets, Receptors, Interleukin, Th2 Cells, Interleukin-13, Receptors, Interleukin-13, Interleukin-13 Receptor alpha1 Subunit
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