Serum and synovial fluid levels of tumor necrosis factor-like ligand 1A and decoy receptor 3 in rheumatoid arthritis

•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 P...

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Veröffentlicht in:Cytokine (Philadelphia, Pa.) Pa.), 2015-04, Vol.72 (2), p.185-189
Hauptverfasser: Xiu, Zijuan, Shen, Hui, Tian, Ye, Xia, Liping, Lu, Jing
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Sprache:eng
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Zusammenfassung:•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. To 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. The 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. Serum 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. TL1A and DcR3 may be of pathogenic and potentially of therapeutic importance in RA patients.
ISSN:1043-4666
1096-0023
DOI:10.1016/j.cyto.2014.12.026