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© 1995 British Society for Rheumatology

research-article

BCL-2 EXPRESSION IS UNALTERED IN UNFRACTIONATED PERIPHERAL BLOOD MONONUCLEAR CELLS IN PATIENTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS

L. M. ROSE*,{dagger},, D. S. LATCHMAN* and D. A. ISENBERG{dagger}

*Medical Molecular Biology Unit, Department of Molecular Pathology, University College London Medical School Cleveland Street, London WIP 6DB
{dagger}Bloomsbury Rheumatology Unit, Arthur Stanley House Tottenham Street, London WIP 9PG

Correspondence to: Correspondence to: L. M. Rose, Medical Molecular Biology Unit, University College London Medical School, Cleveland Street, London WIP 6DB.

It has been postulated that the high levels of autoantibodies observed in systemic lupus erythematosus (SLE) patients could result from abnormal longevity of polyclonally activated B-cells. This increased survival could be due to dysfunction of apoptosis, the normal regulatory process governing their life span. The protein product of the bcl-2 gene can enhance lymphoid cell survival by interfering with apoptosis. Moreover, transgenic mice overexpressing bcl-2 in their B-cells developed an autoimmune syndrome resembling SLE. To determine whether overexpression of bcl-2 occurs in SLE patients, bcl-2 protein was measured in peripheral blood mononuclear cells from 73 SLE patients, 20 healthy individuals and 47 patients with other autoimmune diseases. Only three lupus patients had raised levels of bcl-2 and there were no statistically significant differences in the mean bcl-2 levels measured in SLE patients compared to controls. Bcl-2 levels did not correlate with overall disease activity in SLE patients.

KEY WORDS: Systemic lupus erythematosus, Apoptosis, Lymphocytes, bcl-2


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