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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
IL-22 suppresses IFN-γ-mediated lung inflammation in asthmatic patients.
J. Allergy Clin. Immunol. 131, 562-570 (2013)
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
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
Verlag
Elsevier
Verlagsort
Amsterdam [u.a.]
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute for Allergy Research (IAF)