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Pennino, D. ; Bhavsar, P.K.* ; Effner, R. ; Avitabile, S.* ; Venn, P.* ; Quaranta, M. ; Marzaioli, V. ; Cifuentes, L. ; Durham, S.R.* ; Cavani, A.* ; Eyerich, K.* ; Chung, K.F.* ; Schmidt-Weber, C.B. ; Eyerich, S.

IL-22 suppresses IFN-γ-mediated lung inflammation in asthmatic patients.

J. Allergy Clin. Immunol. 131, 562-570 (2013)
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Background: IL-22 controls tissue homeostasis by both proinflammatory and anti-inflammatory effects. However, the anti-inflammatory mechanisms of IL-22 remain poorly investigated. Objective: We sought to investigate the anti-inflammatory role for IL-22 in human asthma. Methods: T-cell lines derived from lung biopsy specimens of asthmatic patients were characterized by means of flow cytometry. Human bronchial epithelial cells from healthy and asthmatic subjects were stimulated with IL-22, IFN-gamma, or the combination of both cytokines. Effects of cytokine stimulation were investigated by using whole-genome analysis, ELISA, and flow cytometry. The functional consequence of cytokine stimulation was evaluated in an in vitro wound repair model and T cell-mediated cytotoxicity experiments. In vivo cytokine expression was measured by using immunohistochemistry and Luminex assays in bronchoalveolar lavage fluid of healthy and asthmatic patients. Results: The current study identifies a tissue-restricted antagonistic interplay of IL-22 and the proinflammatory cytokine IFN-gamma. On the one hand, IFN-gamma antagonized IL-22-mediated induction of the antimicrobial peptide S100A7 and epithelial cell migration in bronchial epithelial cells. On the other hand, IL-22 decreased epithelial susceptibility to T cell-mediated cytotoxicity by inhibiting the IFN-gamma-induced expression of MHC-I, MHC-II, and CD54/intercellular adhesion molecule 1 molecules. Likewise, IL-22 inhibited IFN-gamma-induced secretion of the proinflammatory chemokines CCL5/RANTES and CXCL10/interferon-inducible protein 10 in vitro. Consistently, the IL-22 expression in bronchoalveolar lavage fluid of asthmatic patients inversely correlated with the expression of CCL5/RANTES and CXCL10/interferon-inducible protein 10 in vivo. Conclusions: IL-22 might control the extent of IFN-gamma-mediated lung inflammation and therefore play a tissue-restricted regulatory role.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter T(h)22 Cells ; Il-22 ; Ifn-gamma ; Asthma ; Human Bronchial Epithelial Cells ; Epithelial Regulation; Natural-killer-cells ; Bronchial Epithelial-cells ; T-cells ; Airway Hyperresponsiveness ; Virus-infection ; Innate Immunity ; Interleukin 22 ; Potential Role ; Keratinocytes ; Expression
Sprache englisch
Veröffentlichungsjahr 2013
HGF-Berichtsjahr 2013
ISSN (print) / ISBN 0091-6749
e-ISSN 1097-6825
Zeitschrift The journal of allergy and clinical immunology
Quellenangaben Band: 131, Heft: 2, Seiten: 562-570 Artikelnummer: , Supplement: ,
Verlag Elsevier
Verlagsort Amsterdam [u.a.]
Begutachtungsstatus Peer reviewed
Institut(e) Institute for Allergy Research (IAF)
POF Topic(s) 80000 - German Center for Lung Research
30503 - Chronic Diseases of the Lung and Allergies
Forschungsfeld(er) Allergy
PSP-Element(e) G-501800-541
G-552600-001
PubMed ID 23174657
DOI 10.1016/j.jaci.2012.09.036
WOS ID WOS:000314661500036
Erfassungsdatum 2013-03-07
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