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rdf:type |
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lifeskim:mentions |
umls-concept:C0004364,
umls-concept:C0024141,
umls-concept:C0030705,
umls-concept:C0152060,
umls-concept:C0205154,
umls-concept:C0205419,
umls-concept:C0683481,
umls-concept:C1306235,
umls-concept:C1335874,
umls-concept:C1415900,
umls-concept:C1515655,
umls-concept:C1881189,
umls-concept:C2346484
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pubmed:issue |
1
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pubmed:dateCreated |
2008-12-25
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pubmed:abstractText |
Increased IFN-alpha signaling is a primary pathogenic factor in systemic lupus erythematosus (SLE). STAT4 is a transcription factor that is activated by IFN-alpha signaling, and genetic variation of STAT4 has been associated with risk of SLE and rheumatoid arthritis. We measured serum IFN-alpha activity and simultaneous IFN-alpha-induced gene expression in PBMC in a large SLE cohort. The risk variant of STAT4 (T allele; rs7574865) was simultaneously associated with both lower serum IFN-alpha activity and greater IFN-alpha-induced gene expression in PBMC in SLE patients in vivo. Regression analyses confirmed that the risk allele of STAT4 was associated with increased sensitivity to IFN-alpha signaling. The IFN regulatory factor 5 SLE risk genotype was associated with higher serum IFN-alpha activity; however, STAT4 showed dominant influence on the sensitivity of PBMC to serum IFN-alpha. These data provide biologic relevance for the risk variant of STAT4 in the IFN-alpha pathway in vivo.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/19109131-11303025,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19109131-11711679,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19109131-12642603,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19109131-15565395,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19109131-15593221,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19109131-16447217,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19109131-17095088,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19109131-17412832,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19109131-17581626,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19109131-17804842,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19109131-17932559,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19109131-18240214,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19109131-18288123,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19109131-18579578,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19109131-18668568
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1550-6606
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
182
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
34-8
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pubmed:dateRevised |
2011-6-9
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pubmed:meshHeading |
pubmed-meshheading:19109131-Alleles,
pubmed-meshheading:19109131-Cell Line,
pubmed-meshheading:19109131-Down-Regulation,
pubmed-meshheading:19109131-Gene Expression Regulation,
pubmed-meshheading:19109131-Genetic Predisposition to Disease,
pubmed-meshheading:19109131-Genetic Variation,
pubmed-meshheading:19109131-Haplotypes,
pubmed-meshheading:19109131-Humans,
pubmed-meshheading:19109131-Interferon Regulatory Factors,
pubmed-meshheading:19109131-Interferon-alpha,
pubmed-meshheading:19109131-Lupus Erythematosus, Systemic,
pubmed-meshheading:19109131-Risk Factors,
pubmed-meshheading:19109131-STAT4 Transcription Factor,
pubmed-meshheading:19109131-Signal Transduction
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pubmed:year |
2009
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pubmed:articleTitle |
Cutting edge: autoimmune disease risk variant of STAT4 confers increased sensitivity to IFN-alpha in lupus patients in vivo.
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pubmed:affiliation |
Section of Rheumatology, University of Chicago, Chicago, IL 60637, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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