Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

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...
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...
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...
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...
Goiter01:27

Goiter

Goiter refers to an abnormal enlargement of the thyroid gland that may appear as a diffuse goiter (uniform enlargement) or nodular (single or multiple nodules). Functionally, it is classified as nontoxic (normal/low hormone levels) or toxic (excess hormone production).PathophysiologyDiffuse thyroid enlargement typically results from prolonged stimulation by thyroid-stimulating hormone (TSH) or TSH-like agents, commonly seen in hypothyroidism or iodine deficiency. In contrast, in hyperthyroid...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

DNA-histone complexes as ligands amplify cell penetration and nuclear targeting of anti-DNA antibodies via energy-independent mechanisms.

Immunology·2015
Same author

Genes and environment as predisposing factors in autoimmunity: acceleration of spontaneous thyroiditis by dietary iodide in NOD.H2(h4) mice.

International reviews of immunology·2015
Same author

Genes and Environment as Predisposing Factors in Autoimmunity: Acceleration of Spontaneous Thyroiditis by Dietary Iodide in NOD.H2<sup>h4</sup> Mice.

International reviews of immunology·2015
Same author

The thyroxine-containing thyroglobulin peptide (aa 2549-2560) is a target epitope in iodide-accelerated spontaneous autoimmune thyroiditis.

Journal of immunology (Baltimore, Md. : 1950)·2014
Same author

Apoptosis of NOD.H2 h4 thyrocytes by low concentrations of iodide is associated with impaired control of oxidative stress.

Thyroid : official journal of the American Thyroid Association·2014
Same author

Identification of pathogenic T cell epitopes near cathepsin cleavage sites in thyroglobulin.

Journal of immunology (Baltimore, Md. : 1950)·2013

Related Experiment Video

Updated: Jun 4, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Molecular parameters linking thyroglobulin iodination with autoimmune thyroiditis.

George Carayanniotis1

  • 1Division of Endocrinology and Biomedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, NL, Canada. gcarayan@mun.ca

Hormones (Athens, Greece)
|February 26, 2011
PubMed
Summary
This summary is machine-generated.

High iodide intake may trigger autoimmune thyroiditis through effects on thyroglobulin peptides and thyroid cell death. Further research is needed to understand these complex mechanisms.

Related Experiment Videos

Last Updated: Jun 4, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Area of Science:

  • Endocrinology
  • Immunology
  • Thyroid Research

Background:

  • Increased iodide intake is associated with hypothyroidism and autoimmune thyroiditis.
  • The precise mechanisms underlying this link are not fully understood.
  • Iodide may influence metabolic or immunological pathways.

Purpose of the Study:

  • To summarize recent findings on the mechanisms linking iodide intake to thyroid autoimmunity.
  • To explore the role of iodinated peptides in thyroglobulin (Tg) in autoimmune responses.
  • To investigate the impact of iodine on thyroid cell apoptosis and necrosis.

Main Methods:

  • Literature review of recent research findings.
  • Analysis of studies focusing on thyroglobulin structure and function.
  • Examination of research on iodine-induced thyroid cell death.

Main Results:

  • Iodinated peptides within thyroglobulin may initiate autoimmune reactions.
  • Iodine exposure can induce apoptosis and necrosis in thyroid cells (thyrocytes).
  • These processes contribute to the development of thyroid disease.

Conclusions:

  • Iodide's role in thyroid autoimmunity involves complex immunological and cellular mechanisms.
  • Further investigation into iodinated peptides and thyrocyte apoptosis is crucial.
  • Understanding these mechanisms can inform prevention and treatment strategies for thyroid disorders.