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Vitamin D receptor-mediated suppression of RelB in antigen presenting cells: a paradigm for ligand-augmented negative transcriptional regulation Griffin MD; Dong X; Kumar RArch Biochem Biophys 2007[Apr]; 460 (2): 218-26The immunological effects of vitamin D receptor (VDR) ligands include inhibition of dendritic cell (DC) maturation, suppression of T-helper type 1 (Th1) T-cell responses and facilitation of antigen-specific immune tolerance in vivo. While studying the molecular profile of DCs cultured in the presence of 1alpha,25(OH)D3 or synthetic D3 analogs we observed that expression of the NF-kappaB family member RelB, which plays an essential role in DC differentiation and maturation, is selectively suppressed by VDR ligands. Further in vitro and in vivo studies of VDR-mediated RelB suppression indicated that the mechanism for this effect involves direct binding of VDR/RXR alpha to a defined region of the relB promoter and assembly of a negative regulatory complex containing HDAC3, HDAC1, SMRT and, most likely, other factors. Interestingly, promoter engagement by VDR and HDAC3, but not the other identified components, is enhanced by addition of a VDR ligand and inhibited by a pro-maturational stimulus (LPS) that results in RelB upregulation. Promoter assays in a panel of cell lines suggest that the VDR ligand-dependent component of relB suppression may occur selectively in antigen presenting cells. Cell type-specific, ligand-enhanced negative transcriptional regulation represents a potentially novel paradigm for VDR-controlled genes. In this report we review the experimental data to support such a mechanism for relB regulation in DCs and present a model for the process.|*Models, Molecular[MESH]|Animals[MESH]|Calcitriol/*pharmacology[MESH]|Cell Differentiation/drug effects/physiology[MESH]|Cell Line[MESH]|Dendritic Cells/cytology/*metabolism[MESH]|Histone Deacetylase 1[MESH]|Histone Deacetylases/metabolism[MESH]|Humans[MESH]|Ligands[MESH]|Protein Binding/drug effects[MESH]|Receptors, Calcitriol/*metabolism[MESH]|Response Elements/physiology[MESH]|Retinoid X Receptor alpha/metabolism[MESH]|Transcription Factor RelB/*metabolism[MESH]|Transcription, Genetic/drug effects/*physiology[MESH]|Up-Regulation/drug effects/physiology[MESH]|Vitamins/metabolism/pharmacology[MESH] |
