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桥本甲状腺炎患者的Th17/Treg细胞失衡与糖皮质激素诱导的肿瘤坏死因子受体配体表达情况

Th17/Treg cells imbalance and GITRL profile in patients with Hashimoto's thyroiditis.

作者信息

Liu Yingzhao, Tang Xinyi, Tian Jie, Zhu Chenlu, Peng Huiyong, Rui Ke, Wang Yungang, Mao Chaoming, Ma Jie, Lu Liwei, Xu Huaxi, Wang Shengjun

机构信息

Department of Laboratory Medicine, the Affiliated People's Hospital, Jiangsu University, Zhenjiang 212002, China.

Institute of Laboratory Medicine, Jiangsu Key Laboratory of Medical Science and Laboratory Medicine, Jiangsu University, Zhenjiang 212013, China.

出版信息

Int J Mol Sci. 2014 Nov 25;15(12):21674-86. doi: 10.3390/ijms151221674.

DOI:10.3390/ijms151221674
PMID:25429429
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4284671/
Abstract

Hashimoto's thyroiditis (HT) is an organ-specific immune disease characterized by the presence of lymphocytic infiltration and serum autoantibodies. Previous studies have confirmed the critical role of Th17 cells in the pathopoiesis of HT patients. Additionally, regulatory T cells (Treg) display a dysregulatory function in autoimmune disease. The purpose of this study is to investigate the alteration of Th17 and Treg cells in HT patients and explore contributing factors. We found there was an increased ratio of Th17/Treg in HT patients and a positive correlation with autoantibodies (anti-TgAb). In addition, there was an increased level of GITRL, which has been demonstrated to be correlated with the increassement of Th17 cells in the serum and thyroid glands of HT patients; the upregulated serum level of GITRL has a positive correlation with the percentage of Th17 cells in HT patients. In summary, an increase in GITRL may impair the balance of Th17/Treg, and contribute to the pathopoiesis of Hashimoto's thyroiditis.

摘要

桥本甲状腺炎(HT)是一种器官特异性免疫疾病,其特征为淋巴细胞浸润和血清自身抗体的存在。先前的研究已经证实Th17细胞在HT患者发病机制中的关键作用。此外,调节性T细胞(Treg)在自身免疫性疾病中表现出调节功能异常。本研究的目的是调查HT患者中Th17和Treg细胞的变化,并探索相关影响因素。我们发现HT患者中Th17/Treg比值升高,且与自身抗体(抗TgAb)呈正相关。此外,GITRL水平升高,已证明其与HT患者血清和甲状腺中Th17细胞的增加相关;血清中GITRL水平上调与HT患者中Th17细胞百分比呈正相关。总之,GITRL的增加可能会破坏Th17/Treg的平衡,并促进桥本甲状腺炎的发病机制。

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