CSF1R regulates monocyte subset differentiation and intracellular metabolism.

Authors

Alexandre Gallerand, Johanna Merlin, Zakariya Caillot, Chloé Delaby, Elisa Bord, Jichang Han, Bastien Dolfi, Michael D Chang, Guilhem R Thierry, Alexia Castiglione, Sacha Grenet, Eloïse Goës, Maxime Franceschini, Gisèle Jarretou, Fairouz N Zair, Evy Boré, Florian Tuffin, David Dombrowicz, Giulia Chinetti, Rodolphe R Guinamard, Maxim N Artyomov, Abdelilah Wakkach, Didier F Pisani, Gwendalyn J Randolph, Adeline Bertola, Patrick Auberger, Arnaud Jacquel, David A Hume, Jesse W Williams, Marc Bajénoff, Jaap G Neels, Stoyan Ivanov

Published in

Nature communications. Jul 04, 2026. Epub Jul 04, 2026.

Abstract

Monocytes are key circulating effectors of vascular homeostasis, innate immunity and inflammation. Following their generation in mouse bone marrow, classical (Ly6C^high) monocytes are mobilized into the blood circulation where they mature into non-classical (Ly6C^low) patrolling monocytes or are recruited into peripheral tissues where they differentiate into tissue resident or inflammatory macrophages. Monocytes and macrophages express CSF1R (CD115), the receptor for lineage-specific growth factors CSF1 and IL-34. Here, we report that acute CSF1R blockade or genetic deletion negatively interferes with monocyte intracellular metabolism and reduces blood Ly6C^low monocytes in part by blunting differentiation of Ly6C^high monocytes. Based upon lineage-specific deletion of Glutamine-Fructose-6-Phosphate Transaminase 1 (GFPT1), the hexosamine biosynthetic pathway (HBP) is identified as an important regulator of CSF1R expression and monocyte subsets. Inhibition of receptor tyrosine kinases CSF1R and FLT3 rewires and partially impairs metabolic activity in human monocytes. Our findings provide insights into the link between CSF1R signaling, metabolic regulation, and monocyte survival and differentiation.

PMID:
42401537
Bibliographic data and abstract were imported from PubMed on 05 Jul 2026.

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