Source:http://linkedlifedata.com/resource/pubmed/id/12634991
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2003-3-13
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pubmed:abstractText |
Accumulative evidence suggests that psoriasis may be a genetically determined immunologenic inflammatory disorder based on an ongoing autoreactive Th-1 response. Various cytokines (e.g. IL-2, interferon-gamma etc.) are released and exert proliferative signals on to keratinocytes, which start proliferation that finally results in an incomplete differentiation. During this pathobiological process keratinocytes themselves express receptors that make them sensitive for growth inducing stimulation and also start the production of a set of cytokines that contribute to and maintain inflammation. Immunosuppressive agents, mostly by affecting T-cells may interfere with or even disrupt by rather unspecific mechanisms, this complex process of mutual stimulation of leucocytes and keratinocytes. In this manuscript we show mode of action, efficacy and side effects of Methotrexate, Ciclosporin A, Tacrolimus and Pimecrolimus, and discuss therapeutic options with mycophenolate mofetil and fumaric acid esters.
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pubmed:language |
ger
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0017-8470
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
54
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
230-6
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:12634991-Autoantibodies,
pubmed-meshheading:12634991-Cytokines,
pubmed-meshheading:12634991-Dose-Response Relationship, Drug,
pubmed-meshheading:12634991-Humans,
pubmed-meshheading:12634991-Immunosuppressive Agents,
pubmed-meshheading:12634991-Keratinocytes,
pubmed-meshheading:12634991-Psoriasis,
pubmed-meshheading:12634991-Th1 Cells,
pubmed-meshheading:12634991-Treatment Outcome
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pubmed:year |
2003
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pubmed:articleTitle |
[New immunosuppressive agents for treating psoriasis].
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pubmed:affiliation |
Department of Dermatology, Stanford Medical School, Stanford, CA, USA.
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pubmed:publicationType |
Journal Article,
English Abstract
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