An etiopathogenic role for the type I IFN system in SLE

Abstract

The type I interferon (IFN) system plays a pivotal role in the etiopathogenesis of systemic lupus erythematosus (SLE). The initial appearance of autoantibody-producing B cells can be precipitated by infection-induced type I IFNs, but the further, significant generation of autoimmune T and B cells is caused by the prolonged production of IFN-alpha, which is maintained by a vicious circle mechanism. This involves the activation of immature dendritic cells, known as natural IFN-producing cells, by continuously formed endogenous IFN-alpha inducers. These IFN-alpha inducers consist of complexes of autoantibodies with nucleic-acid-containing autoantigens derived from apoptotic cells.