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NETosis: A key player in autoimmunity, COVID-19, and long COVID

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dc.creatorRamírez Santana, Heily Carolinaspa
dc.creatorShoenfeld, Yehudaspa
dc.creatorYilmaz, Ahsen Morvaspa
dc.creatorŞahin, Alispa
dc.creatorCelis-Andrade, Marianaspa
dc.creatorGuerrero Acosta, Nicolásspa
dc.creatorAcosta Ampudia, Yeny Yasbleidyspa
dc.creatorMonsalve Carmona, Diana Marcelaspa
dc.date.accessioned2025-07-21T16:50:06Z
dc.date.available2025-07-21T16:50:06Z
dc.date.created2025-02-21spa
dc.date.issued2025-02-21spa
dc.description.abstractNETosis, 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.eng
dc.format.mimetypeapplication/pdfspa
dc.identifier.doihttps://doi.org/10.1016/j.jtauto.2025.100280spa
dc.identifier.issn2589-9090spa
dc.identifier.urihttps://repository.urosario.edu.co/handle/10336/46091
dc.language.isoengspa
dc.publisherElsevierspa
dc.relation.ispartofJournal of Translational Autoimmunity Volume 10, June 2025spa
dc.relation.urihttps://www.sciencedirect.com/science/article/pii/S2589909025000152?via%3Dihubspa
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internationalspa
dc.rights.accesRightsinfo:eu-repo/semantics/openAccessspa
dc.rights.accesoAbierto (Texto Completo)spa
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/spa
dc.sourceJournal of Translational Autoimmunityspa
dc.source.instnameinstname:Universidad del Rosariospa
dc.source.reponamereponame:Repositorio Institucional EdocURspa
dc.subject.keywordInmunologyeng
dc.subject.keywordNETseng
dc.subject.keywordNeutrophilseng
dc.subject.keywordSARS-CoV-2eng
dc.subject.keywordCOVID-19eng
dc.subject.keywordAutoimmunityeng
dc.subject.keywordLong COVIDeng
dc.titleNETosis: A key player in autoimmunity, COVID-19, and long COVIDspa
dc.typearticlespa
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersionspa
dc.type.spaArtículo de revisiónspa
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