Linked Life Data

11180010

Source:http://linkedlifedata.com/resource/pubmed/id/11180010

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pubmed-article:11180010pubmed:dateCreated2001-2-22lld:pubmed
pubmed-article:11180010pubmed:abstractTextPsoriasis is a chronic inflammatory skin disease in which epidermal hyperplasia results from the release of cytokines by infiltrating type 1 T cells. Up- regulation of endogenous interleukin-10 controls type 1 skin responses in animal models; however, interleukin-10 production is low in psoriatic lesions. Consistent with an important role of interleukin-10 in psoriasis, we and colleagues have recently demonstrated clinical efficacy of subcutaneous administration of recombinant interleukin-10 to affected patients. Here, we studied the effects of interleukin-10 on disease-related inflammatory pathways. Patients were treated with recombinant interleukin-10 over 6 wk in an open-label phase II clinical trial. Tissue was obtained before and after therapy and examined by histology/immunohistochemistry, in situ hybridization, and quantitative real-time reverse transcription-polymerase chain reaction. Ten of 14 patients showed a marked reduction of the clinical disease activity. The clinical response was associated with a significant decrease of cutaneous T cell infiltration and the lesional expression of type 1 cytokines interferon-gamma and tumor necrosis factor-alpha. Interleukin-10 inhibited the epidermal interleukin-8 pathway by downregulating the expression of interleukin-8, its receptor CXCR2, and its inducer interleukin-17, and partially reversed the aberrant keratinocyte maturation defining psoriatic epidermal pathology. Remarkably, there was evidence that genetic factors are involved in the response to interleukin-10 as individual variations in the downregulation of tumor necrosis factor-alpha were related to the presence of polymorphisms in the tumor necrosis factor-alpha promoter. These data suggest that excessive production of type 1 cytokines in human skin disease can be counter-regulated by the administration of recombinant interleukin-10. Genotypic analysis may help to identify patients that will preferentially respond to interleukin-10 therapy.lld:pubmed
pubmed-article:11180010pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:11180010pubmed:languageenglld:pubmed
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pubmed-article:11180010pubmed:authorpubmed-author:MaurelEElld:pubmed
pubmed-article:11180010pubmed:authorpubmed-author:ReichKKlld:pubmed
pubmed-article:11180010pubmed:authorpubmed-author:GarbeCClld:pubmed
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pubmed-article:11180010pubmed:volume116lld:pubmed
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pubmed-article:11180010pubmed:pagination319-29lld:pubmed
pubmed-article:11180010pubmed:dateRevised2008-11-21lld:pubmed
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pubmed-article:11180010pubmed:year2001lld:pubmed
pubmed-article:11180010pubmed:articleTitleResponse of psoriasis to interleukin-10 is associated with suppression of cutaneous type 1 inflammation, downregulation of the epidermal interleukin-8/CXCR2 pathway and normalization of keratinocyte maturation.lld:pubmed
pubmed-article:11180010pubmed:affiliationDepartment of Dermatology, Georg-August-University, Von-Siebold-Strasse 3, 37075 Göttingen, Germany. kreich@gwdg.gelld:pubmed
pubmed-article:11180010pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:11180010pubmed:publicationTypeClinical Triallld:pubmed
pubmed-article:11180010pubmed:publicationTypeControlled Clinical Triallld:pubmed
pubmed-article:11180010pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
pubmed-article:11180010pubmed:publicationTypeMulticenter Studylld:pubmed
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