Vitamin D Receptor (VDR) ChIP-seq reported in "Vitamin D receptor and STAT3 cooperate to TET2-mediated acquisition of tolerogenesis"

The active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), induces stable tolerogenesis in dendritic cells (DC). This process involves the Vitamin D receptor (VDR) which translocates to the nucleus, binds its cognate genomic sites and promotes epigenetic and transcriptional remodeling. In this study, we investigated the interplay between the vitamin D receptor (VDR) and transcription factors to induce DNA methylation changes, which might provide phenotypic stability to the tolerogenic phenotype of DCs. Overall design: Vitamin D Receptor (VDR) ChIP-seq on human monocytes (MO) and monocyte-derived dendritic cells in the abscence (DC) or presence (tolDC) of the acitve form of vitamin D (calcitriol)