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Plasmacytoid dendritic cells (pDCs) are first responders to tissue damage and interact with wound CD4 T-cells to orchestrate tissue repair. In diabetes, the role of pDCs and their subsequent influence on wound CD4 T-cells and inflammation during tissue repair is unknown. Using human diabetic wound single cell sequencing, we identified that human wound CD4 T cells are primarily the Th17 phenotype. Thus, we hypothesized that pDCs in the wounds may regulate this inflammatory T cell phenotype, contributing to chronic inflammation. Although pDCs exist in low numbers in the wounds, we isolated wound pDCs from diabetic and control mice and examined them for inflammatory cytokine expression. We found that diabetic pDC produced significantly more IL6 (amongst other inflammatory cytokines) compared to controls. This is important as IL6 has been shown to skew CD4 T-cells towards a Th17 phenotype in tissues. Upon co-culture of diabetic pDCs with naïve CD4 T-cells, a significant increase in Th17 cells was observed by intracellular flow cytometry analysis. In order to examine the increased IL6 from diabetic pDCs we isolated diabetic and control wound pDCs and performed an epigenetic superarray. We identified that histone demethylase Jarid1C was significantly decreased in diabetic pDCs compared to controls. We then isolated diabetic pDCs and performed a ChIP analysis on the IL6 NFkB binding sites in the promoter and identified an increase in tri-methylated lysine 4 on histone 3 (H3K4me3), a marker regulated by Jarid 1C and consistent with increased transcription of IL6. Taken together, this data suggests that in diabetes, pDCs are epigenetically altered to produce increased IL6 and contribute to increased Th17 and inflammation in diabetic wounds.