外源性TGF-β1对实验性自身免疫性脑脊髓炎模型小鼠中IL-23/Th17炎症轴的影响

The effects on the inflammatory axis of IL-23/Th17 cells in the mice model of experimental autoimmune encephalomyelitis mediated by exogenous transforming growth factor β1

目的:观察外源性TGF-β1对实验性自身免疫性脑脊髓炎模型小鼠IL-23/Th17炎症轴的影响,探讨其可能的作用机制。方法:以MOG35-55免疫C57BL/6小鼠制作EAE模型,多时间点皮下注射TGF-β1作为干预,RT-PCR和ELISA检测IL-23、IL-17和IL-6的表达。结果:与EAE组相比,干预组在发病初IL-23、IL-17、IL-6表达均升高(P<0.05,P<0.05,P<0.05);在高峰期IL-23表达下降(P<0.05),IL-17、IL-6表达升高(P<0.05,P<0.05);在慢性期IL-23、IL-17表达下降(P<0.05,P<0.05),而IL-6表达升高(P<0.05)。结论:外源性的TGF-β1可能通过上调IL-23、IL-17的表达使EAE高峰期的症状加重并提前,而在慢性期相对地下调其表达,EAE症状趋于缓解。

Objective：To investigate the variation of IL-23/Th17 axis in the model mice of experimental autoimmune encephalomyelitis administered with exogenous transforming growth factor β1 for its possible pathogenesis.Methods：The C57BL/6 mice were immunized with MOG35-55 to establish the animal model of EAE,which was treated with TGF-β1 after immunization at multiple time points,and the expression of IL-23,IL-17 and IL-6 was analyzed by RT-PCR and ELISA.Results：Compared to those of the EAE group,the expressions of IL-23,IL-17 and IL-6 were all increased significantly at the onset（P〈0.05,P〈0.05,P〈0.05）;And at the peak,the expression of IL-23 was down-regulated（P〈0.05） while the expressions of both IL-17 and IL-6 were still high（P〈0.05,P〈0.05）;And during the chronic phase,it was found that there was low expression of IL-23 and IL-17（P〈0.05,P〈0.05）,and the high expression of IL-6（P〈0.05）.Conclusion：The exogenous TGF-β1 on EAE may up-regulate the expression of IL-23 and IL-17 to accelerate the progress of EAE and increase the symptom at the peak,while down-regulating their expression to ameliorate the symptom during the chronic phase.