Document Detail


IL-27 is expressed in chronic human eczematous skin lesions and stimulates human keratinocytes.
MedLine Citation:
PMID:  19523673     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: IL-27 is produced by antigen-presenting cells early during immune responses. IL-27 has been described to support T-cell polarization along the T(H)1 lineage but also to exert important anti-inflammatory responses in later phases of inflammation in murine models. OBJECTIVE: It was the aim of this study to analyze the potential role of IL-27 in epidermal inflammatory skin responses in human subjects. METHODS: Surface receptor expression and apoptosis of human primary keratinocytes were analyzed by means of flow cytometry. Supernatants of stimulated keratinocytes were either analyzed by means of ELISA or submitted to chemotaxis assays. RT-PCR from lesional skin and phospho-specific Western blotting were performed. RESULTS: Both subunits of IL-27 were expressed in chronic lesional allergic eczematous skin, whereas the IL-27 subunit EBV-induced gene 3 was not detectable in the acute phase of eczema. Human primary keratinocytes responded to IL-27. Stimulation of keratinocytes with IL-27 resulted in activation of the signal transducer and activator of transcription 1 and 3 pathways. Major effects found for IL-27 include CXCL10 production and MHC class I upregulation. Importantly, we could demonstrate that IL-27 acts as a priming signal on keratinocytes able to amplify chemokine production and surface molecule expression when used before a second signal, such as TNF-alpha. The effects of IL-27 could not be mimicked by IL-6, IL-12, or IL-23. CONCLUSION: These results support the notion that IL-27 might act in an inflammatory, disease-maintaining manner in the epidermal compartment of patients with eczema.
Authors:
Miriam Wittmann; Jana Zeitvogel; Dong Wang; Thomas Werfel
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-06-11
Journal Detail:
Title:  The Journal of allergy and clinical immunology     Volume:  124     ISSN:  1097-6825     ISO Abbreviation:  J. Allergy Clin. Immunol.     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-06-29     Completed Date:  2009-07-22     Revised Date:  2010-06-04    
Medline Journal Info:
Nlm Unique ID:  1275002     Medline TA:  J Allergy Clin Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  81-9     Citation Subset:  AIM; IM    
Affiliation:
Department of Immunodermatology and Allergy Research, Hannover Medical School, Hannover, Germany. M.Wittmann@leeds.ac.uk
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MeSH Terms
Descriptor/Qualifier:
Blotting, Western
Cells, Cultured
Chemokine CXCL10 / metabolism
Eczema / immunology,  metabolism*
Flow Cytometry
Gene Expression Regulation*
Humans
Intercellular Adhesion Molecule-1 / metabolism
Interleukin-18 Receptor alpha Subunit / metabolism
Interleukins / metabolism*,  pharmacology*
Keratinocytes / drug effects*
Receptors, Interleukin / metabolism
Recombinant Proteins / genetics
Reverse Transcriptase Polymerase Chain Reaction
STAT1 Transcription Factor / metabolism
STAT3 Transcription Factor / metabolism
Signal Transduction
Up-Regulation
Chemical
Reg. No./Substance:
0/C19orf10 protein, human; 0/Chemokine CXCL10; 0/IL27RA protein, human; 0/Interleukin-18 Receptor alpha Subunit; 0/Interleukins; 0/Receptors, Interleukin; 0/Recombinant Proteins; 0/STAT1 Transcription Factor; 0/STAT1 protein, human; 0/STAT3 Transcription Factor; 126547-89-5/Intercellular Adhesion Molecule-1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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