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Jing Qin [1] and Jin Zhou [1; 2] and Chenling Fan [1] and Na Zhao [1] and Yongping Liu [1] and Shuo Wang [1] and Xuejiao Cui [1] and Mingshi Huang [1] and Haixia Guan [1] and Yushu Li [1] and Zhongyan Shan [1] and Weiping Teng [1]

Academic Editor: Marzia Caproni

1, Department of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning, China, cmu.edu.cn

2, Department of Endocrinology, Affiliated Yantai Yuhuangding Hospital of Qingdao University Medical College, Yantai, Shandong, China, qdu.edu.cn

Received Jun 3, 2017; Accepted Oct 12, 2017

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

1. Introduction

Graves’ disease (GD) is one of the most common organ-specific autoimmune diseases. It is characterized by hyperthyroidism and specific thyroid autoantibodies against thyroid-stimulating hormone receptor (TSHR) and is also commonly accompanied by autoantibodies against thyroglobulin (TG) and thyroid peroxidase (TPO).

Despite the environmental and genetic factors, the aetiology of GD is partly due to the breakdown of immune self-tolerance to thyroid autoantigen TSHR, thus leading to autoreactive T and B cells. It has been widely accepted that the exaggerated T helper (Th) 2 response plays a pivotal role in GD development [1–3]. However, the Th2 theory cannot explain all conditions. Recently, researchers have recognized that two other CD4+ T cell subsets and one B cell subtype, namely, the Th17 and regulatory T (Treg) cells, along with regulatory B (Breg) cells, may participate in GD pathogenesis [4–9].

Th17 cells, a newly identified CD4+ T cell subgroup, function by secreting their signature cytokine, interleukin-17A (IL-17A, also called IL-17). Numerous studies have demonstrated the pathogenic role of Th17 cells in autoimmune diseases, including inflammatory bowel disease, rheumatoid arthritis (RA), psoriasis, and asthma [10–13]. Treg cells, characterized by CD4, CD25, and transcription factor forkhead box P3 (Foxp3) expression, are reported to help maintain immune self-tolerance and to suppress autoreactive T and B cells through cell-to-cell contact or the secretion of regulatory cytokines such as interleukin-10 (IL-10) and transforming growth factor-β (TGF-β) [14]. In a previous study, we...
 

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