目的通过建立实验性自身免疫性肝炎小鼠模型，观察外源性IL-23对实验性自身免疫性肝炎模型小鼠中IL-17的影响，探讨其可能的作用机制。方法以肝抗原S-100免疫C57BL/6小鼠制作自身免疫性肝炎动物模型，提取出脾淋巴细胞，将IL-23加入到抗CD3抗体活化后的脾淋巴细胞中进行培养，免疫组化观察IL-17在肝细胞中的分布及表达水平，RT-PCR和ELISA检测IL-17在脾淋巴细胞中的表达。结果与对照组相比，模型组肝细胞中IL-17表达升高；IL-23作用于模型组活化的脾淋巴细胞后IL-17的表达水平明显高于对照组。结论IL-23/IL-17炎症轴在EAH的病理机制中发挥着重要的作用，IL-23可能通过上调IL-17的表达使AIH模型小鼠症状加重，并为AIH的治疗提供了新的靶点。%Objective To investigate the variation of IL-17 in the model mice of experimental autoimmune hepatitis with exogenous IL-23 for its possible pathogenesis. Methods The C57BL/6 mice were immunized with S-100 to establish the model of experimental autoimmune hepatitis (EAH), the distribution and the expression levels of cytokines (IL)-17 in the murine liver using immunohistochemical method and lymphocyte from murine spleen were activated with anti-CD3 antibody and treated with IL-23 in vitro, the cytokines, IL-17 were detected using reverse transcription-polymerase chain reaction (RT-PCR) and ELISA. Result The results were compared with those of normal controls, the expression of IL-17 were increased;We demonstrated that there were signiifcantly increased IL-17A+cells in livers of AIH mice, compared to normal mice using immunohistochemical method, and the expression of IL-17A was signiifcant increase after treatment with IL-23 vs the non-IL-23-treatment control group and the cultured cells both were activated with anti-CD3 antibody in AIH mice. Conclusion Our ifndings indicate that the IL-23/IL-17 inlfammation axis play an important role in the pathogenesis of AIH, IL-23 on EAH may up-regulate the expression of IL-17 to accelerate the progress EAH, and which might be a target for treatment.
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