Type I interferons (IFN) are primarily regarded as an inhibitor of viral 
replication. However, type I IFN, mainly IFNalpha, plays a major role in 
activation of both the innate and adaptive immune systems. Systemic lupus 
erythematosus (SLE) is a chronic, multi-systemic, inflammatory autoimmune 
disease with undefined etiology. SLE is characterized by dysregulation of both 
the innate and the adaptive immune systems. An increased expression of type I 
IFN-regulated genes, termed IFN signature, has been reported in patients with 
SLE. We review here the role of IFNalpha in the pathogenesis and course of SLE 
and the possible role of IFNalpha inhibition as a novel treatment for lupus 
patients.