Systemic lupus erythematosus (SLE) is characterized by increased numbers of activated B cells, which produce large amounts of immunoglobulins, including autoantibodies. This high numbers of B cells might be the consequence of dysfunction of apoptosis. The priduct of oncogene bcl-2 appears to enhance lymphoid cell survival by interfering with apoptosis.The aim of this work is to study bcl-2 protein expresion in SLE patients and correlate it with the clinical manifestations of the disease, laboratory parameters, concurrent treatment and disease activity. Bcl-2 protein was measured in freshly isolated PBMCs from 50 female SLE patients and 20 control subjects using dual colour flowcytometry. This study revealed that the percentage of circulating bcl-2 +ve lymphocytes in SLE patients was 52.69+ 2.14%, which is significantly elevated compared to its level in the control group (21.79 + 2.57%) P=0.003. No correlation was found between bcl-2 expretion in SLE patients and disease manifestations, organ involvement or with any of the serological parameters. Based on our study, it is concluded that disturbed apoptosis appears to be incriminated in the immunopathogenesis of SLE.