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Related Concept Videos

Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
Functions of Thyroid Hormones01:18

Functions of Thyroid Hormones

The thyroid hormone (TH) plays a pivotal role in the intricate orchestration of physiological processes, exerting profound effects on development, metabolism, and homeostasis throughout different life stages.
TH is indispensable for the normal development and maturation of the skeletal, muscular, and nervous systems during fetal and childhood growth. It facilitates bone mineral turnover and regulates protein synthesis in developing tissues, contributing significantly to overall growth and...
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...
Graves' Disease I: Introduction01:28

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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Related Experiment Video

Updated: Jun 13, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Immunity, thyroid function and pregnancy: molecular mechanisms.

Anthony P Weetman1

  • 1Department of Human Metabolism, Faculty of Medicine, Dentistry and Health, University of Sheffield, The Medical School, Beech Hill Road, Sheffield S10 2RX, UK. a.p.weetman@sheffield.ac.uk

Nature Reviews. Endocrinology
|April 28, 2010
PubMed
Summary
This summary is machine-generated.

Pregnancy temporarily improves autoimmune thyroid disease by increasing regulatory T (TREG) cells, which suppress the immune system. Postpartum, a decline in TREG cells leads to a resurgence of thyroid autoimmunity.

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In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse
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In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse

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Last Updated: Jun 13, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse
04:14

In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse

Published on: October 6, 2023

Area of Science:

  • Immunology
  • Endocrinology
  • Obstetrics

Background:

  • Pregnancy significantly impacts autoimmune thyroid diseases like Graves' disease and postpartum thyroiditis.
  • Maternal immune tolerance to the fetus involves complex hormonal and cellular mechanisms.
  • Regulatory T (TREG) cells are crucial for maintaining immune tolerance during pregnancy.

Purpose of the Study:

  • To elucidate the immunological mechanisms underlying changes in autoimmune thyroid disease during pregnancy and postpartum.
  • To understand the role of regulatory T (TREG) cells in immune tolerance during gestation.

Main Methods:

  • Review of immunological factors during pregnancy, including hormonal changes and cytokine profiles.
  • Analysis of the role and distribution of regulatory T (TREG) cells in maternal circulation and decidua.
  • Correlation of TREG cell dynamics with thyroid autoantibody levels and disease activity.

Main Results:

  • Thyroid autoimmunity, such as Graves' disease, often improves during pregnancy due to immune suppression.
  • Postpartum thyroiditis involves destructive thyroiditis, potentially linked to immune system shifts.
  • Regulatory T (TREG) cells accumulate during pregnancy, suppressing autoimmune responses via linked suppression.
  • A decline in TREG cells postpartum is associated with the exacerbation of autoimmune thyroid conditions.

Conclusions:

  • Regulatory T (TREG) cells play a pivotal role in maintaining immune tolerance during pregnancy, leading to remission of Graves' disease.
  • Postpartum immune system shifts, particularly a decrease in TREG cells, can trigger or worsen autoimmune thyroid diseases.