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- W4320912323 endingPage "1014" @default.
- W4320912323 startingPage "999" @default.
- W4320912323 abstract "Research elucidating the pathogenesis of systemic lupus erythematosus (SLE) has defined two critical families of mediators, type I interferon (IFN-I) and autoantibodies targeting nucleic acids and nucleic acid-binding proteins, as fundamental contributors to the disease. On the fertile background of significant genetic risk, a triggering stimulus, perhaps microbial, induces IFN-I, autoantibody production or most likely both. When innate and adaptive immune system cells are engaged and collaborate in the autoimmune response, clinical SLE can develop. This review describes recent data from genetic analyses of patients with SLE, along with current studies of innate and adaptive immune function that contribute to sustained IFN-I pathway activation, immune activation and autoantibody production, generation of inflammatory mediators and tissue damage. The goal of these studies is to understand disease mechanisms, identify therapeutic targets and stimulate development of therapeutics that can achieve improved outcomes for patients." @default.
- W4320912323 created "2023-02-16" @default.
- W4320912323 creator A5086055060 @default.
- W4320912323 date "2023-02-15" @default.
- W4320912323 modified "2023-10-18" @default.
- W4320912323 title "Pathogenesis of systemic lupus erythematosus: risks, mechanisms and therapeutic targets" @default.
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