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- aggregation classification "A1".
- aggregation creator B584017.
- aggregation creator B584018.
- aggregation creator B584019.
- aggregation creator B584020.
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- aggregation creator B584029.
- aggregation creator person.
- aggregation creator person.
- aggregation date "2011".
- aggregation format "application/pdf".
- aggregation hasFormat 1234726.bibtex.
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- aggregation isPartOf urn:issn:1073-449X.
- aggregation language "eng".
- aggregation rights "I have transferred the copyright for this publication to the publisher".
- aggregation subject "Medicine and Health Sciences".
- aggregation title "Dual role of IL-22 in allergic airway inflammation and its cross-talk with IL-17A".
- aggregation abstract "Rationale: IL-22 has both proinflammatory and antiinflammatory properties. Its role in allergic lung inflammation has not been explored. Objectives: To investigate the expression and roles of IL-22 in the onset and resolution of experimental allergic asthma and its cross-talk with IL-17A. Methods: IL-22 expression was assessed in patient samples and in the lung of mice immunized and challenged with ovalbumin. IL-22 functions in allergic airway inflammation were evaluated using mice deficient in IL-22 or anti-IL-22 neutralizing antibodies. Moreover, the effects of recombinant IL-22 and IL-17A neutralizing antibodies were investigated. Measurements and Main Results: Increased pulmonary IL-22 expression is found in the serum of patients with asthma and mice immunized and challenged with ovalbumin. Allergic lung inflammation is IL-22 dependent because eosinophil recruitment, Th2 cytokine including IL-13 and IL-33, chemokine production, airway hyperreactivity, and mucus production are drastically reduced in mice deficient in IL-22 or by IL-22 antibody neutralization during immunization of wild-type mice. By contrast, IL-22 neutralization during antigen challenge enhanced allergic lung inflammation with increased Th2 cytokines. Consistent with this, recombinant IL-22 given with allergen challenge protects mice from lung inflammation. Finally, IL-22 may regulate the expression and proinflammatory properties of IL-17A in allergic lung inflammation. Conclusions: IL-22 is required for the onset of allergic asthma, but functions as a negative regulator of established allergic inflammation. Our study reveals that IL-22 contributes to the proinflammatory properties of IL-17A in experimental allergic asthma.".
- aggregation authorList BK937081.
- aggregation endPage "1163".
- aggregation issue "9".
- aggregation startPage "1153".
- aggregation volume "183".
- aggregation aggregates 1234728.
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- aggregation similarTo rccm.201008-1383OC.
- aggregation similarTo LU-1234726.