Recent studies of patients with systemic lupus erythematosus, together with data 
from lupus-prone mice, suggest that inappropriate activation of type I 
interferon might have a role in disease pathogenesis. Serum levels of IFN-alpha 
are elevated in SLE patients, and gene expression profiling of peripheral blood 
cells shows that most lupus cases demonstrate an upregulation of IFN-responsive 
genes. Of interest, the IFN gene 'signature' correlates with more severe 
disease. The available data support a model whereby chromatin-containing immune 
complexes circulating in the blood of lupus patients stimulate leukocytes to 
produce IFN, which perpetuates disease. These emerging insights into the 
connection between IFN and lupus provide a host of new diagnostic and 
therapeutic opportunities.