Source:http://linkedlifedata.com/resource/pubmed/id/21635228
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2011-7-5
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pubmed:abstractText |
Studies have indicated that interleukin (IL)-10 has a pathogenic role in systemic lupus erythematosus (SLE); however, a protective effect of IL-10 in SLE was also observed. Because the exact mechanism of IL-10 signalling in the pathogenesis of SLE is unclear, this study sought to assess the expression and signalling of interleukin-10 receptor (IL-10R) in peripheral leucocytes from patients with SLE. We used flow cytometry to examine the expression of IL-10R1 on different peripheral leucocytes from 28 SLE patients, of whom 14 had lupus nephritis (LN) and 14 were healthy controls. We also examined the effects of IL-10 on phosphorylation of signal transducer and activator of transcription (STAT)-3 and STAT-1 in peripheral blood mononuclear cells (PBMCs) obtained from 13 SLE patients and seven healthy controls. Plasma cytokines were detected by flow cytometric bead array (CBA) techniques. Although IL-10R1 expression levels on each peripheral leucocyte subset from 28 SLE patients and 14 healthy controls were similar, the expression levels on CD4(+) T cells from LN patients were significantly lower than on CD4(+) T cells from controls and SLE patients without nephritis (P < 0·01). IL-10R1 expression levels on CD4(+) and CD8(+) T cells were correlated negatively with the SLE disease activity index (P < 0·01). Additionally, the phosphorylation of STAT-3 was delayed and reduced in PBMCs from LN patients and active SLE patients. Plasma IL-10 levels were significantly higher in LN patients than controls. IL-10R1 expression on CD4(+) T cells and signalling in PBMCs were down-regulated in LN patients, indicating that IL-10 and its receptor may have a special role in LN pathogenesis.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/STAT1 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/STAT1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/STAT3 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/STAT3 protein, human
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1365-2249
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pubmed:author | |
pubmed:copyrightInfo |
© 2011 The Authors. Clinical and Experimental Immunology © 2011 British Society for Immunology.
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pubmed:issnType |
Electronic
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pubmed:volume |
165
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
163-71
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pubmed:meshHeading |
pubmed-meshheading:21635228-Adolescent,
pubmed-meshheading:21635228-Adult,
pubmed-meshheading:21635228-CD4-Positive T-Lymphocytes,
pubmed-meshheading:21635228-CD8-Positive T-Lymphocytes,
pubmed-meshheading:21635228-Cells, Cultured,
pubmed-meshheading:21635228-Cytokines,
pubmed-meshheading:21635228-Down-Regulation,
pubmed-meshheading:21635228-Female,
pubmed-meshheading:21635228-Flow Cytometry,
pubmed-meshheading:21635228-Humans,
pubmed-meshheading:21635228-Interleukin-10,
pubmed-meshheading:21635228-Leukocytes, Mononuclear,
pubmed-meshheading:21635228-Lupus Erythematosus, Systemic,
pubmed-meshheading:21635228-Lupus Nephritis,
pubmed-meshheading:21635228-Male,
pubmed-meshheading:21635228-Middle Aged,
pubmed-meshheading:21635228-Phosphorylation,
pubmed-meshheading:21635228-Receptors, Interleukin-10,
pubmed-meshheading:21635228-STAT1 Transcription Factor,
pubmed-meshheading:21635228-STAT3 Transcription Factor,
pubmed-meshheading:21635228-Signal Transduction
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pubmed:year |
2011
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pubmed:articleTitle |
Interleukin-10 receptor expression and signalling were down-regulated in CD4? T cells of lupus nephritis patients.
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pubmed:affiliation |
Department of Rheumatology and Immunology, Shengjing Hospital, Shenyang, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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