[Research advances in the role of neutrophil extracellular traps in childhood-onset systemic lupus erythematosus].

Neutrophil extracellular traps (NETs) represent a form of cell death distinct from apoptosis or necrosis. The imbalance between the formation and degradation of NETs has long been considered to be closely associated with the activity of autoimmune diseases such as systemic lupus erythematous (SLE). Reactive oxygen species derived from the nicotinamide adenine dinucleotide phosphate oxidase pathway or mitochondrial DNA pathway play a key role in the primary stage of NETs formation. The exposure or delayed degradation of abundant autoantigens, such as double-strand DNA, caused by abnormal activation of neutrophils can induce autoantibody to form immune complexes that deposit in local tissues and then induce the plasmacytoid dendritic cells to secrete the interferon alpha and other inflammatory factors. Those inflammatory factors will eventually cause endothelial cell injury. In order to provide a theoretical basis for targeted therapy and diagnosis of childhood-onset SLE, this paper reviews the role of NETs in the pathogenesis of SLE.