Safdari Vahid, Alijani Ebrahim, Nemati Maryam, Jafarzadeh Abdollah
Physiology Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran.
Department of Laboratory Sciences, School of Para-Medicine, Kerman University of Medical Sciences, Kerman, Iran.
Sultan Qaboos Univ Med J. 2017 May;17(2):e174-e180. doi: 10.18295/squmj.2016.17.02.007. Epub 2017 Jun 20.
Imbalances in effector T cell functioning have been associated with a number of autoimmune diseases, including Hashimoto's thyroiditis (HT). Differentiation of effector T helper (Th) 1, Th2, Th17 and regulatory T cell (Treg) lymphocytes is regulated by transcription factors, including Th1-specific T box (T-bet), GATA binding protein-3 (GATA), retinoid-related orphan receptor (ROR)-α and forkhead box P3 (FOXP3). This study aimed to investigate Th1/Th2, Th1/Treg, Th2/Treg and Th17/Treg balances at the level of these transcription factors.
This study took place between October 2015 and August 2016. Peripheral blood mononuclear cells were collected from a control group of 40 healthy women recruited from the Zahedan University of Medical Sciences, Zahedan, Iran, and a patient group of 40 women with HT referred to the Hazrat Ali Asghar Hospital, Zahedan. Total ribonucleic acid extraction was performed and the gene expression of transcription factors was quantitated using a real-time polymerase chain reaction technique.
Expression of T-bet and GATA was significantly elevated, while FOXP3 expression was significantly diminished among HT patients in comparison with the controls ( = 0.03, 0.01 and 0.05, respectively). Expression of RORα was higher among HT patients, although this difference was not significant ( = 0.15). Expression of T-bet/FOXP3, GATA/FOXP3 and RORα/FOXP3 ratios were increased among HT patients in comparison with the controls ( <0.02, <0.01 and <0.01, respectively).
These results indicate that HT patients have imbalances in Th1/Treg, Th2/Treg and Th17/Treg lymphocytes at the level of the transcription factors, deviating towards Th1, Th2 and Th17 cells. Correction of these imbalances may therefore be therapeutic.
效应T细胞功能失衡与包括桥本甲状腺炎(HT)在内的多种自身免疫性疾病相关。效应性辅助性T细胞(Th)1、Th2、Th17和调节性T细胞(Treg)淋巴细胞的分化受转录因子调控,包括Th1特异性T盒(T-bet)、GATA结合蛋白3(GATA)、视黄酸相关孤儿受体(ROR)α和叉头框P3(FOXP3)。本研究旨在探讨这些转录因子水平上的Th1/Th2、Th1/Treg、Th2/Treg和Th17/Treg平衡。
本研究于2015年10月至2016年8月进行。从伊朗扎黑丹医科大学招募的40名健康女性对照组以及转诊至扎黑丹哈扎特·阿里·阿斯加尔医院的40名HT女性患者组中采集外周血单个核细胞。进行总核糖核酸提取,并使用实时聚合酶链反应技术对转录因子的基因表达进行定量。
与对照组相比,HT患者中T-bet和GATA的表达显著升高,而FOXP3表达显著降低(分别为P = 0.03、0.01和0.05)。HT患者中RORα的表达较高,尽管差异不显著(P = 0.15)。与对照组相比,HT患者中T-bet/FOXP3、GATA/FOXP3和RORα/FOXP3比值升高(分别为P <0.02、P <0.01和P <0.01)。
这些结果表明,HT患者在转录因子水平上Th1/Treg、Th2/Treg和Th17/Treg淋巴细胞存在失衡,偏向于Th1、Th2和Th17细胞。因此,纠正这些失衡可能具有治疗作用。