title: The role of the IL-23/IL-17 axis in the pathogenesis of Graves' disease.
abstract: This study is to explore the role of IL-23/IL-17 axis in subjects with Graves' disease, while IL-23/IL-17 axis plays an important role in a number of autoimmune diseases, but it's not clear in Graves' disease. Thirty-three patients with Graves' disease as a GD group, 15 patients with euthyroid GD as eGD group and 22 healthy volunteers as a control group whose age- and sex-matched. Peripheral blood was collected and peripheral blood mononuclear cells (PBMCs) were isolated in the both groups, then PBMCs were cultured in the presence or absence of IL-23 in vitro. The expression of retinoid-related orphan receptor gamma t (RORγt) and IL-17 mRNA were examined by Semi-quantitative RT-PCR, and the levels of IL-17 protein were measured by enzyme-linked immunosorbent assay. The expression of RORγt, IL-17 mRNA and IL-17 protein levels were markedly higher in GD and euthyroid GD group as compared with the control group. IL-17 levels were still higher in euthyroid GD patients. When PBMCs derived from the three groups were cultured in vitro with or without IL-23, the expression of RORγt in GD group with IL-23 dramatically increased as compared with that in GD group without IL-23 and in control group with IL-23. RORγt expression of PBMCs from eGD group cultured with IL-23 was increased compared with that cultured without IL-23. The levels of IL-17 mRNA and the protein were also significantly higher than that of GD and eGD cultured without IL-23 and control group. There was no difference of the expression of RORγt mRNA and IL-17 protein levels between GD and eGD group cultured with or without IL-23. Our studies demonstrated that IL-23/IL-17 axis is associated with the pathogenesis of Graves' disease in it activated term. This effect is not dependent on thyroid function, but may be associated to the immunity.
authors: Department of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
authors: Li
authors: L
authors: Zheng
authors: Peng
authors: P
authors: Ye
authors: Chun
authors: C
authors: Liu
mesh_terms: D000328:Adult; D013956:Antithyroid Agents / Q000627:therapeutic use; D001323:Autoantibodies / Q000032:analysis; D002478:Cells, Cultured; D005260:Female; D006111:Graves Disease / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D020381:Interleukin-17 / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D053760:Interleukin-23 Subunit p19 / Q000378:metabolism*; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000378:metabolism*; D008297:Male; D008713:Methimazole / Q000627:therapeutic use; D008875:Middle Aged; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D058504:Th17 Cells / Q000276:immunology / Q000378:metabolism; D013961:Thyroid Gland / Q000187:drug effects / Q000276:immunology / Q000503:physiopathology*; D015854:Up-Regulation; D055815:Young Adult
chemical_list: D013956:Antithyroid Agents; D001323:Autoantibodies; C508717:IL17A protein, human; C508840:IL23A protein, human; D020381:Interleukin-17; D053760:Interleukin-23 Subunit p19; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D012333:RNA, Messenger; C539900:RORC protein, human; C006606:anti-thyroglobulin; C056626:thyroid microsomal antibodies; D008713:Methimazole