Table 1.
Factors modulating the epigenetic regulation of genes involved in Th17 differentiation, recruitment or plasticity in the context of cancer.
| Genes | Epigenetic Regulation | Factors Modulating the Epigenome | References | |
|---|---|---|---|---|
| Th17 differentiation | IL-17, RORγt | Histone modification complex like HAT or HMT responsible for the deposition of permissive marks | Cytokines of the TME | [9,10,12,13,14,15,16,17,60,61,62,74,75,76,77,80,81,82] |
| DNA demethylation enzymes (5hmc) | Metabolism regulates the biodisponibility of co-factors of epigenetic enzymes | |||
| miRNA | Metabolites produced by gut microbiota modulate epigenetic enzymes activity | |||
| Th17 recruitment through the CCR6-CCL20 axis | CCL20 | long non coding RNA (lncRNA-u50535) | Upregulation of lncRNA-u50535 in colorectal cancer | [64] |
| Th17 plasticity | [74,75,76,77,79,88] | |||
| - Th17 /Treg plasticity | Foxp3 | DNA methylation | Glutamate Metabolism pathway (reduction of 2 hydroxyglutarate level in Th17 cells diminish the Foxp3 promoter methylation status) | |
| - Th17/Th1 cells plasticity | IFN-γ, Tbet | Histone modification complex | Exposition of differentiated Th17 cells to another cytokinic environment |