DNA Damage Signaling Instructs Polyploid Macrophage Fate in Granulomas

نویسندگان

  • Laura Herrtwich
  • Indrajit Nanda
  • Konstantinos Evangelou
  • Teodora Nikolova
  • Veronika Horn
  • Sagar
  • Daniel Erny
  • Jonathan Stefanowski
  • Leif Rogell
  • Claudius Klein
  • Kourosh Gharun
  • Marie Follo
  • Maximilian Seidl
  • Bernhard Kremer
  • Nikolas Münke
  • Julia Senges
  • Manfred Fliegauf
  • Tom Aschman
  • Dietmar Pfeifer
  • Sandrine Sarrazin
  • Michael H. Sieweke
  • Dirk Wagner
  • Christine Dierks
  • Thomas Haaf
  • Thomas Ness
  • Mario M. Zaiss
  • Reinhard E. Voll
  • Sachin D. Deshmukh
  • Marco Prinz
  • Torsten Goldmann
  • Christoph Hölscher
  • Anja E. Hauser
  • Andres J. Lopez-Contreras
  • Dominic Grün
  • Vassilis Gorgoulis
  • Andreas Diefenbach
  • Philipp Henneke
  • Antigoni Triantafyllopoulou
چکیده

Granulomas are immune cell aggregates formed in response to persistent inflammatory stimuli. Granuloma macrophage subsets are diverse and carry varying copy numbers of their genomic information. The molecular programs that control the differentiation of such macrophage populations in response to a chronic stimulus, though critical for disease outcome, have not been defined. Here, we delineate a macrophage differentiation pathway by which a persistent Toll-like receptor (TLR) 2 signal instructs polyploid macrophage fate by inducing replication stress and activating the DNA damage response. Polyploid granuloma-resident macrophages formed via modified cell divisions and mitotic defects and not, as previously thought, by cell-to-cell fusion. TLR2 signaling promoted macrophage polyploidy and suppressed genomic instability by regulating Myc and ATR. We propose that, in the presence of persistent inflammatory stimuli, pathways previously linked to oncogene-initiated carcinogenesis instruct a long-lived granuloma-resident macrophage differentiation program that regulates granulomatous tissue remodeling.

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عنوان ژورنال:
  • Cell

دوره 167  شماره 

صفحات  -

تاریخ انتشار 2016