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- W2117832897 endingPage "1019" @default.
- W2117832897 startingPage "1012" @default.
- W2117832897 abstract "Systemic lupus erythematosus (SLE) is a prototypic multisystem autoimmune disorder where interplay of environmental and genetic risk factors leads to progressive loss of tolerance to nuclear antigens over time, finally culminating in clinical disease. The heterogeneity of clinical manifestations and the disease’s unpredictable course characterized by flares and remissions are very likely a reflection of heterogeneity at the origin of disease, with a final common pathway leading to loss of tolerance to nuclear antigens. Impaired clearance of immune complexes and apoptotic material and production of autoantibodies have long been recognized as major pathogenic events in this disease. Over the past decade the type I interferon cytokine family has been postulated to play a central role in SLE pathogenesis, by promoting feedback loops progressively disrupting peripheral immune tolerance and driving disease activity. The identification of key molecules involved in the pathogenesis of SLE will not only improve our understanding of this complex disease, but also help to identify novel targets for biological intervention. Lupus (2010) 19, 1012—1019." @default.
- W2117832897 created "2016-06-24" @default.
- W2117832897 creator A5041412546 @default.
- W2117832897 creator A5046877204 @default.
- W2117832897 date "2010-08-01" @default.
- W2117832897 modified "2023-09-23" @default.
- W2117832897 title "The interferon-α signature of systemic lupus erythematosus" @default.
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- W2117832897 doi "https://doi.org/10.1177/0961203310371161" @default.
- W2117832897 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3658279" @default.