Expression of galectins-1 and-3 correlates with defective mononuclear cellapoptosis in patients with juvenile idiopathic arthritis

Citation
M. Harjacek et al., Expression of galectins-1 and-3 correlates with defective mononuclear cellapoptosis in patients with juvenile idiopathic arthritis, J RHEUMATOL, 28(8), 2001, pp. 1914-1922
Citations number
51
Categorie Soggetti
Rheumatology,"da verificare
Journal title
JOURNAL OF RHEUMATOLOGY
ISSN journal
0315162X → ACNP
Volume
28
Issue
8
Year of publication
2001
Pages
1914 - 1922
Database
ISI
SICI code
0315-162X(200108)28:8<1914:EOGACW>2.0.ZU;2-F
Abstract
Objective. Juvenile idiopathic arthritis (JIA) is characterized by hyperpla sia of synovial cells and accumulation of mononuclear inflammatory infiltra tes, which are locally maintained through a balance between cell proliferat ion and apoptosis. Although defective clearance of activated T cells in RA joints has been explained by alterations of the Fas-Fas ligand system, this has not been confirmed in synovial tissue of patients with JIA. We evaluat ed the relation between expression of alectin-1 (Gal-1) and galectin-3 (Gal -3) (3-galactoside-binding proteins with pro- and anti-apoptotic properties , respectively) and the apoptosis and proliferation rates of infiltrative l ymphocytes in synovial tissue of patients with JIA. Methods. Using slide cytometry and in situ end labeling we observed dysregu lated apoptosis of infiltrating mononuclear cells within the synovial tissu e of patients with JIA. Results. Patients with pauciarticular JIA showed minimal apoptosis, high Bc l-2 expression, and high or normal proliferation rates, while patients with polyarticular disease showed the lowest apoptotic indexes, accompanied by low Bcl-2 expression and low proliferation rates. We found that Gal-1 expre ssion is downregulated and Gal-3 expression is upregulated in synovial tiss ue from patients with JIA. Conclusion. In patients with polyarticular JIA, accumulation of inflammator y cells is mainly due to downregulated apoptosis, whereas in patients with pauciarticular disease the process results from increased proliferation. De fective mononuclear apoptosis in synovial inflammatory infiltrates from pat ients with JIA could be explained in part by decreased Gal-1 and increased Gal-3 expression.