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Pathophysiology of thyroid-associated orbitopathy.

Alan Chun Hong Lee1, George J Kahaly2

  • 1Division of Endocrinology and Metabolism, Department of Medicine, LKS Faculty of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong SAR, China; Department of Medicine I, Johannes Gutenberg University Medical Center, Mainz 55101, Germany.

Best Practice & Research. Clinical Endocrinology & Metabolism
|February 19, 2022
PubMed
Summary

Thyroid-associated orbitopathy involves orbital fibroblast activation, leading to inflammation and tissue remodeling. Targeting T helper 17 cells and receptor crosstalk offers potential therapeutic strategies for Graves' disease complications.

Keywords:
T helper 17crosstalkinsulin-like growth factor-1 receptororbital fibroblaststhyroid stimulating hormone receptorthyroid-associated orbitopathy

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Area of Science:

  • Ophthalmology
  • Endocrinology
  • Immunology

Background:

  • Thyroid-associated orbitopathy (TAO) is the most frequent extrathyroidal manifestation of Graves' disease.
  • TAO involves orbital inflammatory infiltration and fibroblast activation, causing adipogenesis, hyaluronan production, myofibroblast differentiation, and fibrosis.
  • Immune cell interactions, particularly T cells and B cells with orbital fibroblasts, perpetuate TAO's inflammation and tissue remodeling.

Purpose of the Study:

  • To elucidate the pathogenic mechanisms of Thyroid-associated orbitopathy.
  • To identify key cellular players and signaling pathways involved in TAO.
  • To explore potential novel therapeutic targets for TAO.

Main Methods:

  • Review of current literature on TAO pathogenesis.
  • Analysis of the roles of T helper 17 cells and receptor crosstalk (TSH receptor/IGF-1 receptor) in fibroblast activation.
  • Examination of the significance of disease-specific biomarkers and emerging factors like oxidative stress.

Main Results:

  • T helper 17 cells are identified as key pro-inflammatory and profibrotic CD4+ T cell subsets in TAO.
  • Crosstalk between Thyroid Stimulating Hormone Receptor (TSHR) and Insulin-like Growth Factor-1 Receptor (IGF-1R) is a primary driver of orbital fibroblast activation.
  • Thyroid Stimulating Hormone Receptor autoantibody (TRAb) is a crucial disease-specific biomarker.

Conclusions:

  • Understanding TSHR/IGF-1R signaling and T helper 17 cell involvement is critical for TAO pathogenesis.
  • TRAb serves as a clinically relevant biomarker for TAO.
  • Emerging factors like oxidative stress, gut microbiome, and epigenetics present novel therapeutic avenues for TAO.