Nature Communications (Dec 2018)
A miR-150/TET3 pathway regulates the generation of mouse and human non-classical monocyte subset
- Dorothée Selimoglu-Buet,
- Julie Rivière,
- Hussein Ghamlouch,
- Laura Bencheikh,
- Catherine Lacout,
- Margot Morabito,
- M’boyba Diop,
- Guillaume Meurice,
- Marie Breckler,
- Aurélie Chauveau,
- Camille Debord,
- Franck Debeurme,
- Raphael Itzykson,
- Nicolas Chapuis,
- Christophe Willekens,
- Orianne Wagner-Ballon,
- Olivier A. Bernard,
- Nathalie Droin,
- Eric Solary
Affiliations
- Dorothée Selimoglu-Buet
- INSERM U1170, Gustave Roussy Cancer Center
- Julie Rivière
- INSERM U1170, Gustave Roussy Cancer Center
- Hussein Ghamlouch
- INSERM U1170, Gustave Roussy Cancer Center
- Laura Bencheikh
- INSERM U1170, Gustave Roussy Cancer Center
- Catherine Lacout
- INSERM U1170, Gustave Roussy Cancer Center
- Margot Morabito
- INSERM U1170, Gustave Roussy Cancer Center
- M’boyba Diop
- INSERM US23, CNRS UMS 3655, Gustave Roussy Cancer Center
- Guillaume Meurice
- INSERM US23, CNRS UMS 3655, Gustave Roussy Cancer Center
- Marie Breckler
- INSERM US23, CNRS UMS 3655, Gustave Roussy Cancer Center
- Aurélie Chauveau
- INSERM U1170, Gustave Roussy Cancer Center
- Camille Debord
- INSERM U1170, Gustave Roussy Cancer Center
- Franck Debeurme
- INSERM U1170, Gustave Roussy Cancer Center
- Raphael Itzykson
- INSERM U1170, Gustave Roussy Cancer Center
- Nicolas Chapuis
- Département d’Immuno-Hématologie, Institut Cochin
- Christophe Willekens
- INSERM U1170, Gustave Roussy Cancer Center
- Orianne Wagner-Ballon
- Département d’Hématologie et d’Immunologie Biologiques, Hôpital Henri-Mondor
- Olivier A. Bernard
- INSERM U1170, Gustave Roussy Cancer Center
- Nathalie Droin
- INSERM U1170, Gustave Roussy Cancer Center
- Eric Solary
- INSERM U1170, Gustave Roussy Cancer Center
- DOI
- https://doi.org/10.1038/s41467-018-07801-x
- Journal volume & issue
-
Vol. 9,
no. 1
pp. 1 – 17
Abstract
A decrease in the fraction of non-classical monocytes is a hallmark of chronic myelomonocytic leukaemia. Taking advantage of this abnormal situation, the authors identify a mechanistic link between miR-150 and TET3 as being involved in monocyte subset generation.
