title: Imbalance of Th17/Treg in Different Subtypes of Autoimmune Thyroid Diseases.
abstract: OBJECTIVE
  To clarify the imbalance of Th17/Treg in different subtypes of autoimmune thyroid diseases (AITDs) including Graves' disease(GD), Hashimoto's thyroiditis(HT) and Graves' ophthalmopathy (GO).
  
  
  METHODS
  47 patients with AITD (including 16 GD, 15 HT, and 16 GO) and 12 healthy controls were enrolled in this study. The percentages of Th17 and Treg cells, the ratio of Th17/Treg, as well as their related transcription factors RORγt and Foxp3 mRNA in peripheral blood mononuclear cells (PBMCs) were measured by flow cytometry and real-time quantitative PCR Results: Compared with those in control group, the percentage of CD4+IL-17+T cell(Th17) and the mRNA expression of its transcription factor RORγt were higher in PBMCs of AITDs (P<0.05), particularly in HT subgroup (P<0.01). The percentage of CD4+Foxp3+T (Treg) cells and its transcription factor Foxp3 mRNA were significantly decreased in PBMCs of GD (P<0.05). In addition, the ratio of Th17/Treg was elevated in AITD group and GO subgroup (P<0.01). In GO subgroup, the patients with clinical activity score (CAS) above 4.5 had higher percentages of Th17 than those with CAS ranging from 3 to 4.5 (P<0.05).
  
  
  CONCLUSIONS
  Increased Th17 lymphocytes may play a more important role in the pathogenesis of HT and GO while decreased Treg may be greatly involved in GD.
authors.affiliation: Department of Geriatrics, Xijing Hospital of Fourth Military Medical University, Xi'an China.
authors.forename: Cui
authors.initials: C
authors.lastname: Li
authors.forename: Jianghong
authors.initials: J
authors.lastname: Yuan
authors.forename: Yuan-Feng
authors.initials: YF
authors.lastname: Zhu
authors.forename: Xiang-Ju
authors.initials: XJ
authors.lastname: Yang
authors.forename: Qiong
authors.initials: Q
authors.lastname: Wang
authors.forename: Jian
authors.initials: J
authors.lastname: Xu
authors.forename: Shuang-Tao
authors.initials: ST
authors.lastname: He
authors.forename: Jin-An
authors.initials: JA
authors.lastname: Zhang
mesh_terms: D000328:Adult; D001327:Autoimmune Diseases / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D016022:Case-Control Studies; D005260:Female; D005434:Flow Cytometry; D051858:Forkhead Transcription Factors / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation; D049970:Graves Ophthalmopathy / Q000235:genetics / Q000276:immunology / Q000473:pathology; D050031:Hashimoto Disease / Q000235:genetics / Q000276:immunology / Q000473:pathology; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008297:Male; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D058504:Th17 Cells / Q000276:immunology*; D013959:Thyroid Diseases / Q000235:genetics / Q000276:immunology* / Q000473:pathology
chemical_list: C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D012333:RNA, Messenger