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 and Eric Solary ()
Additional contact information
Dorothée Selimoglu-Buet: Gustave Roussy Cancer Center
Julie Rivière: Gustave Roussy Cancer Center
Hussein Ghamlouch: Gustave Roussy Cancer Center
Laura Bencheikh: Gustave Roussy Cancer Center
Catherine Lacout: Gustave Roussy Cancer Center
Margot Morabito: Gustave Roussy Cancer Center
M’boyba Diop: Gustave Roussy Cancer Center
Guillaume Meurice: Gustave Roussy Cancer Center
Marie Breckler: Gustave Roussy Cancer Center
Aurélie Chauveau: Gustave Roussy Cancer Center
Camille Debord: Gustave Roussy Cancer Center
Franck Debeurme: Gustave Roussy Cancer Center
Raphael Itzykson: Gustave Roussy Cancer Center
Nicolas Chapuis: Institut Cochin
Christophe Willekens: Gustave Roussy Cancer Center
Orianne Wagner-Ballon: Hôpital Henri-Mondor
Olivier A. Bernard: Gustave Roussy Cancer Center
Nathalie Droin: Gustave Roussy Cancer Center
Eric Solary: Gustave Roussy Cancer Center

Nature Communications, 2018, vol. 9, issue 1, 1-17

Abstract: Abstract Non-classical monocyte subsets may derive from classical monocyte differentiation and the proportion of each subset is tightly controlled. Deregulation of this repartition is observed in diverse human diseases, including chronic myelomonocytic leukemia (CMML) in which non-classical monocyte numbers are significantly decreased relative to healthy controls. Here, we identify a down-regulation of hsa-miR-150 through methylation of a lineage-specific promoter in CMML monocytes. Mir150 knock-out mice demonstrate a cell-autonomous defect in non-classical monocytes. Our pulldown experiments point to Ten-Eleven-Translocation-3 (TET3) mRNA as a hsa-miR-150 target in classical human monocytes. We show that Tet3 knockout mice generate an increased number of non-classical monocytes. Our results identify the miR-150/TET3 axis as being involved in the generation of non-classical monocytes.

Date: 2018
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DOI: 10.1038/s41467-018-07801-x

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