Immunological tolerance is critical for maintaining gut homeostasis. An imbalance between interleukin-17 (IL-17)-producing T helper 17 (T_H17) cells and regulatory T cells (T_reg cells) is involved in ulcerative colitis (UC) pathogenesis. Dendritic cells (DCs) are able to induce T cell differentiation. Paeoniflorin (PF) is a monoterpene glucoside that is commonly used for treatment of autoimmune disease. However, the immunological mechanism of PF involvement in UC treatment is unclear. The present study aimed to explore whether PF can restore the T_H17/T_reg balance by modulating DCs. The effects of PF on DCs, T_H17 cells and T_reg cells were measured. Furthermore, PF-treated DCs were injected into mice with 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis. PF inhibited MHC-II and CD86 expression on the DC surface (P < 0.05), decreased interleukin (IL)-12 secretion in vitro and in vivo (P < 0.05), and restored the T_H17/T_reg ratio in the mouse model of colitis (P < 0.05). PF-treated DCs diminished T_H17 differentiation (4.26% in vitro and 1.64% in vivo) and decreased IL-17 expression (P < 0.05) while inducing CD4⁺CD25⁺Foxp3⁺ T_reg differentiation (7.82% in vitro and 6.85% in vivo) and increasing Foxp3 and IL-10 production (P < 0.05). Additionally, both PF and PF-treated DCs improved colonic histopathology in the mouse model of colitis (P < 0.05). In conclusion this study suggested that PF can ameliorate TNBS-induced colitis by modulating the DC-mediated T_H17/T_reg balance.

免疫耐受对维持肠道稳态至关重要。产生白介素17（IL-17）的T辅助17（T _H 17）细胞和调节性T细胞（T _reg细胞）之间的失衡涉及溃疡性结肠炎（UC）发病机理。树突状细胞（DC）能够诱导T细胞分化。eon药苷（PF）是一种单萜糖苷，通常用于治疗自身免疫性疾病。然而，PF参与UC治疗的免疫机制尚不清楚。本研究旨在探讨PF是否可以通过调节DC恢复T _H 17 / T _reg平衡。PF DC上，T的影响_ħ 17个细胞和T _REG测量细胞。此外，用PF处理的DC注射有2,4,6-三硝基苯磺酸（TNBS）诱导的结肠炎的小鼠。PF抑制DC表面MHC-II和CD86表达（P  <0.05），体内外白介素（IL）-12分泌减少（P  <0.05），并恢复小鼠的T _H 17 / T _reg比率结肠炎模型（P  <0.05）。PF处理的DC 诱导CD4 ⁺ CD25 ⁺ Foxp3 ⁺ T _reg减少了T _H 17的分化（体外为4.26％，体内为1.64％）并降低了IL-17表达（P <0.05）。分化（体外7.82％和体内6.85％）并增加Foxp3和IL-10的产生（P  <0.05）。此外，在结肠炎的小鼠模型中，PF和PF处理的DC均可改善结肠组织病理学（P  <0.05）。总之，这项研究表明，PF可以通过调节DC介导的T _H 17 / T _reg平衡来缓解TNBS引起的结肠炎。