Neutrophil extracellular trap: A key player in the pathogenesis of autoimmune diseases

Numerous studies suggest that neutrophils might have a crucial role in the pathogenesis of systemic autoimmune diseases through neutrophil extracellular trap (NET) formation, production of pro-inflammatory cytokines, and organ destruction. NET components that are released into extracellular spaces can be considered autoantigens, which contribute to causing a break in self-tolerance. Subsequently, this leads to the development of autoimmune responses in predisposed individuals. Additionally, an imbalance between NET formation and NET degradation may prolong immune system contact with these modified autoantigens and enhance NET-induced tissue damage. In this review, we discuss the generation and clearance of the NET, as well as the role of NETosis in the path-ogenesis of autoimmune disorders, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (AAV), multiple sclerosis (MS), psoriasis, antiphospholipid syndrome (APS), and Type-1 diabetes mellitus (T1DM).

Automated summary

Numerous studies suggest that neutrophils play a crucial role in the development of systemic autoimmune diseases through the formation of neutrophil extracellular traps (NET), production of pro-inflammatory cytokines, and tissue damage. The components of NET released into the extracellular spaces act as autoantigens, leading to the breakdown of self-tolerance and the development of autoimmune responses. Imbalance between NET formation and degradation can contribute to prolonged exposure of the immune system to modified autoantigens and exacerbate tissue damage. This review discusses the generation and clearance of NET, as well as the role of NETosis in the pathogenesis of various autoimmune disorders.