Type I Interferon as a Target of Treatment in SLE

Author(s): P. Y. Lee, W. H. Reeves

Journal Name: Endocrine, Metabolic & Immune Disorders - Drug Targets
Formerly Current Drug Targets - Immune, Endocrine & Metabolic Disorders

Volume 6 , Issue 4 , 2006

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Systemic lupus erythematosus (SLE) is a multi-organ autoimmune disease characterized by the production of antibodies against a spectrum of autoantigens. Recent evidence suggests that type-I interferons (IFN-I) are critically involved in the pathogenesis of SLE. Initially recognized for their anti-viral properties, IFN-I play important roles in immunity and autoimmunity by promoting DC maturation, T cell survival, and antibody production. Onset of SLE has been reported in patients with hepatitis or neoplastic diseases undergoing treatment with recombinant IFN-I while elevated serum IFN-I and IFN-stimulated gene expression are found in ∼2/3 of SLE patients. This “interferon signature” is clinically important as it correlates with disease activity and renal as well as CNS involvement. Supporting these findings, genetic abnormalities resulting in increased IFN-I production and/or signaling are associated with SLE. In view of the accumulating evidence linking IFN-I to the pathogenesis of SLE, targeting of IFN-I may be beneficial therapeutically while avoiding the side effects associated with conventional immunosuppressive therapy. To this end, IFN-I and IFN-producing cells as well as IFN-inducers and molecules of the IFN signaling pathway may all serve as potential therapeutic targets. Several anti-IFN-I approaches have already shown promising effects in animal studies and clinical trials will likely begin in the near future.

Keywords: interferonα, systemic lupus erythematosus, autoimmunity, dendritic cells, toll-like receptors

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Article Details

Year: 2006
Page: [323 - 330]
Pages: 8
DOI: 10.2174/187153006779025702
Price: $65

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