Abstract
Neutrophil pathogen-killing mechanism termed neutrophil extracellular traps (NETs)
has been recently identified. NETs consist of chromatin and histones along with serine
proteases and myeloperoxidase and are induced by a great variety of infectious and
non-infectious stimuli. NETosis is a kind of programmed neutrophil death characterized by chromatin decondensation
and release of nuclear granular contents, mainly driven by peptidylarginine deiminase
4 citrullination of histones. Although classically related to the protection against
infectious pathogens, nowadays NETs have been described as a player of several pathophysiological
processes. Neutrophil dysregulation has been demonstrated in the pathogenesis of most
representative vascular diseases, such as acute coronary syndrome, stroke and venous
thrombosis. Indeed, NETs have been identified within atherosclerotic lesions and arterial
thrombi in both human beings and animal models. Moreover, an imbalance in this mechanism
has been proposed as a critical source of modified and/or externalized autoantigens
in autoimmune and inflammatory diseases. Finally, an update on the role of NETs in
the pathogenesis of cancer has been included. In the present review, based on papers
released on PubMed and MEDLINE up to July 2017, we point to update the knowledge on
NETs, from their structure to their roles in infectious diseases as well as in cardiovascular
diseases, autoimmunity, metabolic disorders and cancer, with a look to future perspectives
and therapeutic opportunities.
Keywords
NETs - infectious diseases - autoimmune diseases - metabolic disorders - cancer
