Programmed cell death involves an orderly process of morphological disintegration that has been termed apoptosis. Unlike cell degradiation or necrosis, programmed cell death is an active cell suicide process regulated by signals provided by the environment. In general, cells undergoing apoptosis display profound structural changes including a rapid blebbing of the plasma membrane and nuclear disintegration. The nuclear collapse is associated with extensive damage to chromatin and DNA cleavage into oligonucleosomal lenght DNA fragment. The enrichment of mono-and oligonucleosomes in the cytoplasm of the apoptotic cells is due to the fact that DNA degradation occurs several hours before plasma membrane breakdown. Apoptosis plays an important role in the normal immune system development and homeostasis, tumorogenesis, viral infection and autoimmune disorders.To investigate the potential role of apoptosis in SLE pathogenesis, we used flow cytometric analysis of peripheral blood lymphocytes from 15 patients aged 18 to 60 years with different disease activity. The patients were compared with 15 random healthy individuals. Freshly isolated peripheral blood lymphocytes were stained with Propidium iodide (PI) and Fluorescein-12-dUTP. We observed increased number of apoptotic lymphocytes in SLE patients compared with the control group. Approximately 15% of peripheral blood lymphocytes in SLE patients were apoptotic.Our preliminary data support the hypothesis that the production of antinuclear antibody in SLE might be due to the released of intact nuclear antigens (oligonucleosomes) from apoptotic cells.