
It is estimated that more than 5% of the U.S. population suffers from some form
of autoimmune disease. The interferons are at the center of the immune response
and thus play a key role in nearly all autoimmune diseases.
Systemic Lupus Erythematosus (SLE), an often severe autoimmune disease, afflicts
more than 350,000 people in the U.S. alone. An important role for both interferon-α 1
and interferon-γ 2
in SLE has been postulated based on the observation of high interferon
activity in the SLE patient. A number of examples of SLE induced as a side effect
of interferon therapy have been reported 3 and gene expression patterns
have led investigators to conclude there is “a strong rationale for the development
of new therapies to block interferon pathways in human SLE” 4 .
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