Th17 cell plays a role in the pathogenesis of Hashimoto's thyroiditis in patients Dapeng Li a , 1 , Wenqian Cai b , 1 , Runxia Gu c , Yi Zhang b , Huafeng Zhang b , Ke Tang b , Pingwei Xu b , Foad Katirai b , Wei Shi a , Longqiang Wang a , Tao Huang a , ⁎ , Bo Huang b , ⁎⁎ a Department of Breast and Thyroid Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430000, PR China b Department of Biochemistry & Molecular Biology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430000, PR China c Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430000, PR China Received 19 January 2013; accepted with revision 3 October 2013 Available online 11 October 2013 KEYWORDS Hashimoto's thyroiditis; Autoimmune thyroiditis; IL-17; Th17 cell; Iodine; Regulatory T cell Abstract Hashimoto's thyroiditis (HT) has long been epidemiologically associated with excess iodine levels. However, the underlying immunological mechanisms still remain largely unexplored. Th17 cells are commonly recognized as playing vital roles in various autoimmune diseases. Here we show that intra-thyroid infiltrating Th17 cells and serum IL-17 levels were significantly increased in HT patients. However, the concentration of serum IL-17 was inversely correlated with patients' residual thyroid function while the heterogeneously expressed thyroid IL-17 was directly correlated with local fibrosis. Administration of moderate high levels of iodine was found to facilitate the polarization of murine splenic naïve T cells into Th17 cells, whereas extreme high levels of iodine favored Th1 polarization and inhibited Treg development. These findings suggest that both Th1 and Th17 cells may be involved in the pathogenesis of HT and high levels of iodine may play a critical role in this process by modulating T cell differentiation. © 2013 Elsevier Inc. All rights reserved. ⁎ Correspondence to: T. Huang, Department of Breast and Thyroid Surgery, Union Hospital, Wuhan 430000, PR China. ⁎⁎ Corresponding author. E-mail addresses: huangtaowh@163.com (T. Huang), tjhuangbo@hotmail.com (B. Huang). 1 DL and WC contributed equally to this work. 1521-6616/$ - see front matter © 2013 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.clim.2013.10.001 available at www.sciencedirect.com Clinical Immunology www.elsevier.com/locate/yclim Clinical Immunology (2013) 149, 411–420