Abstract
System lupus erythematosus (SLE) is an autoimmune disease with multicellular pathogeneic components.Recent studiessuggestan importantrole for interferon-a (IFN) in the immunopathogenesis of SLE. Data demonstrating a correlationbetween IFN-a and SLE disease severity range from elevated IFN-a levels in patients’serum and induction of IFN-regulated genes in peripheral blood mononuclear cells, to drug induced lupus disease in hepatitis C or cancer patients treated with recombinant IFN-a. In addition, mouse models of lupus in which the IFNR is deleted fail to develop disease manifestations. Thus, targetingIFN-a promises to be therapeuticallyefficacious for SLE.
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