Expansion of CD56dimCD16neg NK Cell Subset and Increased Inhibitory KIRs in Hospitalized COVID-19 Patients

Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV-2) infection induces elevated levels of inflammatory cytokines, which are mainly produced by the innate response to the virus. The role of NK cells, which are potent producers of IFN-γ and cytotoxicity, has not been sufficiently studied in the setting of SARS-CoV-2 infection. We confirmed a different distribution of NK cell subsets in hospitalized COVID-19 patients despite their NK cell deficiency. The impairment of this innate defense is mainly focused on the cytotoxic capacity of the CD56dim NK cells. On the one hand, we found an expansion of the CD56dimCD16neg NK subset, lower cytotoxic capacities, and high frequencies of inhibitory 2DL1 and 2DL1/S1 KIR receptors in COVID-19 patients. On the other hand, the depletion of CD56dimCD16dim/bright NK cell subsets, high cytotoxic capacities, and high frequencies of inhibitory 2DL1 KIR receptors were found in COVID-19 patients. In contrast, no differences in the distribution of CD56bright NK cell subsets were found in this study. These alterations in the distribution and phenotype of NK cells might enhance the impairment of this crucial innate line of defense during COVID-19 infection.

Medienart:

E-Artikel

Erscheinungsjahr:

2021

Erschienen:

2021

Enthalten in:

Zur Gesamtaufnahme - volume:14

Enthalten in:

Viruses - 14(2021), 1 vom: 28. Dez.

Sprache:

Englisch

Beteiligte Personen:

Casado, José L [VerfasserIn]
Moraga, Elisa [VerfasserIn]
Vizcarra, Pilar [VerfasserIn]
Velasco, Héctor [VerfasserIn]
Martín-Hondarza, Adrián [VerfasserIn]
Haemmerle, Johannes [VerfasserIn]
Gómez, Sandra [VerfasserIn]
Quereda, Carmen [VerfasserIn]
Vallejo, Alejandro [VerfasserIn]

Links:

Volltext

Themen:

CD56 Antigen
COVID-19
FCGR3B protein, human
GPI-Linked Proteins
Journal Article
KIR receptors
NCAM1 protein, human
NK cell subsets
Receptors, IgG
Receptors, KIR
Research Support, Non-U.S. Gov't
SARS-CoV-2

Anmerkungen:

Date Completed 03.02.2022

Date Revised 03.02.2022

published: Electronic

Citation Status MEDLINE

doi:

10.3390/v14010046

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM335968414