首页> 中文期刊> 《中国免疫学杂志》 >Graves病患者131 I、甲巯咪唑治疗前后外周血Th17细胞及IL-17水平的变化

Graves病患者131 I、甲巯咪唑治疗前后外周血Th17细胞及IL-17水平的变化

         

摘要

目的:通过比较研究GD患者131 I、甲巯咪唑治疗外周血中Th17细胞、IL-17的变化,探讨Th17细胞在 GD 发病机制中的作用及意义。方法:收集初诊的GD患者31例采用131I治疗,30例采用甲巯咪唑(MMI)治疗,分别在治疗前(T0)及治疗后1个月(T1)、3个月(T3)进行相关指标测定。另选年龄、性别匹配的29例正常人作为正常对照组。应用流式细胞仪技术检测外周血中Th17细胞比例。采用ELISA 法检测各组血清 IL-17水平。结果:2种治疗方案T0组外周血 Th17细胞及IL-17水平明显高于正常对照组( P<0.01)。131 I治疗组外周血Th17细胞及IL-17水平在T0、T1、T3组中水平逐渐下降,仍高于正常对照组(P<0.01),MMI治疗组变化无统计学差异(P>0.05)。采用双变量相关性分析得出Th17细胞比例与IL-17水平呈正相关(r=0.758,P<0.05),且两者与甲状腺相关抗体呈正相关。结论:Th17细胞、IL-17在初发GD中高表达,Th17细胞可能参与了GD的发病过程。另外,放射性131 I可能通过影响Th17细胞及IL-17起到治疗GD的作用。%Objective:To explore the role of Th17 cells in the pathogenesis with Graves′disease (GD),through examining the proportion of peripheral of Th17 cells and the plasma levels of Interleukin-17 ( IL-17 ) before and after 131 I or methimazol ( MMI ) treatment with GD patients.Methods:We studied 31 subjects and 30 subjects with GD after 131 I or MMI treatment as 131 I therapy group and MMI therapy group and examined as before treatment (T0 ),one month (T1)and three months (T3)after the treatment.29 age-and sexmatched healthy subjects were enrolled as the healthy control group.The Th17 lymphocytes cells were investigated by flow cytometry analysis.The levels of serum IL-17 were measured by ELISA.Results:The proportion of peripheral Th17 cells and the levels of IL-17 were significantly increased in the T0 group GD patients compared with the control group( P<0.01).In the 131 I therapy group the levels of Th17 cells,IL-17 in T0,T1,T3 decreased gradually,but still higher than in normal group( P<0.01) .But there was no sig-nificant difference in MMI therapy group (P>0.05).The proportion of peripheral Th17 cells had positive relationship with the level of IL-17( r=0.758,P<0.05 ) .Both of them were associated positively with thyroid autoantibodies.Conclusion: Th17 cells, IL-17 are highly expressed in the GD.Th17 cells may play an important role in the pathogenesis of GD.In addition,radioactive 131 I may also work on GD via Th17 cells and IL-17.

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