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Disharmonic Inflammatory Signatures in COVID-19: Augmented Neutrophils' but Impaired Monocytes' and Dendritic Cells' Responsiveness
Z. Parackova, I. Zentsova, M. Bloomfield, P. Vrabcova, J. Smetanova, A. Klocperk, G. Mesežnikov, LF. Casas Mendez, T. Vymazal, A. Sediva,
Jazyk angličtina Země Švýcarsko
Typ dokumentu časopisecké články, práce podpořená grantem
Grantová podpora
AZV NU20-05-00320
Ministerstvo Zdravotnictví Ceské Republiky - International
NLK
Directory of Open Access Journals
od 2012
Free Medical Journals
od 2012
PubMed Central
od 2012
Europe PubMed Central
od 2012
ProQuest Central
od 2012-03-01
Open Access Digital Library
od 2012-01-01
Open Access Digital Library
od 2012-01-01
ROAD: Directory of Open Access Scholarly Resources
od 2012
PubMed
33003471
DOI
10.3390/cells9102206
Knihovny.cz E-zdroje
- MeSH
- antigeny CD274 genetika metabolismus MeSH
- COVID-19 MeSH
- cytokiny genetika metabolismus MeSH
- dendritické buňky imunologie MeSH
- dospělí MeSH
- imunofenotypizace MeSH
- koronavirové infekce krev imunologie MeSH
- kultivované buňky MeSH
- lidé středního věku MeSH
- lidé MeSH
- monocyty imunologie MeSH
- neutrofily imunologie MeSH
- pandemie MeSH
- přirozená imunita MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- virová pneumonie krev imunologie MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
COVID-19, caused by SARS-CoV-2 virus, emerged as a pandemic disease posing a severe threat to global health. To date, sporadic studies have demonstrated that innate immune mechanisms, specifically neutrophilia, NETosis, and neutrophil-associated cytokine responses, are involved in COVID-19 pathogenesis; however, our understanding of the exact nature of this aspect of host-pathogen interaction is limited. Here, we present a detailed dissection of the features and functional profiles of neutrophils, dendritic cells, and monocytes in COVID-19. We portray the crucial role of neutrophils as drivers of hyperinflammation associated with COVID-19 disease via the shift towards their immature forms, enhanced degranulation, cytokine production, and augmented interferon responses. We demonstrate the impaired functionality of COVID-19 dendritic cells and monocytes, particularly their low expression of maturation markers, increased PD-L1 levels, and their inability to upregulate phenotype upon stimulation. In summary, our work highlights important data that prompt further research, as therapeutic targeting of neutrophils and their associated products may hold the potential to reduce the severity of COVID-19.
Citace poskytuje Crossref.org
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