摘要
Systemic lupus erythematosus(SLE),the most common form of lupus,is a chronic autoimmune disorder characterized by a global loss of self-tolerance and hyper-activation of both innate and adaptive immune systems(Kaul et al.,2016).Neutrophils,the most abundant leukocytes in human blood,have a critical role in maintaining immune surveillance and tissue homeostasis,and its dysregulation is of high relevance to SLE(Ricklin et al.,2010).In patients with SLE,accelerated neutrophil death and the deficiency in clearing dying neutrophils cause nuclear and cytoplasmic antigen exposure,excessive production of type I interferon(IFN),and neutrophil extracellular trap(NET)release,subsequently inducing autoimmune responses(Garcia-Romo et al.,2011).Dysregulated neutrophil death is believed to be a major cause of SLE;however,the underlying mechanism of neutrophil death in SLE is not well-defined.
