NETosis and SARS-COV-2 Infection-Related Autoimmunity: A Narrative Review

Abstract

Background: Neutrophil extracellular traps (NETs) are crucial for antimicrobial defense in sepsis, trapping and neutralizing pathogens while minimizing damage to host cells. Neutrophil extracellular traps, comprising nuclear chromatin, histones, and antimicrobial cytoplasmic granules, are significant. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) triggers multiple complications in patients. Decondensed NETs and associated proteins can become a critical source of autoantigens, presented to the immune system, thereby inducing hyperinflammation and autoimmunity in sepsis and viral diseases. Objectives: This study aimed to explore NETosis and its role in autoimmunity in coronavirus disease 2019 (COVID-19). Methods: We reviewed the PubMed database using keywords (autoimmune disease OR autoimmunity AND SARS-CoV-2 OR COVID-19 AND NETosis OR NETs) to enhance understanding of NETosis in autoimmune diseases and COVID-19, ultimately analyzing 55 articles. Results: Neutrophil extracellular traps play a pivotal role in host defense against pathogens. However, their overproduction can lead to self-tolerance failure and immune system activation, contributing to autoimmunity. Autoimmune phenomena have been observed in many COVID-19 patients, with a pathophysiology similar to other viral infections that induce NET formation. Conclusions: SARS-CoV-2 infections may cause immune system hyperactivation and subsequent autoimmunity. Like in other viral infections, NETosis could play a significant role in the autoimmunity associated with SARS-CoV-2. Modulating NET formation and degradation could potentially reduce the severity of the disease.