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

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.

doi:10.1172/jci31546

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

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 +4 more·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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Macrophages can also regulate or reverse fibrosis through secretion of matrix degrading MMPs and M2 factors (IL-10, RELMα, Arg-1) that suppress fibrosis.
“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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IL‐13Rα2 and IL‐10 coordinately suppress Th2‐dependent Inflammation and Immunopathology.
Wilson, M. S., Elnekave, E., Mentink‐Kane, M. M., Pesce, J. T., Ramalingam, T. R., Thompson, R. C., Flavell, R. A., Cheever, A. W., & Wynn, T. A. (2008) · The FASEB Journal · doi:10.1096/fasebj.22.1_supplement.663.2
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Self-citation

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 › Physiology › 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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