Abstract
Systemic lupus erythematosus (SLE) is a prototypical autoimmune disease. It has recently been suggested that a failure of apoptosis wherein autoreactive lymphocytes continue to survive is a major factor in the pathogenesis of SLE. Fas antigen is increased on peripheral blood lymphocytes from human SLE patients while Bcl-2 protein, which inhibits apoptosis, is highly expressed in peripheral T lymphocytes of SLE patients. The Bcl-2 family includes homologs that are believed to be related to regulation of apoptosis. Of these, Bax is capable of forming heterodimers with Bcl-2, thereby counteracting the action of Bcl-2. The present study examines the ratio of Bcl-2 to Bax in relation to the activity of SLE, with implications relating to the survival or death of lymphocytes. The ratio of Bcl-2 to Bax in active SLE was significantly higher than in inactive SLE and in normal controls. Although the exact role of apoptosis in SLE is still unclear, a high ratio of Bcl-2 to Bax in active SLE patients might support the survival of autoreactive cells.
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