期刊
IMMUNITY
卷 47, 期 3, 页码 582-+出版社
CELL PRESS
DOI: 10.1016/j.immuni.2017.08.016
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资金
- INSERM
- Agence Nationale de la Recherche [ANR-10-LABX-0043, ANR-CHIN-0002, ANR-10-IDEX-0001-02 PSL]
- Institut Curie [CIC IGR-Curie 1428]
- European Research Council [340046 DCBIOX]
- La Ligue Nationale contre le Cancer [EL2014.LNCC/SA]
- Fondation Bristol-Myers Squibb pour la Recherche en Immuno-Oncologie
- National Human Genome Research Institute Centers of Excellence in Genomics Science [P50 HG006193]
- National Human Genome Research Institute [NIH T32 HG002295]
- Banting Postdoctoral Fellowship
- Universite Paris Descartes
- Equipex [ANR-10-EQPX-03]
- France Genomique Consortium [ANR-10-INBS-09-08]
- Canceropole Ile-de-France
- SESAME program from Region Ile-de-France
- SiRIC-Curie program (SiRIC) [INCa-DGOS-4654]
After entering tissues, monocytes differentiate into cells that share functional features with either macrophages or dendritic cells (DCs). How monocyte fate is directed toward monocyte-derived macrophages (mo-Macs) or monocyte-derived DCs (mo-DCs) and which transcription factors control these differentiation pathways remains unknown. Using an in vitro culture model yielding human mo-DCs and moMacs closely resembling those found in vivo in ascites, we show that IRF4 and MAFB were critical regulators of monocyte differentiation into mo-DCs and mo-Macs, respectively. Activation of the aryl hydrocarbon receptor (AHR) promoted mo-DC differentiation through the induction of BLIMP-1, while impairing differentiation into mo-Macs. AhR deficiency also impaired the in vivo differentiation of mousemo-DCs. Finally, AHR activation correlated with mo-DC infiltration in leprosy lesions. These results establish that mo-DCs and mo-Macs are controlled by distinct transcription factors and show that AHR acts as a molecular switch for monocyte fate specification in response to micro-environmental factors.
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