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Immune phenotypes that are associated with subsequent COVID-19 severity inferred from post-recovery samples

Author

Listed:
  • Thomas Liechti

    (ImmunoTechnology Section, Vaccine Research Center, NIAID, NIH)

  • Yaser Iftikhar

    (ImmunoTechnology Section, Vaccine Research Center, NIAID, NIH)

  • Massimo Mangino

    (King’s College of London
    NIHR Biomedical Research Centre at Guy’s and St Thomas’ Foundation Trust)

  • Margaret Beddall

    (ImmunoTechnology Section, Vaccine Research Center, NIAID, NIH)

  • Charles W. Goss

    (Washington University School of Medicine)

  • Jane A. O’Halloran

    (Washington University School of Medicine)

  • Philip A. Mudd

    (Washington University School of Medicine
    Washington University School of Medicine)

  • Mario Roederer

    (ImmunoTechnology Section, Vaccine Research Center, NIAID, NIH)

Abstract

Severe COVID-19 causes profound immune perturbations, but pre-infection immune signatures contributing to severe COVID-19 remain unknown. Genome-wide association studies (GWAS) identified strong associations between severe disease and several chemokine receptors and molecules from the type I interferon pathway. Here, we define immune signatures associated with severe COVID-19 using high-dimensional flow cytometry. We measure the cells of the peripheral immune system from individuals who recovered from mild, moderate, severe or critical COVID-19 and focused only on those immune signatures returning to steady-state. Individuals that suffered from severe COVID-19 show reduced frequencies of T cell, mucosal-associated invariant T cell (MAIT) and dendritic cell (DC) subsets and altered chemokine receptor expression on several subsets, such as reduced levels of CCR1 and CCR2 on monocyte subsets. Furthermore, we find reduced frequencies of type I interferon-producing plasmacytoid DCs and altered IFNAR2 expression on several myeloid cells in individuals recovered from severe COVID-19. Thus, these data identify potential immune mechanisms contributing to severe COVID-19.

Suggested Citation

  • Thomas Liechti & Yaser Iftikhar & Massimo Mangino & Margaret Beddall & Charles W. Goss & Jane A. O’Halloran & Philip A. Mudd & Mario Roederer, 2022. "Immune phenotypes that are associated with subsequent COVID-19 severity inferred from post-recovery samples," Nature Communications, Nature, vol. 13(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:13:y:2022:i:1:d:10.1038_s41467-022-34638-2
    DOI: 10.1038/s41467-022-34638-2
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    1. Brigitta M. Laksono & Rory D. de Vries & R. Joyce Verburgh & Eline G. Visser & Alwin de Jong & Pieter L. A. Fraaij & Wilhemina L. M. Ruijs & David F. Nieuwenhuijse & Henk-Jan van den Ham & Marion P. G, 2018. "Studies into the mechanism of measles-associated immune suppression during a measles outbreak in the Netherlands," Nature Communications, Nature, vol. 9(1), pages 1-10, December.
    2. Michelle Schorer & Nikolas Rakebrandt & Katharina Lambert & Annika Hunziker & Katharina Pallmer & Annette Oxenius & Anja Kipar & Silke Stertz & Nicole Joller, 2020. "TIGIT limits immune pathology during viral infections," Nature Communications, Nature, vol. 11(1), pages 1-14, December.
    3. Erola Pairo-Castineira & Sara Clohisey & Lucija Klaric & Andrew D. Bretherick & Konrad Rawlik & Dorota Pasko & Susan Walker & Nick Parkinson & Max Head Fourman & Clark D. Russell & James Furniss & Ann, 2021. "Genetic mechanisms of critical illness in COVID-19," Nature, Nature, vol. 591(7848), pages 92-98, March.
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    1. Gunther Glehr & Paloma Riquelme & Katharina Kronenberg & Robert Lohmayer & Víctor J. López-Madrona & Michael Kapinsky & Hans J. Schlitt & Edward K. Geissler & Rainer Spang & Sebastian Haferkamp & Jame, 2024. "Restricting datasets to classifiable samples augments discovery of immune disease biomarkers," Nature Communications, Nature, vol. 15(1), pages 1-21, December.

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