The type I interferon (IFN) system plays a pivotal role in the etiopathogen
esis of systemic lupus erythematosus (SLE). The initial appearance of autoa
ntibody-producing B cells can be precipitated by infection-induced type IIF
Ns, but the further, significant generation of autoimmune T and B cells is
caused by the prolonged production of IFN-a, which is maintained by a vicio
us circle mechanism. This involves the activation of immature dendritic cel
ls, known as natural IFN-producing cells, by continuously formed endogenous
IFN-alpha inducers. These IFN-a inducers consist of complexes of autoantib
odies with nucleic-acid-containing autoantigens derived from apoptotic cell
s.