Journal
CELL
Volume 182, Issue 6, Pages 1419-+Publisher
CELL PRESS
DOI: 10.1016/j.cell.2020.08.001
Keywords
-
Categories
Funding
- German Research Foundation (DFG) [SFB-TR84 114933180, INST 37/1049-1, INST 216/981-1, INST 257/605-1, INST 269/768-1, INST 217/988-1, INST 217/577-1, EXC2151/1, SFB TR57, SPP1937, GRK2157, ME 3644/5-1]
- Berlin University Alliance (BUA) (PreEP-Corona grant)
- Berlin Institute of Health (BIH)
- Helmholtz-Gemeinschaft Deutscher Forschungszentren, Germany
- EU [733100, 00160389, 260687, 305147, 860003]
- DZIF, Germany [TTU 04.816, 04.817]
- Hector Foundation [M89]
- Helmholtz Association of German Research Centres
- German Federal Ministry of Education and Research, Germany (BMBF)
- Charite 3R project
- Radboud University Medical Centre Hypatia Grant (2018)
- Marie Curie Actions (MSCA) [860003] Funding Source: Marie Curie Actions (MSCA)
Ask authors/readers for more resources
Coronavirus disease 2019 (COVID-19) is a mild to moderate respiratory tract infection, however, a subset of patients progress to severe disease and respiratory failure. The mechanism of protective immunity in mild forms and the pathogenesis of severe COVID-19 associated with increased neutrophil counts and dysregulated immune responses remain unclear. In a dual-center, two-cohort study, we combined single-cell RNA-sequencing and single-cell proteomics of whole-blood and peripheral-blood mononuclear cells to determine changes in immune cell composition and activation in mild versus severe COVID-19 (242 samples from 109 individuals) over time. HLA-DR(hi)CD11c(hi) inflammatory monocytes with an interferon-stimulated gene signature were elevated in mild COVID-19. Severe COVID-19 was marked by occurrence of neutrophil precursors, as evidence of emergency myelopoiesis, dysfunctional mature neutrophils, and HLA-DRlo monocytes. Our study provides detailed insights into the systemic immune response to SARS-CoV-2 infection and reveals profound alterations in the myeloid cell compartment associated with severe COVID-19.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available