Source:http://linkedlifedata.com/resource/pubmed/id/11473831
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
2001-7-27
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pubmed:abstractText |
The type I interferon (IFN) system plays a pivotal role in the etiopathogenesis of systemic lupus erythematosus (SLE). The initial appearance of autoantibody-producing B cells can be precipitated by infection-induced type I IFNs, but the further, significant generation of autoimmune T and B cells is caused by the prolonged production of IFN-alpha, which is maintained by a vicious circle mechanism. This involves the activation of immature dendritic cells, known as natural IFN-producing cells, by continuously formed endogenous IFN-alpha inducers. These IFN-alpha inducers consist of complexes of autoantibodies with nucleic-acid-containing autoantigens derived from apoptotic cells.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1471-4906
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
22
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
427-31
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading | |
pubmed:year |
2001
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pubmed:articleTitle |
An etiopathogenic role for the type I IFN system in SLE.
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pubmed:affiliation |
Dept of Medical Sciences, Section of Rheumatology, University Hospital, S-751 85 Uppsala, Sweden. Lars.Ronnblom@medsci.uu.se
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pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't
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