Severe COVID-19 is marked by a dysregulated myeloid cell compartment. Schulte-Schrepping et al., 2020

Published: 28 July 2020| Version 1 | DOI: 10.17632/hwxhw2sxys.1
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Supplemental tables of the publication "Severe COVID-19 is marked by a dysregulated myeloid cell compartment." Schulte-Schrepping et al., 2020. Table S1 - Cohort details (related to all Figures) Table S2 - Detailed information on antibody panels used for mass cytometry analysis (related to Figure 1,3,6) Table S3 - List of antibodies used for multi-color flow cytometry (related to Figure 1,3,6). Table S4 - Cluster-specific marker gene lists from the scRNA-seq analyses (related to Figure 2,4,5,7 + S2-4,S6) Severe COVID-19 is marked by a dysregulated myeloid cell compartment Jonas Schulte-Schrepping, Nico Reusch, Daniela Paclik, Kevin Baßler, Stephan Schlickeiser, Bowen Zhang, Benjamin Krämer, Tobias Krammer, Sophia Brumhard, Lorenzo Bonaguro, Elena De Domenico, Daniel Wendisch, Martin Grasshoff, Theodore S. Kapellos, Michael Beckstette, Tal Pecht, Adem Saglam, Oliver Dietrich, Henrik E. Mei, Axel R. Schulz, Claudia Conrad, Désirée Kunkel, Ehsan Vafadarnejad, Cheng-Jian Xu, Arik Horne, Miriam Herbert, Anna Drews, Charlotte Thibeault, Moritz Pfeiffer, Stefan Hippenstiel, Andreas Hocke, Holger Müller-Redetzky, Katrin-Moira Heim, Felix Machleidt, Alexander Uhrig, Laure Bosquillon de Jarcy, Linda Jürgens, Miriam Stegemann, Christoph R. Glösenkamp, Hans-Dieter Volk, Christine Goffinet, Markus Landthaler, Emanuel Wyler, Philipp Georg, Maria Schneider, Chantip Dang-Heine, Nick Neuwinger, Kai Kappert, Rudolf Tauber, Victor Corman, Jan Raabe, Kim Melanie Kaiser, Michael To Vinh, Gereon Rieke, Christian Meisel, Thomas Ulas, Matthias Becker, Robert Geffers, Martin Witzenrath, Christian Drosten, Norbert Suttorp, Christof von Kalle, Florian Kurth, Kristian Händler, Joachim L. Schultze, Anna C Aschenbrenner, Yang Li, Jacob Nattermann, Birgit Sawitzki, Antoine-Emmanuel Saliba, Leif Erik Sander, Deutsche COVID-19 OMICS Initiative (DeCOI) Coronavirus Disease 2019 (COVID-19) is a mild to moderate respiratory tract infection, however, a subset of patients progresses 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, remains 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 vs. severe COVID-19 (242 samples from 109 individuals) over time. HLA-DR high CD11c high 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-DR low monocytes. Our study provides detailed insights into the systemic immune response to SARS-CoV-2 infection and it reveals profound alterations in the myeloid cell compartment associated with severe COVID-19.

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Proteomics, Neutrophil, Transcriptomics, Monocyte, COVID-19

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