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Mitroulis, I.* ; Ruppova, K.* ; Wang, B.* ; Chen, L.S.* ; Grzybek, M. ; Grinenko, T.* ; Eugster, A.* ; Troullinaki, M.* ; Palladini, A. ; Kourtzelis, I.* ; Chatzigeorgiou, A.* ; Schlitzer, A.* ; Beyer, M.* ; Joosten, L.A.B.* ; Isermann, B.* ; Lesche, M.* ; Petzold, A.* ; Simons, K.* ; Henry, I.* ; Dahl, A.* ; Schultze, J.L.* ; Wielockx, B.* ; Zamboni, N.* ; Mirtschink, P.* ; Coskun, Ü. ; Hajishengallis, G.* ; Netea, M.G.* ; Chavakis, T.*

Modulation of myelopoiesis progenitors is an integral component of trained immunity.

Cell 172, 147-161.e12 (2018)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold (Paid Option)
Creative Commons Lizenzvertrag
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 beta-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-1 beta 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.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Gm-csf ; Cholesterol Biosynthesis ; Glycolysis ; Inflammation ; Innate Immune Memory ; Interleukin-1β ; Myelopoiesis ; Myelosuppression ; Trained Innate Immunity ; β-glucan; Hematopoietic Stem-cells; High-throughput; Self-renewal; Mass-spectrometry; Lineage Commitment; Global Analysis; Hypoxic Niche; Proliferation; Dormancy; Mice
ISSN (print) / ISBN 0092-8674
e-ISSN 1097-4172
Zeitschrift Cell
Quellenangaben Band: 172, Heft: 1-2, Seiten: 147-161.e12 Artikelnummer: , Supplement: ,
Verlag Cell Press
Verlagsort Cambridge, Mass.
Begutachtungsstatus
Institut(e) Institute for Pancreatic Beta Cell Research (IPI)