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@ARTICLE{Mitroulis:139724,
      author       = {Mitroulis, Ioannis and Ruppova, Klara and Wang, Baomei and
                      Chen, Lan-Sun and Grzybek, Michal and Grinenko, Tatyana and
                      Eugster, Anne and Troullinaki, Maria and Palladini,
                      Alessandra and Kourtzelis, Ioannis and Chatzigeorgiou,
                      Antonios and Schlitzer, Andreas and Beyer, Marc and Joosten,
                      Leo A B and Isermann, Berend and Lesche, Mathias and
                      Petzold, Andreas and Simons, Kai and Henry, Ian and Dahl,
                      Andreas and Schultze, Joachim L and Wielockx, Ben and
                      Zamboni, Nicola and Mirtschink, Peter and Coskun, Ünal and
                      Hajishengallis, George and Netea, Mihai G and Chavakis,
                      Triantafyllos},
      title        = {{M}odulation of {M}yelopoiesis {P}rogenitors {I}s an
                      {I}ntegral {C}omponent of {T}rained {I}mmunity.},
      journal      = {Cell},
      volume       = {172},
      number       = {1-2},
      issn         = {0092-8674},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DZNE-2020-06046},
      pages        = {147-161.e12},
      year         = {2018},
      abstract     = {Trained innate immunity fosters a sustained favorable
                      response of myeloid cells to a secondary challenge, despite
                      their short lifespan in circulation. We thus hypothesized
                      that trained immunity acts via modulation of hematopoietic
                      stem and progenitor cells (HSPCs). Administration of
                      β-glucan (prototypical trained-immunity-inducing agonist)
                      to mice induced expansion of progenitors of the myeloid
                      lineage, which was associated with elevated signaling by
                      innate immune mediators, such as IL-1β and
                      granulocyte-macrophage colony-stimulating factor (GM-CSF),
                      and with adaptations in glucose metabolism and cholesterol
                      biosynthesis. The trained-immunity-related increase in
                      myelopoiesis resulted in a beneficial response to secondary
                      LPS challenge and protection from chemotherapy-induced
                      myelosuppression in mice. Therefore, modulation of myeloid
                      progenitors in the bone marrow is an integral component of
                      trained immunity, which to date, was considered to involve
                      functional changes of mature myeloid cells in the
                      periphery.},
      keywords     = {Animals / Cells, Cultured / Granulocyte-Macrophage
                      Colony-Stimulating Factor: metabolism / Immunity, Innate /
                      Immunologic Memory / Interleukin-1beta: metabolism / Male /
                      Mice / Mice, Inbred C57BL / Myeloid Progenitor Cells: drug
                      effects / Myeloid Progenitor Cells: immunology /
                      Myelopoiesis: immunology / beta-Glucans: pharmacology /
                      Interleukin-1beta (NLM Chemicals) / beta-Glucans (NLM
                      Chemicals) / Granulocyte-Macrophage Colony-Stimulating
                      Factor (NLM Chemicals)},
      cin          = {PRECISE / AG Schultze / AG Beyer},
      ddc          = {610},
      cid          = {I:(DE-2719)1013031 / I:(DE-2719)1013038 /
                      I:(DE-2719)1013035},
      pnm          = {341 - Molecular Signaling (POF3-341) / 342 - Disease
                      Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-341 / G:(DE-HGF)POF3-342},
      experiment   = {EXP:(DE-2719)PRECISE-20190321},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29328910},
      pmc          = {pmc:PMC5766828},
      doi          = {10.1016/j.cell.2017.11.034},
      url          = {https://pub.dzne.de/record/139724},
}