Tc17细胞及相关细胞因子在银屑病样皮炎模型小鼠中的表达

Expression of Tc17 Cells and Related Cytokines in Psoriasiform Dermatitis Model Mice

目的观察Tc17细胞及相关细胞因子在银屑病样皮炎模型小鼠的表达。方法将BALB/c雄性小鼠随机分为模型组及正常对照组各10只,模型组局部皮肤涂抹5%咪喹莫特软膏60 mg·d^(-1),连续7 d。流式细胞术检测分选出小鼠血液细胞毒性Tc17细胞与辅助性Th17细胞比例,逆转录聚合酶链反应检测小鼠Tc17细胞中白细胞介素-17A(IL-17A)、IL-22、视黄酸相关孤儿受体(RORγt)及信号传导与转录激活因子(STAT3)表达水平。结果模型组Tc17与Th17细胞占比分别为(4.63±0.10)%,(8.30±1.67)%,正常对照组分别为(0.30±0.07)%,(1.47±0.40)%,模型组均显著高于正常对照组(P<0.01);模型组Tc17细胞中IL-17A、IL-22、RORγt和STAT3表达量分别为(3.13±0.49),(2.41±0.22),(3.35±0.22),(2.02±0.40);正常对照组分别为(0.95±0.21),(1.11±0.10),(1.09±0.27),(0.89±0.17),模型组均较正常对照组增高(P<0.01)。结论Tc17细胞参与银屑病样皮炎过程,且分化及作用机制与Th17相似;咪喹莫特诱导的银屑病样皮炎小鼠模型能模拟免疫相关的细胞因子变化。

Objective To analyze the proportion of cytotoxic T-17(Tc17)cells in imiquimod-induced psoriasiform dermatitis in mice and the expression of related cytokines.Methods BALB/c male mice were randomly divided into two groups:the psoriasiform dermatitis model group induced by topically applying 5%imiquimod(IQM)ointment and the normal control group.The percentage of Tc17 and helper T-17(Th17)cells were detected and sorted by flow cytometry in the blood of the two groups,and the expression levels of IL-17A,IL-22,RORγt,and STAT3 in Tc17 cells were detected by real-time quantitative PCR(RT-qPCR).Results The percentage of Tc17 and Th17 cells in the model group was(4.63±0.10)%and(8.30±1.67)%,respectively.Moreover,those in the normal control group were(0.30±0.07)%and(1.47±0.40)%,which were significantly higher in the model group than in the normal control group(P<0.01).The expression levels of IL-17A,IL-22,RORγt and STAT3 in Tc17 cells in model group after flow sorting were(3.13±0.49),(2.41±0.22),(3.35±0.22),(2.02±0.40),significantly higher(P<0.01)than those in the normal control group[(0.95±0.21),(1.11±0.10),(1.09±0.27),(0.89±0.17)],respectively.Conclusion Tc17 cells are involved in the pathogenesis of psoriasiform dermatitis,and their differentiation and action mechanism are similar to those of Th17.The mice models induced by IMQ can mimic the changes of immune-related cytokines.