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• W3021401127 abstract "Abstract Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by systemic inflammation and the production of numerous autoantibodies, many of which are directed to nuclear antigens. The disease exhibits female predominance and is more common in individuals of African or Asian descent than in Caucasians. Although the precise etiology is not known, it is clear that both genetic predisposition and environmental triggers are factors. Approximately 50 risk alleles have been identified, yet severity and age of onset of disease relate only partially to the number of risk alleles present in an individual. Years before clinical symptomatology and diagnosis, immune perturbations of both myeloid cells and B cells can be identified. Progression from immune perturbation to clinical disease can occur through multiple mechanisms, possibly related to genetic factors, and can account for the variability in clinical presentation and disease course. Evidence from patients and from mouse models of disease suggests that most tissue injury is initiated by autoantibody deposition, with subsequent activation of myeloid cells through Fc receptor–mediated mechanisms. This, in turn, leads to altered function in tissue resident cells. Nucleic acid containing immune complexes can lead to systemic inflammation through activation of endosomal Toll-like receptors. The impetus for the production of autoantibodies, and in particular antibodies to nuclear antigens, is not known; however, it is thought to be secondary in some individuals to impaired mechanisms for the clearance of apoptotic debris, and in others it is perhaps secondary to cross-reactivity with microbial antigens. Numerous organ systems can be affected by SLE. Skin and musculoskeletal manifestations are most common. Neuropsychiatric manifestations, especially cognitive impairment, are increasing and appreciated as a component of disease. Mortality in SLE is due primarily to active disease—most commonly nephritis—to accelerated atherosclerosis, and to infection secondary to immunosuppressive treatment regimens. At present, treatment strategies are globally immunosuppressive and are inadequate, with limited efficacy and potentially devastating toxicities. A number of clinical trials of novel biologicals in SLE have been unsuccessful, suggesting the need for better understanding of pathogenic mechanisms and better mouse models of disease." @default.
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• W3021401127 date "2008-01-01" @default.
• W3021401127 modified "2023-10-17" @default.
• W3021401127 title "Systemic lupus erythematosus" @default.
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• W3021401127 doi "https://doi.org/10.1016/b978-0-323-04404-2.10051-x" @default.
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