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IL-13Rα2 and IL-10 coordinately suppress airway inflammation, airway-hyperreactivity, and fibrosis in mice
Open accessAbstract
Development of persistent Th2 responses in asthma and chronic helminth infections are a major health concern. IL-10 has been identified as a critical regulator of Th2 immunity, but mechanisms for controlling Th2 effector function remain unclear. IL-10 also has paradoxical effects on Th2-associated pathology, with IL-10 deficiency resulting in increased Th2-driven inflammation but also reduced airway hyperreactivity (AHR), mucus hypersecretion, and fibrosis. We demonstrate that increased IL-13 receptor alpha 2 (IL-13Ralpha2) expression is responsible for the reduced AHR, mucus production, and fibrosis in BALB/c IL-10(-/-) mice. Using models of allergic asthma and chronic helminth infection, we demonstrate that IL-10 and IL-13Ralpha2 coordinately suppress Th2-mediated inflammation and pathology, respectively. Although IL-10 was identified as the dominant antiinflammatory mediator, studies with double IL-10/IL-13Ralpha2-deficient mice illustrate an indispensable role for IL-13Ralpha2 in the suppression of AHR, mucus production, and fibrosis. Thus, IL-10 and IL-13Ralpha2 are both required to control chronic Th2-driven pathological responses.
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“Macrophages, however, can also regulate or reverse fibrosis through the secretion of matrix degrading MMPs and other M2 factors that have been shown to suppress fibrosis (IL-10, RELMα, Arg-1) [102,138–140].”
From Macrophage polarization: an opportunity for improved outcomes in biomaterials and regenerative medicine (2012) · cites this paper as [140]
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Metadata
- Authors
- Wilson, M. S., Elnekave, E., Mentink-Kane, M. M., Hodges, M. G., Pesce, J. T., Ramalingam, T. R., Thompson, R. W., Kamanaka, M., Flavell, R. A., Keane-Myers, A., Cheever, A. W., & Wynn, T. A.
- Affiliations
- National Institutes of Health (US)
- Yale University (US)
- Biomedical Research Institute (US)
- Corresponding author
- Wynn, Thomas A.
- ORCID
- Venue
- Journal of Clinical Investigation
- Published
- 2007-10-01
- Volume
- 117
- Issue
- 10
- Pages
- 2941-2951
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC1978425
- OpenAlex
- W2135565397
- Cited by
- 137
- References
- 63
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 2 · 2023: 8 · 2022: 2 · 2021: 5 · 2020: 8 · 2019: 9 · 2018: 6 · 2017: 6 · 2016: 12 · 2015: 11 · 2014: 5 · 2013: 6 · 2012: 12
- FWCI
- 5.59
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Allergy and Infectious Diseases
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Asthma and respiratory diseases
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- IL-13 receptor alpha 2, IL-10, airway hyperresponsiveness, airway fibrosis, mucus hypersecretion, Th2 immune response, allergic asthma, chronic helminth infection, airway inflammation, IL-10-deficient mice, double knockout mice
- MeSH terms
- Animals, Asthma, Bronchitis, Fibrosis, Granuloma, Mice, Mutant Strains, Mucus, Bronchial Hyperreactivity, Interleukin-10, Th1 Cells, Th2 Cells, Mice, Interleukin-13 Receptor alpha2 Subunit
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