期刊
NATURE MEDICINE
卷 27, 期 5, 页码 904-+出版社
NATURE PORTFOLIO
DOI: 10.1038/s41591-021-01329-2
关键词
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资金
- Wellcome Human Cell Atlas Strategic Science Support [WT211276/Z/18/Z]
- Wellcome [WT211276/Z/18/Z, WT107931/Z/15/Z, 206328/Z/17/Z, WT206194, 207556_Z_17_Z, 211153/Z/18/Z, 203151/Z/16/Z]
- Lister Institute for Preventive Medicine
- Newcastle NIHR Biomedical Research Centre
- MRC [203151/Z/16/Z, MR/S036113/1]
- Aging Biology Foundation
- ERC
- EU MRG-Grammar awards
- Medical Research Council Human Cell Atlas Research Grant [MR/S035842/1]
- Cancer Research UK [C9545/A29580]
- European Molecular Biology Laboratory
- Versus Arthritis Cure Challenge Research Grant [21777]
- NIHR Research Professorship [RP-2017-08-ST2-002]
- Sir Henry Wellcome Postdoctoral Fellowship [213555/Z/18/Z]
- Chan Zuckerberg Initiative [2017-174169]
- Sanger Core [WT206194]
- UKRI Innovation/Rutherford Fund Fellowship by the MRC
- UK Regenerative Medicine Platform [MR/5005579/1]
- Rosetrees Trust [M944]
- University College London, Birkbeck MRC Doctoral Training Programme.
- Jikei University School of Medicine
- NIHR [ACF-2018-01-004]
- BMA Foundation
- NIHR Clinical Lectureship [CL-2017-01-004]
- Action Medical Research [GN2779]
- DFG Research Fellowship [ME 5209/11]
- Barbour Foundation
- Barbour Foundation PhD studentship
- Wellcome/Royal Society [107630/Z/15/Z]
- BBSRC [BB/P002293/1, BB/V006738/1]
- GOSH Children's charity [COVID_CSmith_017]
- Wellcome Trust [212516/Z/18/Z]
- NIHR GOSH Biomedical research centre
- UKRI/NIHR through the UK Coronavirus Immunology Consortium.
- MRC
- BBSRC [BB/V006738/1, BB/P002293/1] Funding Source: UKRI
- MRC [MR/S036113/1, MR/W014556/1] Funding Source: UKRI
- Wellcome Trust [107630/Z/15/Z, 213555/Z/18/Z, 212516/Z/18/Z, 211153/Z/18/Z] Funding Source: Wellcome Trust
Transcriptomic and proteomic profiling of blood samples from individuals with COVID-19 reveals immune cell and hematopoietic progenitor cell alterations that are differentially associated with disease severity.
Analysis of human blood immune cells provides insights into the coordinated response to viral infections such as severe acute respiratory syndrome coronavirus 2, which causes coronavirus disease 2019 (COVID-19). We performed single-cell transcriptome, surface proteome and T and B lymphocyte antigen receptor analyses of over 780,000 peripheral blood mononuclear cells from a cross-sectional cohort of 130 patients with varying severities of COVID-19. We identified expansion of nonclassical monocytes expressing complement transcripts (CD16(+)C1QA/B/C+) that sequester platelets and were predicted to replenish the alveolar macrophage pool in COVID-19. Early, uncommitted CD34(+) hematopoietic stem/progenitor cells were primed toward megakaryopoiesis, accompanied by expanded megakaryocyte-committed progenitors and increased platelet activation. Clonally expanded CD8(+) T cells and an increased ratio of CD8(+) effector T cells to effector memory T cells characterized severe disease, while circulating follicular helper T cells accompanied mild disease. We observed a relative loss of IgA2 in symptomatic disease despite an overall expansion of plasmablasts and plasma cells. Our study highlights the coordinated immune response that contributes to COVID-19 pathogenesis and reveals discrete cellular components that can be targeted for therapy. Transcriptomic and proteomic profiling of blood samples from individuals with COVID-19 reveals immune cell and hematopoietic progenitor cell alterations that are differentially associated with disease severity.
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