Transcriptional Changes in CD16+ Monocytes May Contribute to the Pathogenesis of COVID-19

Autor: Vanessa Chilunda, Pablo Martinez-Aguado, Li C. Xia, Laura Cheney, Aniella Murphy, Veronica Veksler, Vanessa Ruiz, Tina M. Calderon, Joan W. Berman
Jazyk: angličtina
Rok vydání: 2021
Předmět:
0301 basic medicine
Male
Transcription
Genetic

Severity of Illness Index
Monocytes
0302 clinical medicine
cell movement
Interferon
Immunology and Allergy
RNA-Seq
Original Research
Middle Aged
030220 oncology & carcinogenesis
Host-Pathogen Interactions
Interferon Regulatory Factors
Cytokines
Female
medicine.symptom
Inflammation Mediators
Single-Cell Analysis
Cell activation
medicine.drug
Adult
Antigen presentation
Immunology
Inflammation
CD16
Biology
GPI-Linked Proteins
Peripheral blood mononuclear cell
Mitochondrial Proteins
03 medical and health sciences
Young Adult
Immune system
medicine
Humans
Aged
Innate immune system
SARS-CoV-2
Gene Expression Profiling
Receptors
IgG

COVID-19
RC581-607
030104 developmental biology
inflammation
Case-Control Studies
Immunologic diseases. Allergy
non-classical monocytes
Apoptosis Regulatory Proteins
Transcriptome
single-cell transcriptomics
Zdroj: Frontiers in Immunology
Frontiers in Immunology, Vol 12 (2021)
ISSN: 1664-3224
DOI: 10.3389/fimmu.2021.665773
Popis: The COVID-19 pandemic has caused more than three million deaths globally. The severity of the disease is characterized, in part, by a dysregulated immune response. CD16+ monocytes are innate immune cells involved in inflammatory responses to viral infections, and tissue repair, among other functions. We characterized the transcriptional changes in CD16+ monocytes from PBMC of people with COVID-19, and from healthy individuals using publicly available single cell RNA sequencing data. CD16+ monocytes from people with COVID-19 compared to those from healthy individuals expressed transcriptional changes indicative of increased cell activation, and induction of a migratory phenotype. We also analyzed COVID-19 cases based on severity of the disease and found that mild cases were characterized by upregulation of interferon response and MHC class II related genes, whereas the severe cases had dysregulated expression of mitochondrial and antigen presentation genes, and upregulated inflammatory, cell movement, and apoptotic gene signatures. These results suggest that CD16+ monocytes in people with COVID-19 contribute to a dysregulated host response characterized by decreased antigen presentation, and an elevated inflammatory response with increased monocytic infiltration into tissues. Our results show that there are transcriptomic changes in CD16+ monocytes that may impact the functions of these cells, contributing to the pathogenesis and severity of COVID-19.
Databáze: OpenAIRE