alexa Elevated production of galectin-3 is correlated with juvenile idiopathic arthritis disease activity, severity, and progression.
Immunology

Immunology

Journal of Clinical & Cellular Immunology

Author(s): Ezzat MH, ElGammasy TM, Shaheen KY, Osman AO

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Abstract OBJECTIVES: Galectin-3 is a carbohydrate-binding protein that plays many important regulatory roles in inflammation, immunity and cancers. Recent studies indicate that galectin-3 plays a role in rheumatoid arthritis (RA) pathogenesis and progression. Therefore, we sought to characterize the expression pattern and role of galectin-3 in juvenile idiopathic arthritis (JIA) and to explore whether galectin-3 investigated in serum and synovial fluid was associated with clinical, laboratory and radiological variables of JIA disease activity and severity. METHODS: Levels of galectin-3 in serum and synovial fluid from patients with JIA and controls were determined by enzyme-linked immunosorbent assay. RESULTS: Median (interquartile range) serum galectin-3 concentrations (ng/mL) were increasingly higher across the following groups: healthy controls (8.1 [4.9-16.7]), total JIA children with inactive disease (18.6 [9.7-28.8], P = 0.00039 vs. controls) and active disease (35.8 [15.8-60.8], P = 0.000012 vs. controls) (inactive vs. active, P = 0.00016). Highest serum expression was found in polyarthritic children. Galectin-3 concentrations in paired sera and synovial fluid samples could be related to each other. Serum and synovial concentrations of galectin-3 were positively correlated with total number of joints with active arthritis and with overall articular severity score. Patients with Larsen index and total radiographic score ≥ 1 had significant higher serum galectin-3 levels than patients with indices and scores < 1. CONCLUSIONS: These results suggest that serum levels of galectin-3 are increased in active JIA children and galectin-3 can be a new biomarker indicating JIA disease activity, severity and progression, although its increment is not disease-specific. © 2011 The Authors. International Journal of Rheumatic Diseases © 2011 Asia Pacific League of Associations for Rheumatology and Blackwell Publishing Asia Pty Ltd. This article was published in Int J Rheum Dis and referenced in Journal of Clinical & Cellular Immunology

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