| pubmed-article:17703177 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17703177 | lifeskim:mentions | umls-concept:C0085295 | lld:lifeskim |
| pubmed-article:17703177 | lifeskim:mentions | umls-concept:C0032403 | lld:lifeskim |
| pubmed-article:17703177 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:17703177 | lifeskim:mentions | umls-concept:C0086860 | lld:lifeskim |
| pubmed-article:17703177 | lifeskim:mentions | umls-concept:C0443199 | lld:lifeskim |
| pubmed-article:17703177 | lifeskim:mentions | umls-concept:C1882417 | lld:lifeskim |
| pubmed-article:17703177 | lifeskim:mentions | umls-concept:C0127400 | lld:lifeskim |
| pubmed-article:17703177 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:17703177 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:17703177 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:17703177 | pubmed:dateCreated | 2007-10-24 | lld:pubmed |
| pubmed-article:17703177 | pubmed:abstractText | Systemic lupus erythematosus (SLE) is a complex, multifactorial autoimmune disease characterized by the dysregulation of T and B cells that leads to hyperactivity of B cells and production of autoantibodies, and involves both environmental and genetic factors. Interleukin-10 (IL-10) is a candidate susceptibility gene in SLE. In particular, three IL-10 promoter single-nucleotide polymorphisms (SNPs; -1082A/G, -819T/C and -592A/C) are strongly associated with the pathogenesis of SLE. We found that the homozygous GCC haplotype linked to greater SLE severity confers higher IL-10 gene transcriptional activity than the ATA haplotype in macrophages that encounter apoptotic cells, because of the differential DNA binding to the -592 SNP by a nuclear protein uniquely induced by apoptotic cells. We identified this protein as poly(ADP-ribose) polymerase-1, confirmed its physiological role and characterized its molecular properties in modulating IL-10 production during phagocytosis of apoptotic cells. This study unveils a novel direct link between DNA damage repair/apoptosis pathways and IL-10-mediated immune regulation. | lld:pubmed |
| pubmed-article:17703177 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17703177 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17703177 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17703177 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17703177 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17703177 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:17703177 | pubmed:issn | 1466-4879 | lld:pubmed |
| pubmed-article:17703177 | pubmed:author | pubmed-author:LiuJJ | lld:pubmed |
| pubmed-article:17703177 | pubmed:author | pubmed-author:ONOS ISI | lld:pubmed |
| pubmed-article:17703177 | pubmed:author | pubmed-author:ZhangYY | lld:pubmed |
| pubmed-article:17703177 | pubmed:author | pubmed-author:ChungE YEY | lld:pubmed |
| pubmed-article:17703177 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17703177 | pubmed:volume | 8 | lld:pubmed |
| pubmed-article:17703177 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17703177 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17703177 | pubmed:pagination | 577-89 | lld:pubmed |
| pubmed-article:17703177 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:17703177 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17703177 | pubmed:articleTitle | Differential expression in lupus-associated IL-10 promoter single-nucleotide polymorphisms is mediated by poly(ADP-ribose) polymerase-1. | lld:pubmed |
| pubmed-article:17703177 | pubmed:affiliation | Department of Microbiology and Immunology, Weill Medical College of Cornell University, New York, NY 10021, USA. | lld:pubmed |
| pubmed-article:17703177 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17703177 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:17703177 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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