Systemic lupus erythematosus (SLE) is an autoimmune multisystem disease identified by the presence of autoantibodies. 1 SLE is marked by phases of remission and exacerbation and has different symptoms such as arthritis, skin lesions, nephritis, serositis, and nervous system symptoms. 1 SLE mainly affects women of child-bearing age. 1 SLE has multifactorial etiology including genetic, hormonal, and environmental factors that leads to immune dysfunction. 1 Recently, it has been indicated that free radical damage and oxidative stress has a remarkable function in SLE pathogenesis. 2 Oxidative stress causes T helper 17/regulatory T (Th17/Treg) cells imbalance in SLE subjects. Under normal situation, Th17 and Treg cells are in balance, whilst oxidative stress generated in SLE can stimulate and increase proinflammatory Th17 cells and suppresses anti-inflammatory Treg cells, thereby exacerbating autoimmune injury. 3 Moreover, oxidative stress can lead to abnormal activation of apoptosis and delay in the apoptotic bodies clearance. This delay in clearance of apoptotic cells
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