Vitamin C enhances NF-κB-driven epigenomic reprogramming and boosts the immunogenic properties of dendritic cells

Nucleic Acids Res. 2022 Oct 28;50(19):10981-10994. doi: 10.1093/nar/gkac941.

Abstract

Dendritic cells (DCs), the most potent antigen-presenting cells, are necessary for effective activation of naïve T cells. DCs' immunological properties are modulated in response to various stimuli. Active DNA demethylation is crucial for DC differentiation and function. Vitamin C, a known cofactor of ten-eleven translocation (TET) enzymes, drives active demethylation. Vitamin C has recently emerged as a promising adjuvant for several types of cancer; however, its effects on human immune cells are poorly understood. In this study, we investigate the epigenomic and transcriptomic reprogramming orchestrated by vitamin C in monocyte-derived DC differentiation and maturation. Vitamin C triggers extensive demethylation at NF-κB/p65 binding sites, together with concordant upregulation of antigen-presentation and immune response-related genes during DC maturation. p65 interacts with TET2 and mediates the aforementioned vitamin C-mediated changes, as demonstrated by pharmacological inhibition. Moreover, vitamin C increases TNFβ production in DCs through NF-κB, in concordance with the upregulation of its coding gene and the demethylation of adjacent CpGs. Finally, vitamin C enhances DC's ability to stimulate the proliferation of autologous antigen-specific T cells. We propose that vitamin C could potentially improve monocyte-derived DC-based cell therapies.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Ascorbic Acid* / pharmacology
  • Cell Differentiation / genetics
  • Cellular Reprogramming
  • Dendritic Cells*
  • Epigenesis, Genetic*
  • Humans
  • NF-kappa B* / metabolism
  • T-Lymphocytes / metabolism

Substances

  • Ascorbic Acid
  • NF-kappa B
  • RELA protein, human
  • TET2 protein, human