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Nat Immunol. 2013 Mar;14(3):211-20. doi: 10.1038/ni.2526. Epub 2013 Jan 27.

Epigenetic silencing of retinoblastoma gene regulates pathologic differentiation of myeloid cells in cancer.

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  • 1Departments of Immunology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida, USA.

Abstract

Two major populations of myeloid-derived suppressor cells (MDSCs), monocytic MDSCs (M-MDSCs) and polymorphonuclear MDSCs (PMN-MDSCs) regulate immune responses in cancer and other pathologic conditions. Under physiologic conditions, Ly6C(hi)Ly6G(-) inflammatory monocytes, which are the normal counterpart of M-MDSCs, differentiate into macrophages and dendritic cells. PMN-MDSCs are the predominant group of MDSCs that accumulates in cancer. Here we show that a large proportion of M-MDSCs in tumor-bearing mice acquired phenotypic, morphological and functional features of PMN-MDSCs. Acquisition of this phenotype, but not the functional attributes of PMN-MDSCs, was mediated by transcriptional silencing of the retinoblastoma gene through epigenetic modifications mediated by histone deacetylase 2 (HDAC-2). These data demonstrate a new regulatory mechanism of myeloid cells in cancer.

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PMID:
23354483
[PubMed - indexed for MEDLINE]
PMCID:
PMC3578019
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