[1]郑仁东,刘超.白细胞介素-6与甲状腺疾病[J].国际内分泌代谢杂志,2016,36(05):352-354.[doi:10.3760/cma.j.issn.1673-4157.2016.05.18]
 Zheng Rendong,Liu Chao.Interleukin-6 and thyroid disease[J].International Journal of Endocrinology and Metabolism,2016,36(05):352-354.[doi:10.3760/cma.j.issn.1673-4157.2016.05.18]
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白细胞介素-6与甲状腺疾病()
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《国际内分泌代谢杂志》[ISSN:1673-4157/CN:12-1383/R]

卷:
36
期数:
2016年05期
页码:
352-354
栏目:
综述
出版日期:
2016-09-20

文章信息/Info

Title:
Interleukin-6 and thyroid disease
作者:
郑仁东刘超
210028 南京,中国中医科学院江苏分院,南京中医药大学附属中西医结合医院内分泌代谢病院区
Author(s):
Zheng Rendong Liu Chao
Endocrine and Diabetes Center, Jiangsu Province Hospital on Integration of Chinese and Western Medicine, Nanjing University of Traditional Chinese Medicine, Jiangsu Branch of China Academy of Chinese Medicine Science, Nanjing 210028, China
关键词:
白细胞介素-6 Graves病 桥本甲状腺炎 甲状腺癌
Keywords:
Interleukin-6 Graves' disease Hashimoto's thyroiditis Thyroid carcinoma
DOI:
10.3760/cma.j.issn.1673-4157.2016.05.18
摘要:
白细胞介素-6(IL-6)是一种多功能的细胞因子,参与细胞多种生物功能。IL-6的跨膜信号转导主要 分为两种,即经典通路和反式信号通路,通过IL-6/酪氨酸激酶-1(JAK-1)/信号转导和转录激活因子-3(STAT-3) 途径发挥其生物学作用。研究发现,IL-6能够抑制甲状腺细胞的分泌功能及摄碘功能。其次,在临床中发现,IL -6水平升高不仅与Graves病、桥本甲状腺炎显著相关,而且IL-6基因多态性与Graves病及桥本甲状腺炎的发病 关系密切。另外,研究发现,IL-6在甲状腺癌的发病机制中亦扮演重要的角色。
Abstract:
Interleukin(IL)-6 is a multifunctional cytokine involved in multiple biological functions of cells. Transmembrane signaling of IL-6 is divided into two types, the classical pathway and the trans-signaling pathway, and it plays biological effect via IL-6/Janus kinase-1 (JAK1)/signal transducers and activators of transcription-3(STAT3)signal pathway. The study found that IL-6 could inhibit the secretion of thyroid cells and iodine uptake function. Secondly, clinical study found that the level of IL-6 was increased significantly in Graves' disease and Hashimoto's thyroiditis, and IL-6 gene polymorphism was closely related with Graves' disease and Hashimoto's thyroiditis. In addition, IL-6 also plays an important role in the pathogenesis of thyroid carcinoma.

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备注/Memo

备注/Memo:
通信作者:刘超,Email:liuchao@nfmcn.com
更新日期/Last Update: 2016-11-20