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. 2019 Jul 4;10:1525. doi: 10.3389/fimmu.2019.01525

Figure 3.

Figure 3

Epigenetics orchestrating interactions between immune and stroma cells in psoriasis. Increased expression of miR-210 in CD4+ T cells from psoriasis patients reduces the expression of the immune regulatory molecule FOXP3. Together with increased histone deacetylase (HDAC) levels that contribute to increased pro-inflammatory cytokine expression (particularly IL-17A), this leads to an imbalance between effector T cells (Th17 cell) and regulatory T cells. Effector CD3+CD4−CD8− “double negative” (DN) T cells in psoriasis patients are epigenetically primed for IFN-γ expression through decreased CpG DNA methylation at a distal enhancer element of the IFNG gene. Keratinocytes from psoriasis patients exhibit elevated miR-203 expression which results in reduced expression of SOCS3, a negative regulator of STAT3 signaling. This contributes to increased STAT3 phosphorylation (activation) and subsequently increases pro-inflammatory cytokine expression and effector T cell differentiation. Expression of miR-31 in keratinocytes contributes to the activation of NFκB and subsequent production of IL-1β, CXCL1,-5 and-8. Elevated levels of miR-155 induce AIM2 and NLRP3 inflammasome activation through unknown mechanisms which results in enhanced IL-1β release.