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Cutting Edge: Hyperinflammatory Monocytes Expressing CD56 Abound in Severe COVID-19 Patients.

Authors :
Campana S
De Pasquale C
Sidoti Migliore G
Pezzino G
Cavaliere R
Venanzi Rullo E
Nunnari G
Caramori G
David A
Bonaccorsi I
Pollicino T
Carrega P
Ferlazzo G
Source :
Journal of immunology (Baltimore, Md. : 1950) [J Immunol] 2022 Aug 15; Vol. 209 (4), pp. 655-659. Date of Electronic Publication: 2022 Jul 27.
Publication Year :
2022

Abstract

Proinflammatory monocytes play a preponderant role in the development of a cytokine storm causing fatal consequences in coronavirus disease 2019 (COVID-19) patients, highlighting the importance of analyzing in more detail monocyte distribution in these patients. In this study, we identified an atypical monocyte subpopulation expressing CD56 molecules that showed a low level of HLA-DR and high level of l-selectin. They released higher amounts of TNF-α and IL-6 and expressed genes associated with an excessive inflammatory process. Remarkably, the frequency of CD56 <superscript>+</superscript> monocytes inversely correlated with that of CD16 <superscript>+</superscript> monocytes and a high CD56 <superscript>+</superscript> /CD16 <superscript>+</superscript> monocyte ratio was associated with both disease severity and mortality, as well as with serum concentration of type I IFN, a factor able to induce the appearance of CD56 <superscript>+</superscript> monocytes. In conclusion, severe COVID-19 is characterized by the abundance of hyperinflammatory CD56 <superscript>+</superscript> monocytes, which could represent a novel marker with prognostic significance and, possibly, a therapeutic target for controlling the inflammatory process occurring during COVID-19.<br /> (Copyright © 2022 by The American Association of Immunologists, Inc.)

Details

Language :
English
ISSN :
1550-6606
Volume :
209
Issue :
4
Database :
MEDLINE
Journal :
Journal of immunology (Baltimore, Md. : 1950)
Publication Type :
Academic Journal
Accession number :
35896335
Full Text :
https://doi.org/10.4049/jimmunol.2200021