Impaired function and delayed regeneration of dendritic cells in COVID-19.
Journal
PLoS pathogens
ISSN: 1553-7374
Titre abrégé: PLoS Pathog
Pays: United States
ID NLM: 101238921
Informations de publication
Date de publication:
10 2021
10 2021
Historique:
received:
28
06
2021
accepted:
23
09
2021
revised:
18
10
2021
pubmed:
7
10
2021
medline:
3
11
2021
entrez:
6
10
2021
Statut:
epublish
Résumé
Disease manifestations in COVID-19 range from mild to severe illness associated with a dysregulated innate immune response. Alterations in function and regeneration of dendritic cells (DCs) and monocytes may contribute to immunopathology and influence adaptive immune responses in COVID-19 patients. We analyzed circulating DC and monocyte subsets in 65 hospitalized COVID-19 patients with mild/moderate or severe disease from acute illness to recovery and in healthy controls. Persisting reduction of all DC subpopulations was accompanied by an expansion of proliferating Lineage-HLADR+ cells lacking DC markers. Increased frequency of CD163+ CD14+ cells within the recently discovered DC3 subpopulation in patients with more severe disease was associated with systemic inflammation, activated T follicular helper cells, and antibody-secreting cells. Persistent downregulation of CD86 and upregulation of programmed death-ligand 1 (PD-L1) in conventional DCs (cDC2 and DC3) and classical monocytes associated with a reduced capacity to stimulate naïve CD4+ T cells correlated with disease severity. Long-lasting depletion and functional impairment of DCs and monocytes may have consequences for susceptibility to secondary infections and therapy of COVID-19 patients.
Identifiants
pubmed: 34614036
doi: 10.1371/journal.ppat.1009742
pii: PPATHOGENS-D-21-01334
pmc: PMC8523079
doi:
Substances chimiques
Antigens, CD
0
PDCD1 protein, human
0
Programmed Cell Death 1 Receptor
0
Types de publication
Clinical Trial
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
e1009742Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
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