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SARS-CoV-2 proteins

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    Suppressive myeloid cells are a hallmark of severe COVID-19 MESHD

    Authors: 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 Bousquillon de Jarcy; Linda Jürgens; Miriam Stegemann; Christoph R. Glösenkamp; Hans-Dieter Volk; Christine Goffinet; 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)

    doi:10.1101/2020.06.03.20119818 Date: 2020-06-05 Source: medRxiv

    'Severe Acute Respiratory Syndrome MESHD - Coronavirus-2' ( SARS-CoV-2) infection MESHD causes Coronavirus Disease 2019 MESHD ( COVID-19 MESHD), a mild to moderate respiratory tract infection MESHD in the majority of patients. A subset of patients, however, progresses to severe disease and respiratory failure MESHD with acute respiratory distress syndrome MESHD ( ARDS MESHD). Severe COVID-19 MESHD has been associated with increased neutrophil counts and dysregulated immune responses. The mechanisms of protective immunity in mild forms and the pathogenesis of dysregulated inflammation MESHD in severe courses of COVID-19 MESHD remain largely unclear. Here, we combined two single-cell RNA-sequencing technologies and single-cell proteomics in whole blood and peripheral blood mononuclear cells (PBMC) to determine changes in immune cell composition and activation in two independent dual-center patient cohorts (n=46 + n=54 COVID-19 MESHD samples), each with mild and severe cases of COVID-19 MESHD. We observed a specific increase of HLA-DR high CD11c HGNC high inflammatory monocytes that displayed a strong interferon (IFN)-stimulated gene signature in patients with mild COVID-19 MESHD, which was absent in severe disease. Instead, we found evidence of emergency myelopoiesis, marked by the occurrence of immunosuppressive pre-neutrophils and immature neutrophils and populations of dysfunctional MESHD and suppressive mature neutrophils, as well as suppressive HLA-DR low monocytes in severe COVID-19 MESHD. Our study provides detailed insights into systemic immune response to SARS-CoV-2 infection MESHD and it reveals profound alterations in the peripheral myeloid cell compartment associated with severe courses of COVID-19 MESHD.

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MeSH Disease
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SARS-CoV-2 Proteins


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