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• W2016758677 abstract "Systemic lupus erythematosus (SLE) is a severe multisystem autoimmune disease that results from both genetic predisposition and environmental factors. Many lines of investigation support interferon alpha (IFN-α) as a causal agent in human lupus, and high levels of serum IFN-α are a heritable risk factor for SLE. Interferon regulatory factors (IRFs) are a family of transcription factors involved in host defense, which can induce transcription of IFN-α and other immune response genes after activation. In SLE, circulating immune complexes that contain nucleic acid are prevalent. These complexes are recognized by endosomal Toll-like receptors, resulting in activation of downstream IRF proteins. Genetic variants in the IRF5 and IRF7 genes have been associated with SLE susceptibility, and these same variants are associated with increased serum IFN-α in SLE patients. The increase in serum IFN-α related to IRF5 and 7 genotypes is observed only in patients with particular antibody specificities. This suggests that chronic stimulation of the endosomal Toll-like receptors by autoantibody immune complexes is required for IRF SLE-risk variants to cause elevation of circulating IFN-α and subsequent risk of SLE. Recently, genetic variation in the IRF8 gene has been associated with SLE and multiple sclerosis, and studies support an impact of IRF8 genotype on the IFN-α pathway. In summary, the SLE-associated polymorphisms in the IRF family of proteins seem to be gain-of-function variants, and understanding the impact of these variants on the IFN-α pathway in vivo may guide therapeutic strategies directed at the Toll-like receptor/IRF/IFN-α pathway in SLE. Systemic lupus erythematosus (SLE) is a severe multisystem autoimmune disease that results from both genetic predisposition and environmental factors. Many lines of investigation support interferon alpha (IFN-α) as a causal agent in human lupus, and high levels of serum IFN-α are a heritable risk factor for SLE. Interferon regulatory factors (IRFs) are a family of transcription factors involved in host defense, which can induce transcription of IFN-α and other immune response genes after activation. In SLE, circulating immune complexes that contain nucleic acid are prevalent. These complexes are recognized by endosomal Toll-like receptors, resulting in activation of downstream IRF proteins. Genetic variants in the IRF5 and IRF7 genes have been associated with SLE susceptibility, and these same variants are associated with increased serum IFN-α in SLE patients. The increase in serum IFN-α related to IRF5 and 7 genotypes is observed only in patients with particular antibody specificities. This suggests that chronic stimulation of the endosomal Toll-like receptors by autoantibody immune complexes is required for IRF SLE-risk variants to cause elevation of circulating IFN-α and subsequent risk of SLE. Recently, genetic variation in the IRF8 gene has been associated with SLE and multiple sclerosis, and studies support an impact of IRF8 genotype on the IFN-α pathway. In summary, the SLE-associated polymorphisms in the IRF family of proteins seem to be gain-of-function variants, and understanding the impact of these variants on the IFN-α pathway in vivo may guide therapeutic strategies directed at the Toll-like receptor/IRF/IFN-α pathway in SLE. Timothy B. Niewold, MD, FACR, is an Assistant Professor in the Section of Rheumatology and Gwen Knapp Center for Lupus and Immunology Research, University of Chicago, Pritzker School of Medicine. His article is based on a presentation given at the Combined Annual Meeting of the Central Society for Clinical Research and Midwestern Section American Federation for Medical Research held in Chicago, Ill, April 2010. Linking interferon regulatory factors to the pathogenesis of human lupusTranslational ResearchVol. 157Issue 6PreviewSystemic lupus erythematosus (SLE) is a chronic autoimmune disorder that is characterized by the involvement of 1 or more organ systems. In individual patients, the severity of specific disease manifestations, as well as the overall prognosis, can vary significantly.1 Despite decades of research, the causes of lupus are not well understood. This has slowed drug development and frustrated both patients and their physicians. Until recently, corticosteroids, antimalarial compounds, and aspirin were the only medications approved by the Federal Drug Administration (FDA) for lupus. Full-Text PDF" @default.
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• W2016758677 date "2011-06-01" @default.
• W2016758677 modified "2023-10-16" @default.
• W2016758677 title "Interferon regulatory factors in human lupus pathogenesis" @default.
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• W2016758677 doi "https://doi.org/10.1016/j.trsl.2011.01.006" @default.
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