期刊
SCANDINAVIAN JOURNAL OF RHEUMATOLOGY
卷 42, 期 2, 页码 102-107出版社
TAYLOR & FRANCIS LTD
DOI: 10.3109/03009742.2012.725769
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资金
- National Council for Science and Technology [SALUD-2007-C0171161]
- PROMEP-SEP/UAEM [2005-07]
Background: Several studies have confirmed that galectin-1 (Gal-1) plays a role in controlling the immune response because of its pro-apoptotic effect. Although studies based on a rheumatoid arthritis (RA) mouse model have suggested a crucial role for Gal-1 in inflammation, clinical data are lacking. We have detected the presence of autoantibodies against galectinsin blood, but their physiological meaning remains unknown. Objectives: To compare plasma and synovial levels of Gal-1 in RA patients and in healthy controls, and correlate them with clinical parameters. Methods: Plasma and synovial (non-arthritic knee effusion) samples were collected from RA patients and healthy donors. All patients were receiving treatment with steroids and/or disease-modifying anti-rheumatic drugs (DMARDs). A blood sample was taken at a baseline visit to determine plasma anti-cyclic citrullinated peptide (anti-CCP) antibodies, tumour necrosis factor alpha (TNF-alpha), Gal-1, and anti-Gal-1 autoantibodies. Results: Although plasma levels of Gal-1 were similar in patients and controls, the concentration of Gal-1 was significantly reduced in the synovial fluid of patients with RA. This reduction was not correlated with TNF-a or C-reactive protein (CRP) levels. However, the decrease in synovial Gal-1 correlated with a significant increase in anti-Gal-1 autoantibodies and anti-CCP antibody titres, suggesting a physiological effect of autoantibodies limiting the amount Gal-1 and potentially blocking its biological effect in RA patients. Conclusion: Gal-1 levels were significant reduced at the synovial level in RA patients, possibly as a consequence of the increase in anti-Gal-1 autoantibodies.
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