To date, the pathogenesis of systemic lupus erythematosus (SLE) is only 
partially understood. A characteristic feature of this disease is the occurrence 
of antibodies against nuclear antigens. Further, SLE is characterized by a 
type-I interferon gene signature. A dysregulation of apoptosis and phagocytosis 
of apoptotic cells is discussed as a central pathogenetic mechanism in the 
development of SLE. Several publications in recent years have described an 
accumulation of autoantigens within apoptotic cells, as well as an exposition of 
these antigens on the surface of apoptotic cells. During late stages of 
apoptosis, autoantigens are posttranslationally modified, leading to the 
formation of neoantigens. Subcellular fragments such as apoptotic microparticles 
also seem to be involved in the pathogenesis of SLE. It has been shown that 
microparticles contain relevant antigens and stimulate B- and T-lymphocytes. 
Moreover, apoptotic microparticles have the ability to stimulate plasmacytoid 
dendritic cells, causing a secretion of interferon alpha. These observations 
provide a link between dysregulation of apoptosis and phagocytosis and the 
type-I interferon signature observed in SLE patients.