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Graves' Disease I: Introduction

Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...

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Hyperthyroidism I: Introduction

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Related Experiment Video

Updated: May 7, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Breaking tolerance to thyroid antigens: changing concepts in thyroid autoimmunity.

Sandra M McLachlan¹, Basil Rapoport

¹Thyroid Autoimmune Disease Unit, Cedars-Sinai Research Institute, and University of California-Los Angeles School of Medicine, Los Angeles, California 90048.

Endocrine Reviews

|October 5, 2013

Summary

Thyroid autoimmunity results from genetic susceptibility and environmental factors. Preventing autoimmune thyroid disease requires predicting at-risk individuals and using antigen-specific therapies, not broad approaches.

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Last Updated: May 7, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

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Published on: March 17, 2023

Interrogating Individual Autoreactive Germinal Centers by Photoactivation in a Mixed Chimeric Model of Autoimmunity

Interrogating Individual Autoreactive Germinal Centers by Photoactivation in a Mixed Chimeric Model of Autoimmunity

Published on: April 11, 2019

Area of Science:

Immunology
Endocrinology
Genetics

Background:

Thyroid autoimmunity arises from a loss of self-tolerance to thyroid proteins like TSHR, TPO, and Tg.
Mechanisms include central T-cell deletion and peripheral regulatory T cells, but these proteins have unique immunogenic properties.
Genetic predisposition and environmental factors play crucial roles in developing these conditions.

Purpose of the Study:

To explore the complex mechanisms underlying the loss of self-tolerance to thyroid proteins.
To understand the roles of central and peripheral tolerance in autoimmune thyroid diseases.
To identify factors contributing to the breakdown of tolerance and inform therapeutic strategies.

Main Methods:

Analysis of spontaneous and induced animal models of thyroid autoimmunity.
Investigation of intrathymic and peripheral T-cell tolerance mechanisms.
Examination of the immunogenicity of TSHR, TPO, and Tg, including genetic and environmental influences.

Main Results:

Intrathymic expression controls TSHR tolerance, but not TPO or Tg.
Regulatory T cells are not involved in TSHR self-tolerance but modulate Graves' disease and thyroiditis.
TSHR tolerance breakdown involves MHC, TSHR polymorphisms, and alternative splicing; Tg tolerance loss precedes TPO loss.
Environmental factors often reveal existing autoimmunity; interferon-α therapy and T-cell depletion can trigger thyroid autoimmunity.
Micro-organisms may act via bystander stimulation.

Conclusions:

No single mechanism explains the loss of tolerance to thyroid proteins.
Preventing autoimmune thyroid disease necessitates predicting at-risk individuals.
Future therapies should be antigen-specific rather than broad-acting.