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 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...
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...
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...
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...
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

[Exploration on the application of perineal lateral arc-shaped incision in the resection of complex tumors on the lateral side of the pelvic floor].

Zhonghua zhong liu za zhi [Chinese journal of oncology]·2026
Same author

[Utilizing machine learning and SHAP analysis to develop a prognostic survival prediction model for gastric cancer patients following radical gastrectomy].

Zhonghua wei chang wai ke za zhi = Chinese journal of gastrointestinal surgery·2026
Same author

[Surgical techniques for the safe and rapid resection of primary or secondary sacral tumors located between the second and fourth sacral vertebrae].

Zhonghua zhong liu za zhi [Chinese journal of oncology]·2025
Same author

Biomechanical strength of triceps tendon repairs: systematic review and meta-regression analysis of human cadaveric studies.

Musculoskeletal surgery·2024
Same author

[Clinical efficacy of autologous biological patch in preventing rectovaginal fistula after pelvic exenteration].

Zhonghua wei chang wai ke za zhi = Chinese journal of gastrointestinal surgery·2024
Same author

[Exploration of the method and efficacy of treatments for intractable pelvic pain caused by rectal or bladder fistula].

Zhonghua zhong liu za zhi [Chinese journal of oncology]·2024

Related Experiment Video

Updated: May 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

Hyperthyroid monkeys: a nonhuman primate model of experimental Graves' disease.

Y Wang1, L P Wu, J Fu

  • 1Department of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University School of Medicine, Xi'an 710061, People's Republic of China.

The Journal of Endocrinology
|September 14, 2013
PubMed
Summary

Researchers developed a new Graves' disease (GD) model in rhesus monkeys using the TSHR A-subunit. This model mimics human GD, showing elevated antibodies and thyroid hormones, aiding future prevention and treatment strategies.

Keywords:
Graves' diseaserhesus monkeysthyrotropin receptor A-subunit

More Related Videos

Characterization of Metabolic Status in Nonhuman Primates with the Intravenous Glucose Tolerance Test
06:59

Characterization of Metabolic Status in Nonhuman Primates with the Intravenous Glucose Tolerance Test

Published on: November 13, 2016

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
07:01

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma

Published on: April 17, 2013

Related Experiment Videos

Last Updated: May 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

Characterization of Metabolic Status in Nonhuman Primates with the Intravenous Glucose Tolerance Test
06:59

Characterization of Metabolic Status in Nonhuman Primates with the Intravenous Glucose Tolerance Test

Published on: November 13, 2016

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
07:01

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma

Published on: April 17, 2013

Area of Science:

  • Immunology
  • Endocrinology
  • Autoimmune Diseases

Background:

  • Graves' disease (GD) is a prevalent organ-specific autoimmune disorder affecting women.
  • Evidence suggests the thyrotropin receptor (TSHR) A-subunit, not the full receptor, is the primary autoantigen in GD.
  • Existing rodent models do not fully replicate human GD characteristics.

Purpose of the Study:

  • To establish a novel non-human primate model for Graves' disease using rhesus monkeys.
  • To investigate the immunological and physiological changes associated with GD induction in this model.
  • To provide a more accurate preclinical tool for studying GD pathogenesis and therapeutic development.

Main Methods:

  • Induction of Graves' disease in female rhesus monkeys via adenovirus expressing the TSHR A-subunit (A-sub-Ad).
  • Monitoring of TSHR antibody levels, thyroid hormone concentrations (T₄, free T₄), and incidence of goiter.
  • Quantitative analysis of CD4+ T helper cell subpopulations, including Th1, Th2, Th17, and regulatory T cells (Tregs).

Main Results:

  • All A-sub-Ad injected monkeys exhibited significantly elevated TSHR antibody levels compared to controls.
  • Fifty percent of the test monkeys developed goiter and showed increased total and free thyroxine (T₄) levels.
  • Immunological analysis revealed a mixed Th1/Th2 response, decreased Treg proportions, and an elevated Th17:Treg ratio.

Conclusions:

  • The rhesus monkey model successfully replicates key features of human Graves' disease.
  • This model offers a valuable platform for advancing the understanding of GD pathogenesis.
  • The model has the potential to accelerate the development of effective prevention and treatment strategies for human GD.