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dc.contributor.authorPietrobon, Anna Juliapt_BR
dc.contributor.authorAndrejew, Robertapt_BR
dc.contributor.authorCustódio, Ricardo Wesley Albercapt_BR
dc.contributor.authorOliveira, Luana de Mendonçapt_BR
dc.contributor.authorScholl, Juliete Nathalipt_BR
dc.contributor.authorTeixeira, Franciane Mouradian Emidiopt_BR
dc.contributor.authorBrito, Cyro Alves dept_BR
dc.contributor.authorGlaser, Talitapt_BR
dc.contributor.authorKazmierski, Juliapt_BR
dc.contributor.authorGoffinet, Christinept_BR
dc.contributor.authorTurdo, Anna Claudiapt_BR
dc.contributor.authorYendo, Tatianapt_BR
dc.contributor.authorAoki, Valériapt_BR
dc.contributor.authorFigueiró, Fabríciopt_BR
dc.contributor.authorBattastini, Ana Maria Oliveirapt_BR
dc.contributor.authorUlrich, Henningpt_BR
dc.contributor.authorBenard, Gillpt_BR
dc.contributor.authorDuarte, Alberto Jose da Silvapt_BR
dc.contributor.authorSato, Maria Notomipt_BR
dc.date.accessioned2022-12-09T04:58:49Zpt_BR
dc.date.issued2022pt_BR
dc.identifier.issn1664-3224pt_BR
dc.identifier.urihttp://hdl.handle.net/10183/252574pt_BR
dc.description.abstractEctonucleotidases modulate inflammatory responses by balancing extracellular ATP and adenosine (ADO) and might be involved in COVID-19 immunopathogenesis. Here, we explored the contribution of extracellular nucleotide metabolism to COVID-19 severity in mild and severe cases of the disease. We verified that the gene expression of ectonucleotidases is reduced in the whole blood of patients with COVID-19 and is negatively correlated to levels of CRP, an inflammatory marker of disease severity. In line with these findings, COVID-19 patients present higher ATP levels in plasma and reduced levels of ADO when compared to healthy controls. Cell type-specific analysis revealed higher frequencies of CD39+ T cells in severely ill patients, while CD4+ and CD8+ expressing CD73 are reduced in this same group. The frequency of B cells CD39+CD73+ is also decreased during acute COVID-19. Interestingly, B cells from COVID-19 patients showed a reduced capacity to hydrolyze ATP into ADP and ADO. Furthermore, impaired expression of ADO receptors and a compromised activation of its signaling pathway is observed in COVID-19 patients. The presence of ADO in vitro, however, suppressed inflammatory responses triggered in patients’ cells. In summary, our findings support the idea that alterations in the metabolism of extracellular purines contribute to immune dysregulation during COVID-19, possibly favoring disease severity, and suggest that ADO may be a therapeutic approach for the disease.en
dc.format.mimetypeapplication/pdfpt_BR
dc.language.isoengpt_BR
dc.relation.ispartofFrontiers in immunology. Lausanne. Vol. 13 (2022), 1012027, 12 p.pt_BR
dc.rightsOpen Accessen
dc.subjectAdenosineen
dc.subjectCOVID-19pt_BR
dc.subjectTrifosfato de adenosinapt_BR
dc.subjectATPen
dc.subjectCD39en
dc.subjectPurinérgicospt_BR
dc.subjectAdenosinapt_BR
dc.subjectCD73en
dc.subjectCOVID-19en
dc.subject5'-nucleotidasept_BR
dc.subjectSARS-CoV-2en
dc.subjectPurinergic signalingen
dc.titleDysfunctional purinergic signaling correlates with disease severity in COVID-19 patientspt_BR
dc.typeArtigo de periódicopt_BR
dc.identifier.nrb001155287pt_BR
dc.type.originEstrangeiropt_BR


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