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Haacke, N.* ; Wang, H.* ; Yan, S.* ; Barovic, M.* ; Li, X.* ; Nagai, K.* ; Botezatu, A.* ; Hatzioannou, A.* ; Gercken, B.* ; Trimaglio, G.* ; Shah, A.U.* ; Wang, J.* ; Ye, L.* ; Jaykar, M.T.* ; Rauner, M.* ; Wielockx, B.* ; Chung, K.J.* ; Netea, M.G.* ; Kalafati, L.* ; Hajishengallis, G.* ; Chavakis, T.

Innate immune training of osteoclastogenesis promotes inflammatory bone loss in mice.

Dev. Cell 60, 1854-1870 (2025)
Verlagsversion Forschungsdaten DOI PMC
Open Access Hybrid
Creative Commons Lizenzvertrag
We previously demonstrated that long-term trained immunity (TRIM) involves adaptations that imprint innate immune memory in long-lived myelopoiesis precursors and their progeny, monocytes/macrophages and neutrophils, which thereby acquire enhanced responsiveness to future challenges. Here, we show that a distinct component of myeloid biology, osteoclastogenesis, can also undergo innate immune training. Indeed, β-glucan-induced TRIM was associated with an increased osteoclastogenesis bias in the bone marrow and an expansion of monocytes/osteoclast progenitors in the periphery, resulting in aggravated severity of experimental periodontitis and arthritis. In the setting of trained inflammatory osteoclastogenesis, we observed transcriptomic rewiring in synovial myeloid cells of arthritic mice, featuring prominent upregulation of the transcription factor melanogenesis-associated transcription factor (MITF). Adoptive transfer of splenic monocytes from β-glucan-trained mice to naive recipients exacerbated arthritis in the latter in a strictly MITF-dependent manner. Our findings establish trained osteoclastogenesis as a maladaptive component of TRIM and potentially provide therapeutic targets in inflammatory bone loss disorders.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Inflammatory Bone Loss ; Innate Immune Memory ; Monocytes ; Osteoclastogenesis ; Trained Immunity; Autoimmune Arthritis; Hematopoietic Stem; Progenitor Cells; Dendritic Cells; Induction; Differentiation; Macrophages; Activation; Glucan; Identification
Sprache englisch
Veröffentlichungsjahr 2025
HGF-Berichtsjahr 2025
ISSN (print) / ISBN 1534-5807
e-ISSN 1878-1551
Zeitschrift Developmental Cell
Quellenangaben Band: 60, Heft: 13, Seiten: 1854-1870 Artikelnummer: , Supplement: ,
Verlag Elsevier
Verlagsort 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Pancreatic Islet Research (IPI)
POF Topic(s) 90000 - German Center for Diabetes Research
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-502600-008
Förderungen Saxon State Ministry of Science, Culture and Tourism (SMWK)
European Research Council (LOSYSINCHRON)
NIH
Deutsche Forschungsgemeinschaft
Stiftung fur Pathobiochemie und Molekulare Diagnostik
DOI 10.1016/j.devcel.2025.02.001
WOS ID 001532712700006
Scopus ID 105000648610
PubMed ID 40020679
Erfassungsdatum 2025-04-30
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