Communications Biology (Feb 2022)

Macrophage migration inhibitory factor is overproduced through EGR1 in TET2 low resting monocytes

  • Elodie Pronier,
  • Aygun Imanci,
  • Dorothée Selimoglu-Buet,
  • Bouchra Badaoui,
  • Raphael Itzykson,
  • Thierry Roger,
  • Chloé Jego,
  • Audrey Naimo,
  • Maëla Francillette,
  • Marie Breckler,
  • Orianne Wagner-Ballon,
  • Maria E. Figueroa,
  • Marine Aglave,
  • Daniel Gautheret,
  • Françoise Porteu,
  • Olivier A. Bernard,
  • William Vainchenker,
  • François Delhommeau,
  • Eric Solary,
  • Nathalie M. Droin

DOI
https://doi.org/10.1038/s42003-022-03057-w
Journal volume & issue
Vol. 5, no. 1
pp. 1 – 15

Abstract

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To improve our understanding of the pathological role of TET2 mutations, Pronier, Imanci et al. use mice and human cells to show that TET2 downregulation promotes the production of macrophage migration inhibitory factor (MIF). In addition they show that whilst TET2 is recruited to the MIF promoter in healthy monocytes, decreased TET2 expression results in chronic overproduction of MIF - suggesting that MIF signaling could therefore constitute a potential therapeutic target for conditions associated with TET2 mutations.