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NETosis: A key player in autoimmunity, COVID-19, and long COVID
Título de la revista
Autores
Ramírez Santana, Heily Carolina
Shoenfeld, Yehuda
Yilmaz, Ahsen Morva
Şahin, Ali
Celis-Andrade, Mariana
Guerrero Acosta, Nicolás
Acosta Ampudia, Yeny Yasbleidy
Monsalve Carmona, Diana Marcela
Fecha
2025-02-21
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Elsevier
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Resumen
Abstract
NETosis, the process through which neutrophils release neutrophil extracellular traps (NETs), has emerged as a crucial mechanism in host defense and the pathogenesis of autoimmune responses. During the SARS-CoV-2 pandemic, this process received significant attention due to the central role of neutrophil recruitment and activation in infection control. However, elevated neutrophil levels and dysregulated NET formation have been linked to coagulopathy and endothelial damage, correlating with disease severity and poor prognosis in COVID-19. Moreover, it is known that SARS-CoV-2 can induce persistent low-grade systemic inflammation, known as long COVID, although the underlying causes remain unclear. It has been increasingly acknowledged that excessive NETosis and NET generation contribute to further pathophysiological abnormalities following SARS-CoV-2 infection. This review provides an updated overview of the role of NETosis in autoimmune diseases, but also the relationship between COVID-19 and long COVID with autoimmunity (e.g., latent and overt autoimmunity, molecular mimicry, epitope spreading) and NETosis (e.g., immune responses, NET markers). Finally, we discuss potential therapeutic strategies targeting dysregulated NETosis to mitigate the severe complications of COVID-19 and long COVID.
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Keywords
Inmunology , NETs , Neutrophils , SARS-CoV-2 , COVID-19 , Autoimmunity , Long COVID
