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.