SLE is a heterogeneous and complex group of disorders of uncertain cause. R
ecent studies have suggested that abnormalities in the apoptotic cell death
process may play an important role in the initiation and propagation of th
is spectrum of disease by altering the generation and cleavage of antigens,
and through abnormalities in immunoregulation. The clustering and concentr
ation of autoantigens in and on the surface blebs of apoptotic cells, modif
ications of antigen structure during certain forms of apoptotic death, and
abnormalities in apoptotic cell clearance in humans with SLE and in certain
animal models are reviewed and synthesized into a comprehensive model of s
ystemic autoimmunity.