Cited by 137Asthma and respiratory diseasesIL-33, ST2, and ILC PathwaysT-cell and B-cell Immunology

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IL-13Rα2 and IL-10 coordinately suppress airway inflammation, airway-hyperreactivity, and fibrosis in mice

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Wilson, Mark S., Elnekave, Eldad, Mentink-Kane, Margaret M., Hodges, Marcus G., Pesce, John T., Ramalingam, Thirumalai R., Thompson, Robert W., Kamanaka, Masahito, Flavell, Richard A., Keane-Myers, Andrea, Cheever, Allen W., Wynn, Thomas A.·2007·Journal of Clinical Investigation

DOI 10.1172/jci31546PMC PMC1978425

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Abstract

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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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: Wilson, Mark S.
Elnekave, Eldad
Ramalingam, Thirumalai R.
Thompson, Robert W.
Flavell, Richard A.
Wynn, Thomas A.
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2007-10-01
Volume: 117
Issue: 10
Pages: 2941-2951
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci31546
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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IL-13Rα2 and IL-10 coordinately suppress airway inflammation, airway-hyperreactivity, and fibrosis in mice

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