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@ARTICLE{Frishberg:164649,
      author       = {Frishberg, Amit and Kooistra, Emma and Nuesch-Germano,
                      Melanie and Pecht, Tal and Milman, Neta and Reusch, Nico and
                      Warnat-Herresthal, Stefanie and Bruse, Niklas and Händler,
                      Kristian and Theis, Heidi and Kraut, Michael and van
                      Rijssen, Esther and van Cranenbroek, Bram and Koenen, Hans
                      JPM. and Heesakkers, Hidde and van den Boogaard, Mark and
                      Zegers, Marieke and Pickkers, Peter and Becker, Matthias Kai
                      Holger and Aschenbrenner, Anna Christin and Ulas, Thomas and
                      Theis, Fabian J. and Shen-Orr, Shai S. and Schultze, Joachim
                      and Kox, Matthijs},
      title        = {{M}ature neutrophils and a {NF}-κ{B}-to-{IFN} transition
                      determine the unifying disease recovery dynamics in
                      {COVID}-19},
      journal      = {Cell reports},
      volume       = {3},
      number       = {6},
      issn         = {2666-3791},
      address      = {Maryland Heights, MO},
      publisher    = {Elsevier},
      reportid     = {DZNE-2022-01179},
      pages        = {100652},
      year         = {2022},
      note         = {(CC BY-NC-ND)},
      abstract     = {Disease recovery dynamics are often difficult to assess, as
                      patients display heterogeneous recovery courses. To model
                      recovery dynamics, exemplified by severe COVID-19, we apply
                      a computational scheme on longitudinally sampled blood
                      transcriptomes, generating recovery states, which we then
                      link to cellular and molecular mechanisms, presenting a
                      framework for studying the kinetics of recovery compared
                      with non-recovery over time and long-term effects of the
                      disease. Specifically, a decrease in mature neutrophils is
                      the strongest cellular effect during recovery, with direct
                      implications on disease outcome. Furthermore, we present
                      strong indications for global regulatory changes in gene
                      programs, decoupled from cell compositional changes,
                      including an early rise in T cell activation and
                      differentiation, resulting in immune rebalancing between
                      interferon and NF-κB activity and restoration of cell
                      homeostasis. Overall, we present a clinically relevant
                      computational framework for modeling disease recovery,
                      paving the way for future studies of the recovery dynamics
                      in other diseases and tissues.},
      keywords     = {COVID-19 / Cell Differentiation / Humans / Interferons:
                      metabolism / NF-kappa B: genetics / Neutrophils: metabolism
                      / Signal Transduction / COVID-19 (Other) / cell
                      deconvolution (Other) / disease modeling (Other) / disease
                      recovery (Other) / gene regulation (Other) / immunology
                      (Other) / medicine (Other) / systems biology (Other) / viral
                      infection (Other) / NF-kappa B (NLM Chemicals) / Interferons
                      (NLM Chemicals)},
      cin          = {AG Schultze / $R\&D$ PRECISE / Modular High Performance
                      Computing},
      ddc          = {610},
      cid          = {I:(DE-2719)1013031 / I:(DE-2719)5000031 /
                      I:(DE-2719)5000079},
      pnm          = {354 - Disease Prevention and Healthy Aging (POF4-354)},
      pid          = {G:(DE-HGF)POF4-354},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC9110324},
      pubmed       = {pmid:35675822},
      doi          = {10.1016/j.xcrm.2022.100652},
      url          = {https://pub.dzne.de/record/164649},
}