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Pathogenesis, Prevalence, And Affected Individuals

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SLE: Pathogenesis, prevalence, and affected individuals. In general, the term “lupus” is used to describe a multi-systemic inflammation that results from an abnormal immunological function. It includes four main types: neonatal and pediatric lupus erythematosus (NLE); discoid lupus erythematosus (DLE); drug-induced lupus (DIL); and systemic lupus erythematosus (SLE). The latter is the most common type, and it is referred to simply as “lupus”. SLE is a complex rheumatic disease of an autoimmune origin, with an unknown etiology and thus individuals at risk are unable to prevent the disease’s progression. Genetic, hormonal, environmental factors as well an immunological abnormalities have been contributed to its pathogenesis. The most agreed upon theory is that the diseases develop as a consequence of the formation and deposition of autoantibodies and immune complexes in various organ systems, leading to eventual organ damage. Studies focusing on SLE as a genetic diseases have shown that there is a genetic predisposition within families. For example first-degree relatives of patients with SLE are significantly more likely to have the disease compared to the rest of population (Maidhof & Hilas, 2012).Recent technological advances have led to breakthroughs in the identification of susceptibility factors involved in SLE, among which DNA methylation alterations has shown great potential. Incomplete concordance for SLE has been found in homozygotic twins, suggesting that

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