EXPRESSION OF BCL-2 IN RHEUMATOID-ARTHRITIS

Citation
P. Isomaki et al., EXPRESSION OF BCL-2 IN RHEUMATOID-ARTHRITIS, British journal of rheumatology, 35(7), 1996, pp. 611-619
Citations number
54
Categorie Soggetti
Rheumatology
ISSN journal
02637103
Volume
35
Issue
7
Year of publication
1996
Pages
611 - 619
Database
ISI
SICI code
0263-7103(1996)35:7<611:EOBIR>2.0.ZU;2-B
Abstract
Since defective apoptosis has been suggested to play a role in the dev elopment of autoimmune diseases, we have investigated the expression o f the proto-oncogene bcl-2 in patients with rheumatoid arthritis (RA). The expression of bcl-2 was studied in peripheral blood (PB) and syno vial fluid (SF) lymphocytes and synovial tissues (ST) from patients wi th RA using immunohistochemistry, flow cytometry and nucleic acid hybr idization. Patients with reactive arthritis (ReA) or osteoarthritis (O A) and healthy individuals were used as controls. The expression of bc l-2 protein in PB lymphocytes and the expression of bcl-2 mRNA in PB m ononuclear cells (PBMC) was similar in healthy controls and patients w ith RA. However, bcl-2 protein expression was significantly reduced in SF lymphocytes when compared to PB lymphocytes. Similar results were observed with lymphocytes from patients with ReA, and irrespective of whether total lymphocytes, T cells or different T-cell subsets were st udied. In the synovial sections, the expression of bcl-2 was restricte d to lymphocytes, and bcl-2+ cells were observed in the majority of sa mples from patients with RA, OA and ReA. These data indicate that the expression of bcl-2 is not increased in the lymphocytes or ST derived from patients with RA. Instead, decreased expression of bcl-2 protein in SF lymphocytes compared to PB lymphocytes was demonstrated. We sugg est that bcl-2 does not play a significant role in the pathogenesis of RA.