T、B淋巴细胞在自身免疫性甲状腺疾病中的作用机制研究进展

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摘要自身免疫性甲状腺疾病（AITD）的发病率呈现上升趋势，复杂的环境因素、遗传因素以及内分泌激素的相互作用可能是该病的病因，AITD的发病机制主要为T淋巴细胞和B淋巴细胞活化，产生针对甲状腺组织的自身抗体，从而使甲状腺产生不同程度的损伤并发生功能变化。T淋巴细胞中与AITD密切相关的是辅助性T淋巴细胞，其存在多种亚型（Th1、Th2、Th17、Treg等），其中Th1/Th2细胞失衡及Th17细胞活化均参与了AITD的发生，而Treg细胞可发挥重要免疫抑制功能；B淋巴细胞活化是Graves病发生的核心病理过程，而Breg细胞可抑制自身免疫反应，并能调控T淋巴细胞的效应，是极具潜力的AITD治疗靶点。本文综述了T、B淋巴细胞在AITD中的作用机制，为寻找有效的治疗途径提供一定思路。

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	李扬左新河华川赵勇

关键词 ：自身免疫性甲状腺疾病, T淋巴细胞, B淋巴细胞, 机制

Abstract：The incidence rate of autoimmune thyroid diseases (AITD) is on the rise. The interaction of complex environmental factors, genetic factors and endocrine hormone may be the causes of the disease. The pathogenesis of AITD is mainly the activation of T lymphocytes and B lymphocytes, which produce autoantibodies targeted at thyroid tissues, so as to cause different degrees of thyroid injury and produce functional changes. In T lymphocytes, helper T lymphocytes are closely related to AITD. It has many subtypes, such as Th1, Th2, Th17, Treg, and so on. Th1/Th2 cell imbalance and Th17 cell activation are involved in the occurrence of AITD, while Treg cells can play an important role in immune suppression function; B lymphocyte activation is the core pathological process of the occurrence of Graves′ disease, while Breg cells can inhibit the autoimmune response and regulate the effect of T lymphocytes, which is a potential therapeutic target of AITD. This paper reviews the mechanism of T and B lymphocytes involved in AITD, which provides some ideas for finding effective therapeutic approaches.

Key words： Autoimmune thyroid disease T lymphocyte B lymphocyte Mechanism

基金资助:湖北省自然科学基金面上青年项目（2018CFB2 78）；
全国名中医传承工作室建设项目（国中医药办人教函〔2018〕119号）。

作者简介: 李扬（1982.7-），女，博士，主要从事甲状腺疾病等内分泌代谢性疾病的研究。

引用本文:

李扬左新河华川赵勇. T、B淋巴细胞在自身免疫性甲状腺疾病中的作用机制研究进展[J]. 中国医药导报, 2019, 16(23): 49-52.
LI Yang ZUO Xinhe HUA Chuan ZHAO Yong. Research progress on the mechanism of T and B lymphocytes involved in autoimmune thyroid disease. 中国医药导报, 2019, 16(23): 49-52.

链接本文:

http://www.yiyaodaobao.com.cn/CN/ 或 http://www.yiyaodaobao.com.cn/CN/Y2019/V16/I23/49

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