基础医学与临床 ›› 2018, Vol. 38 ›› Issue (2): 218-223.

• 研究论文 • 上一篇    下一篇

Treg在亚急性甲状腺炎发病免疫机制中的作用

王小玲1,吕合作1,甘怀勇1,项平2,张小凤1,徐二琴3,裴晓艳4,金国玺1   

  1. 1. 蚌埠医学院第一附属医院
    2. 蚌埠医学院第一附属医院中心实验室
    3. 蚌埠医学院
    4. 蚌埠医学院第一附属医院内分泌科
  • 收稿日期:2017-02-06 修回日期:2017-04-24 出版日期:2018-02-05 发布日期:2018-01-24
  • 通讯作者: 金国玺 E-mail:jyzjyz1999@163.com
  • 基金资助:
    蚌埠医学院研究生科研创新计划项目;蚌埠市科技局科技指导项目

Role of Treg in the immune pathogenesis of subacute thyroiditis

  • Received:2017-02-06 Revised:2017-04-24 Online:2018-02-05 Published:2018-01-24

摘要: 目的 探讨调节性T细胞(Treg)在亚急性甲状腺炎(SAT)发病的免疫机制中的作用。方法 用流式细胞计量术检测46例SAT患者及15名对照者外周血中Treg占CD4+T细胞的比例;ELISA检测血清中白细胞介素10(IL-10)、转化生长因子β1(TGF-β1)及前列腺素E2(PGE2)的浓度;免疫组织化学方法检测29例SAT患者及20名对照者甲状腺组织中叉头蛋白3(Foxp3)阳性细胞。结果 SAT患者外周血Treg比例明显低于对照者(P<0.05);SAT患者血清中TGF-β1明显高于对照者(P<0.05);SAT患者甲状腺组织中Foxp3阳性率明显高于对照者甲状腺组织(P<0.05)。结论 Treg的减少可能在SAT发病的免疫机制中起着重要的作用。

关键词: 亚急性甲状腺炎, 调节性T细胞, 白细胞介素-10, 转化生长因子-β1, 前列腺素E2

Abstract: Objective To explore the role of regulatory T-lymphocytes(Treg) in the immune pathogenesis of subacute thyroiditis(SAT). Methods The proportion of Treg in CD4+T cells in peripheral blood of 46 SAT patients and 15 controls was detected using flow cytometry. And the concentration of interleukin-10(IL-10), transforming growth factor-beta1(TGF-β1) and prostaglandin E2(PGE2) in serum of 46 SAT patients and 15 controls was measured with ELISA. In addition, the Forkhead box protein 3(Foxp3) positive cells in thyroid tissue of 29 SAT patients and 20 controls was detected by immunohistochemistry. Results The proportion of Treg in peripheral blood of SAT patients was significantly lower than that of controls (P<0.05). And the concentration of TGF-β1 in serum of SAT patients was apparently higher than that of controls(P<0.05). Additionally, the positive rate of Foxp3 in thyroid tissue of SAT patients was markedly higher than that of controls(P<0.05). Conclusions The decrease of Treg may play an important role in the immune pathogenesis of SAT.

Key words: subacute thyroiditis, regulatory T-lymphocytes(Treg), interleukin-10(IL-10), transforming growth factor-beta1(TGF-β1), prostaglandin E2(

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