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IL-13Ralpha2 and IL-10 coordinately suppress airway inflammation, airway-hyperreactivity, and fibrosis in mice.

Authors: Wilson, MS  Elnekave, E  Mentink-Kane, MM  Hodges, MG  Pesce, JT  Ramalingam, TR  Thompson, RW  Kamanaka, M  Flavell, RA  Keane-Myers, A  Cheever, AW  Wynn, TA 
Citation: Wilson MS, etal., J Clin Invest. 2007 Oct;117(10):2941-51.
Pubmed: (View Article at PubMed) PMID:17885690
DOI: Full-text: DOI:10.1172/JCI31546

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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CRRD Object Information
CRRD ID: 4892649
Created: 2011-02-28
Species: All species
Last Modified: 2011-02-28
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.