A significant role for IFNα in the pathogenesis of systemic lupus erythematosus 
is well supported, and clinical trials of anti-IFNα monoclonal antibodies are in 
progress in this disease. In other autoimmune diseases characterized by 
substantial inflammation and tissue destruction, the role of type I interferons 
is less clear. Gene expression analysis of peripheral blood cells from patients 
with rheumatoid arthritis and multiple sclerosis demonstrate an interferon 
signature similar to but less intense than that seen in patients with lupus. In 
both of those diseases, presence of the interferon signature has been associated 
with more significant clinical manifestations. At the same time, evidence 
supports an anti-inflammatory and beneficial role of IFNβ locally in the joints 
of patients with rheumatoid arthritis and in murine arthritis models, and many 
patients with multiple sclerosis show a clinical response to recombinant IFNβ. 
As can also be proposed for type I diabetes mellitus, type I interferon appears 
to contribute to the development of autoimmunity and disease progression in 
multiple autoimmune diseases, while maintaining some capacity to control 
established disease - particularly at local sites of inflammation. Recent 
studies in both rheumatoid arthritis and multiple sclerosis suggest that 
quantification of type I interferon activity or target gene expression might be 
informative in predicting responses to distinct classes of therapeutic agents.