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Related Concept Videos

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...
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...
Autoimmune Disorders01:29

Autoimmune Disorders

Autoimmune diseases are a group of disorders in which the body's immune system mistakenly attacks its own cells, tissues, and organs. This results from an overactive immune response against substances and tissues normally present in the body. Let's delve into the concept and mechanism of autoimmune diseases from an immune system point of view, explore different causes and examples of such diseases, and discuss potential solutions.
Concept and Mechanism of Autoimmune Diseases
The immune system...
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...
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...
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...

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Related Experiment Video

Updated: Jun 7, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

SLC26A4 expression among autoimmune thyroid tissues.

Salima Belguith-Maalej1, Sandra A Rebuffat, Ilhem Charfeddine

  • 1Unité Cibles pour le Diagnostic et la Thérapie, Centre de Biotechnologie de Sfax, Tunisia.

Immunobiology
|November 2, 2010
PubMed
Summary

The PDS gene (SLC26A4) expression is altered in autoimmune thyroid diseases (AITD). Pendrin, the PDS gene product, shows altered localization and expression in Graves

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An Ex vivo Culture System to Study Thyroid Development
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An Ex vivo Culture System to Study Thyroid Development

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Related Experiment Videos

Last Updated: Jun 7, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

An Ex vivo Culture System to Study Thyroid Development
08:33

An Ex vivo Culture System to Study Thyroid Development

Published on: June 6, 2014

Area of Science:

  • Endocrinology
  • Genetics
  • Immunology

Background:

  • The Pendred syndrome (PS) gene, SLC26A4 (PDS), is linked to autoimmune thyroid diseases (AITD).
  • Pendrin, the PDS gene product, is a newly identified autoantigen in Graves' disease (GD) and Hashimoto thyroiditis (HT).

Purpose of the Study:

  • To quantify PDS gene expression in various thyroid conditions.
  • To evaluate the in vivo and in vitro immunolocalization of pendrin.

Main Methods:

  • Analysis of 52 thyroid tissue samples including GD, HT, multinodular goiter (MNG), normal thyroid, and thyroid carcinomas.
  • Quantitative RT-PCR and immuno-detection methods for PDS and pendrin expression.
  • Immunofluorescence studies on primary cell cultures from GD tissues to assess TSH and thyroglobulin (Tg) effects on pendrin.

Main Results:

  • PDS transcript levels were significantly increased in GD thyroid tissues (27.17-fold higher than normal).
  • PDS expression was decreased in HT (92.05-fold lower), MNG (14.3-fold lower), and carcinoma tissues.
  • Immunofluorescence revealed apical and cytoplasmic pendrin localization in GD tissues, reduced expression in HT, and improved apical trafficking with TSH/Tg stimulation in GD cells.

Conclusions:

  • A significant relationship exists between SLC26A4 (PDS) gene expression and autoimmune thyroid diseases.
  • Altered pendrin expression and localization correlate with thyroid dysfunction in AITD.