Source:http://linkedlifedata.com/resource/pubmed/id/15685590
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2005-2-23
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pubmed:abstractText |
Recent studies have suggested that type I interferons (IFN) play a role in the pathogenesis of lupus erythematosus (LE), an autoimmune disease of unknown aetiology. Natural interferon-producing plasmacytoid cells have been demonstrated in cutaneous LE (CLE) lesions, along with elevated levels of IFN-alpha mRNA. The hypothesis in the current study was that local production of type I IFNs in CLE induces Th1-biased inflammation via induction of IFN-inducible chemokines such as IP10/CXCL10 leading to the recruitment of chemokine receptor CXCR3 expressing T-cells into skin lesions. Skin biopsies from 21 patients suffering from different types of active cutaneous LE were analysed for the expression of MxA, a protein specifically induced by type I interferons, the IFN-inducible protein IP10/CXCL10, and the chemokine receptor CXCR3, characteristic for Th1 cells, by immunohistochemistry. Additionally, peripheral CD4+ and CD8+ T-cells were investigated for the expression of MxA and CXCR3 by flow cytometry. Cutaneous LE lesions were characterized by strong expression of MxA indicating the induction of localized type I IFN signalling in the skin. Large numbers of infiltrating CXCR3 positive lymphocytes were detected in CLE skin lesions, and correlated closely with lesional MxA expression (epidermis: Spearman's rho = 0.56, p < 0.001; dermis: rho = 0.82, p < 0.001). Intracellular MxA levels of circulating CD4+ and CD8+ T-cells were significantly enhanced in patients with active CLE lesions. The percentage of peripheral T-cells expressing CXCR3 was significantly decreased in specific CLE subtypes. Expression of IP10/CXCL10 in the epidermis links type I IFN signalling and recruitment of CXCR3+ T cells. These results suggest an important role for type I interferon signalling in the pathogenesis of cutaneous lupus erythematosus. It is proposed that type I IFNs induce a Th1-biased inflammatory immune response, with recruitment of CXCR3-expressing T-lymphocytes into the skin.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CXCL10 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/CXCR3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL10,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CXC,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CXCR3,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Chemokine,
http://linkedlifedata.com/resource/pubmed/chemical/myxovirus resistance proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0022-3417
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
205
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
435-42
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:15685590-CD8-Positive T-Lymphocytes,
pubmed-meshheading:15685590-Cells, Cultured,
pubmed-meshheading:15685590-Chemokine CXCL10,
pubmed-meshheading:15685590-Chemokines, CXC,
pubmed-meshheading:15685590-Female,
pubmed-meshheading:15685590-GTP-Binding Proteins,
pubmed-meshheading:15685590-Humans,
pubmed-meshheading:15685590-Immunity, Cellular,
pubmed-meshheading:15685590-Interferon Type I,
pubmed-meshheading:15685590-Keratinocytes,
pubmed-meshheading:15685590-Lupus Erythematosus, Cutaneous,
pubmed-meshheading:15685590-Lupus Erythematosus, Discoid,
pubmed-meshheading:15685590-Male,
pubmed-meshheading:15685590-Receptors, CXCR3,
pubmed-meshheading:15685590-Receptors, Chemokine,
pubmed-meshheading:15685590-Signal Transduction,
pubmed-meshheading:15685590-Skin,
pubmed-meshheading:15685590-Th1 Cells
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pubmed:year |
2005
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pubmed:articleTitle |
Enhanced type I interferon signalling promotes Th1-biased inflammation in cutaneous lupus erythematosus.
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pubmed:affiliation |
Department of Dermatology, University of Bonn, Germany. joerg.wenzel@ukb.uni-bonn.de
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pubmed:publicationType |
Journal Article
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