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  3. Macrophage phagocytosis of SARS-CoV-2-infected cells mediates potent plasmacytoid dendritic cell activation.
 

Macrophage phagocytosis of SARS-CoV-2-infected cells mediates potent plasmacytoid dendritic cell activation.

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BORIS DOI
10.48350/183044
Date of Publication
July 2023
Publication Type
Article
Division/Institute

Institut für Virologi...

Author
Garcia Nicolas, Obdulio
Institut für Virologie und Immunologie (IVI)
Godel, Aurélie
Institut für Virologie und Immunologie (IVI)
Zimmer, Gert
Institut für Virologie und Immunologie (IVI)
Summerfield, Arturorcid-logo
Institut für Virologie und Immunologie (IVI)
Department of Infectious Diseases and Pathobiology (DIP) Universität Bern
Subject(s)

600 - Technology::630...

Series
Cellular & molecular immunology
ISSN or ISBN (if monograph)
1672-7681
Publisher
Nature Publ. Group
Language
English
Publisher DOI
10.1038/s41423-023-01039-4
PubMed ID
37253946
Uncontrolled Keywords

Inflammatory cytokine...

COVID-19

Description
Early and strong interferon type I (IFN-I) responses are usually associated with mild COVID-19 disease, whereas persistent or unregulated proinflammatory cytokine responses are associated with severe disease outcomes. Previous work suggested that monocyte-derived macrophages (MDMs) are resistant and unresponsive to SARS-CoV-2 infection. Here, we demonstrate that upon phagocytosis of SARS-CoV-2-infected cells, MDMs are activated and secrete IL-6 and TNF. Importantly, activated MDMs in turn mediate strong activation of plasmacytoid dendritic cells (pDCs), leading to the secretion of high levels of IFN-α and TNF. Furthermore, pDC activation promoted IL-6 production by MDMs. This kind of pDC activation was dependent on direct integrin-mediated cell‒cell contacts and involved stimulation of the TLR7 and STING signaling pathways. Overall, the present study describes a novel and potent pathway of pDC activation that is linked to the macrophage-mediated clearance of infected cells. These findings suggest that a high infection rate by SARS-CoV-2 may lead to exaggerated cytokine responses, which may contribute to tissue damage and severe disease.
Handle
https://boris-portal.unibe.ch/handle/20.500.12422/167536
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FileFile TypeFormatSizeLicensePublisher/Copright statementContent
s41423-023-01039-4.pdftextAdobe PDF2.16 MBpublishedOpen
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