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Impaired function and delayed regeneration of dendritic cells in COVID-19.
Winheim, Elena; Rinke, Linus; Lutz, Konstantin; Reischer, Anna; Leutbecher, Alexandra; Wolfram, Lina; Rausch, Lisa; Kranich, Jan; Wratil, Paul R; Huber, Johanna E; Baumjohann, Dirk; Rothenfusser, Simon; Schubert, Benjamin; Hilgendorff, Anne; Hellmuth, Johannes C; Scherer, Clemens; Muenchhoff, Maximilian; von Bergwelt-Baildon, Michael; Stark, Konstantin; Straub, Tobias; Brocker, Thomas; Keppler, Oliver T; Subklewe, Marion; Krug, Anne B.
  • Winheim E; Institute for Immunology, Biomedical Center (BMC), Faculty of Medicine, LMU Munich; Munich, Germany.
  • Rinke L; Institute for Immunology, Biomedical Center (BMC), Faculty of Medicine, LMU Munich; Munich, Germany.
  • Lutz K; Institute for Immunology, Biomedical Center (BMC), Faculty of Medicine, LMU Munich; Munich, Germany.
  • Reischer A; Department of Medicine III, University Hospital, LMU Munich; Munich, Germany.
  • Leutbecher A; Laboratory for Translational Cancer Immunology, Gene Center, LMU Munich; Munich, Germany.
  • Wolfram L; Department of Medicine III, University Hospital, LMU Munich; Munich, Germany.
  • Rausch L; Laboratory for Translational Cancer Immunology, Gene Center, LMU Munich; Munich, Germany.
  • Kranich J; Institute for Immunology, Biomedical Center (BMC), Faculty of Medicine, LMU Munich; Munich, Germany.
  • Wratil PR; Institute for Immunology, Biomedical Center (BMC), Faculty of Medicine, LMU Munich; Munich, Germany.
  • Huber JE; Institute for Immunology, Biomedical Center (BMC), Faculty of Medicine, LMU Munich; Munich, Germany.
  • Baumjohann D; Max von Pettenkofer Institute of Hygiene and Medical Microbiology, Faculty of Medicine & Gene Center, Virology, National Reference Center for Retroviruses, LMU Munich; Munich, Germany.
  • Rothenfusser S; German Center for Infection Research (DZIF), partner site Munich, Germany.
  • Schubert B; Institute for Immunology, Biomedical Center (BMC), Faculty of Medicine, LMU Munich; Munich, Germany.
  • Hilgendorff A; Institute for Immunology, Biomedical Center (BMC), Faculty of Medicine, LMU Munich; Munich, Germany.
  • Hellmuth JC; Medical Clinic III for Oncology, Hematology, Immuno-Oncology and Rheumatology, University Hospital Bonn, University of Bonn, Bonn, Germany.
  • Scherer C; Division of Clinical Pharmacology, University Hospital, LMU Munich; Munich, Germany.
  • Muenchhoff M; Unit Clinical Pharmacology (EKLiP), Helmholtz Zentrum München, German Research Center for Environmental Health (HMGU), Neuherberg, Germany.
  • von Bergwelt-Baildon M; Institute of Computational Biology, Helmholtz Zentrum München-German Research Center for Environmental Health, Neuherberg, Germany.
  • Stark K; Department of Mathematics, Technical University of Munich, Garching, Germany.
  • Straub T; Institute for Lung Biology and Disease and Comprehensive Pneumology Center with the CPC-M bioArchive, Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.
  • Brocker T; Center for Comprehensive Developmental Care (CDeCLMU), Dr. Von Haunersche Children's Hospital, University Hospital LMU Munich; Munich, Germany.
  • Keppler OT; Department of Medicine III, University Hospital, LMU Munich; Munich, Germany.
  • Subklewe M; COVID-19 Registry of the LMU Munich (CORKUM), University Hospital, LMU Munich; Munich, Germany.
  • Krug AB; COVID-19 Registry of the LMU Munich (CORKUM), University Hospital, LMU Munich; Munich, Germany.
PLoS Pathog ; 17(10): e1009742, 2021 10.
Article in English | MEDLINE | ID: covidwho-1456098
Preprint
This scientific journal article is probably based on a previously available preprint. It has been identified through a machine matching algorithm, human confirmation is still pending.
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ABSTRACT
Disease manifestations in COVID-19 range from mild to severe illness associated with a dysregulated innate immune response. Alterations in function and regeneration of dendritic cells (DCs) and monocytes may contribute to immunopathology and influence adaptive immune responses in COVID-19 patients. We analyzed circulating DC and monocyte subsets in 65 hospitalized COVID-19 patients with mild/moderate or severe disease from acute illness to recovery and in healthy controls. Persisting reduction of all DC subpopulations was accompanied by an expansion of proliferating Lineage-HLADR+ cells lacking DC markers. Increased frequency of CD163+ CD14+ cells within the recently discovered DC3 subpopulation in patients with more severe disease was associated with systemic inflammation, activated T follicular helper cells, and antibody-secreting cells. Persistent downregulation of CD86 and upregulation of programmed death-ligand 1 (PD-L1) in conventional DCs (cDC2 and DC3) and classical monocytes associated with a reduced capacity to stimulate naïve CD4+ T cells correlated with disease severity. Long-lasting depletion and functional impairment of DCs and monocytes may have consequences for susceptibility to secondary infections and therapy of COVID-19 patients.
Subject(s)

Full text: Available Collection: International databases Database: MEDLINE Main subject: Regeneration / Dendritic Cells / SARS-CoV-2 / COVID-19 Limits: Adult / Female / Humans / Male / Middle aged Language: English Journal: PLoS Pathog Year: 2021 Document Type: Article Affiliation country: Journal.ppat.1009742

Full text: Available Collection: International databases Database: MEDLINE Main subject: Regeneration / Dendritic Cells / SARS-CoV-2 / COVID-19 Limits: Adult / Female / Humans / Male / Middle aged Language: English Journal: PLoS Pathog Year: 2021 Document Type: Article Affiliation country: Journal.ppat.1009742