کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2794087 1155248 2015 5 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Serum and synovial fluid levels of tumor necrosis factor-like ligand 1A and decoy receptor 3 in rheumatoid arthritis
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی علوم غدد
پیش نمایش صفحه اول مقاله
Serum and synovial fluid levels of tumor necrosis factor-like ligand 1A and decoy receptor 3 in rheumatoid arthritis
چکیده انگلیسی


• Serum TL1A levels were higher in RA and correlated with disease activity.
• DcR3 was also elevated in sera of RA patients.
• TL1A and DcR3 levels were higher in SF samples than in paired sera.
• The level of serum TL1A and DcR3 decreased after anti-TNF treatment.
• rhTL1A increased production of IL-17 by PBMC from RA patients.

ObjectiveTo measure the levels of Tumor necrosis factor (TNF)-like ligand 1A (TL1A) and decoy receptor 3 (DcR3) in serum and synovial fluid (SF) of patients with rheumatoid arthritis (RA). To evaluate the effect of recombinant human (rh) TL1A on interleukin (IL)-17 production and IL-17mRNA expression.MethodsThe serum and SF levels of TL1A and DcR3, and the production of IL-17 by rhTL1A-treated PBMC were measured by enzyme-linked immunosorbent assay (ELISA). The expression of IL-17 mRNA by rhTL1A-treated PBMC was measured by real-time reverse transcriptase polymerase chain reaction (RT-PCR). We also tested the change of TL1A and DcR3 level following TNF-α blockade therapy.ResultsSerum TL1A and DcR3 levels were higher in RA patients. This increase was more significant in RF and anti-CCP positive patients. TL1A and DcR3 levels were higher in SF samples than in paired sera. TL1A and DcR3 decreased after anti-TNF treatment. rhTL1A increased the production of IL-17 protein and the expression of IL-17mRNA.ConclusionTL1A and DcR3 may be of pathogenic and potentially of therapeutic importance in RA patients.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cytokine - Volume 72, Issue 2, April 2015, Pages 185–189
نویسندگان
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