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Vitamin C enhances NF-κB-driven epigenomic reprogramming andboosts the immunogenic properties of dendritic cells.


Morante-Palacios O. et al.

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.

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Antibody
IPure kit

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Published
October, 2022

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Products used in this publication

  • default alt
    C03010015
    IPure kit v2
  • ChIP-seq Grade
    C15310256
    NFKB p65 polyclonal antibody
  • Mouse IgG
    C15200179
    TET2 monoclonal antibody
  • Mouse IgG
    C15410206
    Rabbit IgG

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