Paeoniflorin inhibits the maturation and immunostimulatory function of allergen-induced murine dendritic cells

• Paeoniflorin inhibited immaturation of dendritic cells (DCs) in response to allergen.
• Paeoniflorin-treated DCs had impaired ability to produce proinflammatory cytokines.
• Paeoniflorin-treated DCs increased production of anti-inflammatory cytokines.
• Paeoniflorin-treated DCs had diminished capacity to induce Th1 proliferation.
• Paeoniflorin-treated DCs induced the proliferation of T regulatory cells.

Dendritic cells (DCs) as the front lines of defense play a crucial role in allergic contact dermatitis (ACD). Paeoniflorin (PF) has been clinically proven to be effective in the treatment of inflammatory skin diseases such as ACD. However, the mechanisms underlying the anti-inflammatory effect of PF remain unclear. The aim of this study was to explore the effect of PF on the maturation and immunostimulatory function of DCs in the murine model of ACD in vitro. Murine bone marrow-derived DCs were stimulated with the contact sensitizer 1-chloro-2, 4-dinitrobenze (DNCB) in vitro. Surface antigen expression of DCs (MHC II, CD40, CD80, and CD86), as an indicator of maturation DCs and cytokines (IL-12, IFN-γ, IL-10, and TGF-β) after DNCB stimulation in the absence or presence of PF at different doses, was detected. Then, we detected that PF-treated DCs stimulated T cells in response to DNCB. PF inhibited the up-regulation of MHC II, CD80, CD86, and CD40, decreased IL-12p70 secretion, while increased the production of IL-10 and TGF-β, and had no effect on IFN-γ cytokine production by murine bone marrow-derived DCs in response to DNCB. DCs exposed to PF had diminished capacity to stimulate allogeneic T cell proliferation and to activate IFN-γ-producing CD4+ T cells and induced CD4+CD25+Foxp3+ T cells and IL-10-producing T cell expansion from naïve CD4+ T cells. These results indicate that PF may be effective in preventing and treating ACD in vitro and other inflammatory responses possibly through inhibiting maturation of DCs and limiting their capacity to stimulate T cell responses.