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A dynamic COVID-19 immune signature includes associations with poor prognosis
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Abstract
Improved understanding and management of COVID-19, a potentially life-threatening disease, could greatly reduce the threat posed by its etiologic agent, SARS-CoV-2. Toward this end, we have identified a core peripheral blood immune signature across 63 hospital-treated patients with COVID-19 who were otherwise highly heterogeneous. The signature includes discrete changes in B and myelomonocytic cell composition, profoundly altered T cell phenotypes, selective cytokine/chemokine upregulation and SARS-CoV-2-specific antibodies. Some signature traits identify links with other settings of immunoprotection and immunopathology; others, including basophil and plasmacytoid dendritic cell depletion, correlate strongly with disease severity; while a third set of traits, including a triad of IP-10, interleukin-10 and interleukin-6, anticipate subsequent clinical progression. Hence, contingent upon independent validation in other COVID-19 cohorts, individual traits within this signature may collectively and individually guide treatment options; offer insights into COVID-19 pathogenesis; and aid early, risk-based patient stratification that is particularly beneficial in phasic diseases such as COVID-19.
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“Certain cytokines, such as IL-1β and IL-6, have clearly emerged as key to promoting inflammaging.83,229–232”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [232]
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Metadata
- Authors
- Laing, A. G., Lorenc, A., del Molino del Barrio, I., Das, A., Fish, M., Monin, L., Muñoz-Ruiz, M., McKenzie, D. R., Hayday, T. S., Francos-Quijorna, I., Kamdar, S., Joseph, M., Davies, D., Davis, R., Jennings, A., Zlatareva, I., Vantourout, P., Wu, Y., Sofra, V., Cano, F., Greco, M., Theodoridis, E., Freedman, J. D., Gee, S., Chan, J. N. E., Ryan, S., Bugallo-Blanco, E., Peterson, P., Kisand, K., Haljasmägi, L., Chadli, L., Moingeon, P., Martinez, L., Merrick, B., Bisnauthsing, K., Brooks, K., Ibrahim, M. A. A., Mason, J., Lopez Gomez, F., Babalola, K., Abdul-Jawad, S., Cason, J., Mant, C., Seow, J., Graham, C., Doores, K. J., Di Rosa, F., Edgeworth, J., Shankar-Hari, M., & Hayday, A. C.
- Affiliations
- King's College London (GB)
- Guy's Hospital (GB)
- The Francis Crick Institute (GB)
- Royal Free London NHS Foundation Trust (GB)
- University of Tartu (EE)
- Servier (France) (FR)
- Guy's and St Thomas' NHS Foundation Trust (GB)
- King's College Hospital NHS Foundation Trust (GB)
- European Bioinformatics Institute (GB)
- Corresponding author
- Hayday, Adrian C.
- ORCID
- Laing, Adam G.
- Lorenc, Anna
- Das, Abhishek
- Fish, Matthew
- Monin, Leticia
- McKenzie, Duncan R.
- Hayday, Thomas S.
- Francos-Quijorna, Isaac
- Kamdar, Shraddha
- Joseph, Magdalene
- Davies, Daniel
- Davis, Richard
- Jennings, Aislinn
- Zlatareva, Iva
- Vantourout, Pierre
- Wu, Yin
- Cano, Florencia
- Greco, Maria
- Freedman, Joshua D.
- Gee, Sarah
- Chan, Julie Nuo En
- Ryan, Sarah
- Bugallo-Blanco, Eva
- Peterson, Pärt
- Kisand, Kai
- Haljasmägi, Liis
- Chadli, Loubna
- Moingeon, Philippe
- Martinez, Lauren
- Merrick, Blair
- Bisnauthsing, Karen
- Brooks, Kate
- Ibrahim, Mohammad A. A.
- Mason, Jeremy
- Lopez Gomez, Federico
- Babalola, Kola
- Abdul-Jawad, Sultan
- Mant, Christine
- Seow, Jeffrey
- Doores, Katie J.
- Edgeworth, Jonathan
- Shankar-Hari, Manu
- Hayday, Adrian C.
- Venue
- Nature Medicine
- Published
- 2020-08-17
- Volume
- 26
- Issue
- 10
- Pages
- 1623-1635
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W3049325061
- Cited by
- 946
- References
- 94
- Citations by year
- 2026: 24 · 2025: 50 · 2024: 110 · 2023: 123 · 2022: 216 · 2021: 322 · 2020: 97
- FWCI
- 25.06
- Type
- journal article
- Language
- en
- Update notices
- Open access
- bronze
- doi.org
- Locations
- Nature Medicine (publishedVersion)
- medRxiv (acceptedVersion)
- PubMed (publishedVersion)
- Funders
- Wellcome Trust (106292/Z/4/Z)
- National Institute for Academic Anaesthesia (WKR0-2018-0047)
- Topics
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Health Sciences › Medicine › Clinical Neurology › Long-Term Effects of COVID-19
- Keywords
- COVID-19 pandemic, SARS-CoV-2, immune signatures, peripheral immune cells, B cells, myelomonocytic cells, T cell phenotype, cytokines and chemokines, SARS-CoV-2 antibodies, plasmacytoid dendritic cells, disease severity, prognostic factors, CXCL10, IL-10, interleukin-6, patient stratification
- MeSH terms
- Betacoronavirus, COVID-19, SARS-CoV-2, Aged, Antibodies, Viral, B-Lymphocytes, Basophils, Cell Cycle, Dendritic Cells, Female, Flow Cytometry, Hospitalization, Humans, Immunologic Memory, Leukocyte Count, Lymphocyte Activation, Male, Middle Aged, Pneumonia, Viral, Prognosis, Severity of Illness Index, T-Lymphocytes, Cohort Studies, Interleukin-6, Up-Regulation, Case-Control Studies, Immunophenotyping, B-Lymphocyte Subsets, T-Lymphocyte Subsets, Cytokines, Interleukin-10, Coronavirus Infections, Disease Progression, Chemokines, Chemokine CXCL10, Pandemics
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