Imbalance of Th17/Treg in Different Subtypes of Autoimmune Thyroid Diseases

Cell Physiol Biochem. 2016;40(1-2):245-252. doi: 10.1159/000452541. Epub 2016 Nov 18.

Abstract

Aims: 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).

Conclusion: 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.

MeSH terms

  • Adult
  • Autoimmune Diseases / genetics
  • Autoimmune Diseases / immunology*
  • Autoimmune Diseases / pathology
  • Case-Control Studies
  • Female
  • Flow Cytometry
  • Forkhead Transcription Factors / genetics
  • Forkhead Transcription Factors / metabolism
  • Gene Expression Regulation
  • Graves Ophthalmopathy / genetics
  • Graves Ophthalmopathy / immunology
  • Graves Ophthalmopathy / pathology
  • Hashimoto Disease / genetics
  • Hashimoto Disease / immunology
  • Hashimoto Disease / pathology
  • Humans
  • Leukocytes, Mononuclear / metabolism
  • Male
  • Nuclear Receptor Subfamily 1, Group F, Member 3 / genetics
  • Nuclear Receptor Subfamily 1, Group F, Member 3 / metabolism
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • T-Lymphocytes, Regulatory / immunology*
  • Th17 Cells / immunology*
  • Thyroid Diseases / genetics
  • Thyroid Diseases / immunology*
  • Thyroid Diseases / pathology

Substances

  • FOXP3 protein, human
  • Forkhead Transcription Factors
  • Nuclear Receptor Subfamily 1, Group F, Member 3
  • RNA, Messenger