title: Increased differentiation of Th22 cells in Hashimoto's thyroiditis.
abstract: As Th22 subsets are identified, their involvement in the pathogenesis of numerous autoimmune diseases has become apparent. In this study, we investigated differentiation of Th22 cells in the autoimmune thyroid diseases including Hashimoto's thyroiditis (HT) and Graves' disease (GD). Besides, we also explored the involvement of Th22 cells in an iodine-induced autoimmune thyroiditis (AIT) model (i.e., NOD.H-2(h4) mice). In HT patients, we showed the level of circulating Th22 cells correlated with the level of serum IL-22, and was significantly higher than in GD patients and healthy control subjects. Levels of serum IL-6, a major Th22 cell differentiation effector, were also higher in HT, and correlated with Th22 cells concentration. Peripheral blood mononuclear cells isolated from HT patients produced larger amounts of IL-6 in vitro than did those isolated from other groups. Furthermore, unlike those from GD patients, T lymphocytes from HT patients showed an enhanced differentiation in vitro into Th22 cells in the presence of recombinant IL-6 and TNF-α. In addition, levels of circulating Th22 cells and titers of thyroid peroxidase antibody were positively correlated in HT patients. In NOD.H-2(h4) mice, higher numbers of Th22 cells were observed in the spleens of the AIT group, while splenocytes of this group also produced larger amounts of IL-6 and IL-22 in vitro compared with the control. Intra-thyroid infiltrating IL-22+ lymphocytes were significantly increased in mice of the AIT group compared with the control. Our results indicate that Th22 cells may contribute to the pathogenesis of HT.
authors.affiliation: Department of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, The First Affiliated Hospital of China Medical University, Shenyang 110001, China.
authors.forename: Xue
authors.initials: X
authors.lastname: Bai
authors.forename: Jie
authors.initials: J
authors.lastname: Sun
authors.forename: Weiwei
authors.initials: W
authors.lastname: Wang
authors.forename: Zhongyan
authors.initials: Z
authors.lastname: Shan
authors.forename: Hongzhi
authors.initials: H
authors.lastname: Zheng
authors.forename: Yushu
authors.initials: Y
authors.lastname: Li
authors.forename: Yuhang
authors.initials: Y
authors.lastname: Zhao
authors.forename: Ming
authors.initials: M
authors.lastname: Gong
authors.forename: Weiping
authors.initials: W
authors.lastname: Teng
mesh_terms: D000328:Adult; D000818:Animals; D001323:Autoantibodies / Q000032:analysis; D015551:Autoimmunity; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D002478:Cells, Cultured; D005260:Female; D006111:Graves Disease / Q000097:blood / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D050031:Hashimoto Disease / Q000097:blood / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D015850:Interleukin-6 / Q000097:blood / Q000378:metabolism; D007378:Interleukins / Q000097:blood / Q000378:metabolism*; D007453:Iodide Peroxidase / Q000037:antagonists & inhibitors; D038041:Lymphopoiesis; D008297:Male; D016688:Mice, Inbred NOD; D011897:Random Allocation; D013154:Spleen / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D013961:Thyroid Gland / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D013967:Thyroiditis, Autoimmune / Q000097:blood / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D015854:Up-Regulation; D000097043:Interleukin-22
chemical_list: D001323:Autoantibodies; D015850:Interleukin-6; D007378:Interleukins; D007453:Iodide Peroxidase; D000097043:Interleukin-22