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Cellular Differentiation of Human Monocytes Is Regulated by Time-Dependent Interleukin-4 Signaling and the Transcriptional Regulator NCOR2.

Immunity | Dec 19, 2017

Human in vitro generated monocyte-derived dendritic cells (moDCs) and macrophages are used clinically, e.g., to induce immunity against cancer. However, their physiological counterparts, ontogeny, transcriptional regulation, and heterogeneity remains largely unknown, hampering their clinical use. High-dimensional techniques were used to elucidate transcriptional, phenotypic, and functional differences between human in vivo and in vitro generated mononuclear phagocytes to facilitate their full potential in the clinic. We demonstrate that monocytes differentiated by macrophage colony-stimulating factor (M-CSF) or granulocyte macrophage colony-stimulating factor (GM-CSF) resembled in vivo inflammatory macrophages, while moDCs resembled in vivo inflammatory DCs. Moreover, differentiated monocytes presented with profound transcriptomic, phenotypic, and functional differences. Monocytes integrated GM-CSF and IL-4 stimulation combinatorically and temporally, resulting in a mode- and time-dependent differentiation relying on NCOR2. Finally, moDCs are phenotypically heterogeneous and therefore necessitate the use of high-dimensional phenotyping to open new possibilities for better clinical tailoring of these cellular therapies.

Pubmed ID: 29262348 RIS Download

Mesh terms: Cell Differentiation | Cell Lineage | Dendritic Cells | Gene Expression Profiling | Gene Expression Regulation | Granulocyte-Macrophage Colony-Stimulating Factor | Humans | Immunophenotyping | Interleukin-4 | Macrophage Activation | Macrophage Colony-Stimulating Factor | Macrophages | Monocytes | Nuclear Receptor Co-Repressor 2 | Primary Cell Culture | Signal Transduction | Time Factors | Transcription, Genetic

Research resources used in this publication

Data used in this publication

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Associated grants

  • Agency: Medical Research Council, Id: 204464/Z/16/Z
  • Agency: Wellcome Trust, Id:

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.

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