NETosis in autoimmune diseases with focus on psoriasis

Neutrophil granulocytes are a key player in host innate immunity and they provide antimicrobial protection also by NETosis, amongst other mechanisms. NETosis involves the formation of intricate web-like structures, composed of DNA-histone complexes and proteins released by activated neutrophils, commonly referred to as neutrophil extracellular traps (NETs) with sticky and antimicrobial effects on extracellular pathogens. The dysregulation of neutrophils and NETosis may result in autoimmune diseases, due to the formation of autoantibodies, consequent exaggerated immune stimulation, overexpression of various molecules related to NETosis, and infiltration of cutaneous lesions with neutrophils and other immune cell populations. Furthermore, a neutrophil subpopulation was found to be strongly linked to the pathogenesis of these diseases. The interest in the implications of NETosis in autoimmunity has grown in the past years; researchers found new biomarkers and evaluated therapeutics targeted towards this cell death pathway correlated to psoriasis and autoimmunity. Thus, future studies are needed on this matter in order to increase the quality of life in autoimmune disease patients, as NETosis represents a promising therapeutic target. This review article aimed to thoroughly examine neutrophil functions and their association with NETosis in the context of autoimmune diseases, with a particular focus on psoriasis.