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Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by an overproduction of autoantibodies. The loss of self-tolerance in SLE is believed to be caused by the dysregulation of both innate and adaptive immune systems. Neutrophils, the most abundant effector cells of innate immunity, have long been shown to be associated with SLE. However, their role in the pathogenesis of SLE was not clear until recent studies discovered abnormal regulation of neutrophil extracellular traps (NETs) in SLE patients. NETs are web-like structures composed of chromatin backbones and granular molecules. They are released by activated neutrophils through a process called “NETosis”. Nets were first described in 2004 as a novel host defense mechanism to trap and kill foreign pathogens. Recent evidence shows that NETs also participate in the pathogenesis of a variety of inflammatory and autoimmune diseases, including SLE. An imbalance between NET formation and clearance in SLE patients may play a prominent role in the perpetuation of autoimmunity and the exacerbation of disease, as well as the induction of end-organ manifestations. This review summarizes the current findings regarding the contribution of NETs to the pathogenesis of SLE.