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

You might also read

Related Articles

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

Sort by
Same author

Growth patterns and bone maturation in children with sex chromosomal (45,X/46,XY) differences of sex development.

European journal of endocrinology·2026
Same author

Diabetes Mellitus and COVID-19 in Adults: A Systematic Review of Pathophysiological Connections, Clinical Outcomes, and Therapeutic Considerations.

International journal of molecular sciences·2026
Same author

Comparison of Severe COVID-19 Outcomes in Vaccinated and Unvaccinated Patients, with and Without Diabetes Mellitus in a Romanian Tertiary Healthcare Pneumology Hospital-A Retrospective Study.

International journal of molecular sciences·2026
Same author

MASH in Type 2 Diabetes: Pathophysiology, Diagnosis, and Therapeutic Management-A Narrative Review.

Medicina (Kaunas, Lithuania)·2026
Same author

Gonadal Function and Its Evolution in 46,XX Testicular/Ovotesticular DSD.

The Journal of clinical endocrinology and metabolism·2025
Same author

Relationship Between Insulin Resistance Indicators and Type 2 Diabetes Mellitus in Romania.

International journal of molecular sciences·2025
Same journal

Severe Persistent Hypereosinophilia of Undetermined Significance: Diagnostic Challenges in Clinical Practice and Two-Year Follow-Up.

Romanian journal of internal medicine = Revue roumaine de medecine interne·2026
Same journal

Immune Checkpoint Inhibitor-Associated Myocarditis: A Retrospective Case Series.

Romanian journal of internal medicine = Revue roumaine de medecine interne·2026
Same journal

Mortality predictors in patients with ST-segment elevation myocardial infarction presenting no-reflow phenomenon after primary PCI: experience of a tertiary center.

Romanian journal of internal medicine = Revue roumaine de medecine interne·2026
Same journal

Pancreatic stone protein predicts hospital stay in community-acquired infections.

Romanian journal of internal medicine = Revue roumaine de medecine interne·2026
Same journal

Clinical features and hematological indices predicting all-cause mortality in patients undergoing hemodialysis; a retrospective cohort study.

Romanian journal of internal medicine = Revue roumaine de medecine interne·2026
Same journal

Clinical construct validity and subgroup stability of the Romanian version of the Boston Carpal Tunnel Questionnaire in nerve-conduction-confirmed carpal tunnel syndrome - a cross-sectional study.

Romanian journal of internal medicine = Revue roumaine de medecine interne·2026
See all related articles

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

The thyroid and autoimmunity.

Corina Lichiardopol1, Maria Moţa

  • 1Department of Endocrinology, University of Medicine and Pharmacy, Craiova, Romania. corinalich@gmail.com

Romanian Journal of Internal Medicine = Revue Roumaine De Medecine Interne
|May 8, 2010
PubMed
Summary
This summary is machine-generated.

Autoimmune thyroid diseases arise from disrupted self-tolerance, leading to abnormal immune interactions. Understanding these complex mechanisms is key for preventing and managing thyroid disorders.

Related Experiment Videos

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

Area of Science:

  • Immunology
  • Endocrinology
  • Pathogenesis of Autoimmune Diseases

Background:

  • Autoimmune thyroid diseases are common globally, particularly in women, influenced by sex steroids and X chromosome.
  • Disrupted thyroid self-tolerance, often infection-induced, triggers aberrant thyroid-immune crosstalk involving cytokines.
  • Thyrocytes act as antigen-presenting cells, activating immune cells amid deficient regulatory T cells, leading to thyroid autoimmunity.

Purpose of the Study:

  • To elucidate the complex pathogenesis of autoimmune thyroid disorders.
  • To highlight the role of immune cell interactions and hormonal influences in thyroid autoimmunity.
  • To emphasize the importance of understanding these mechanisms for disease prevention and management.

Main Methods:

  • Review of existing literature on thyroid autoimmunity.
  • Analysis of immune cell interactions, including T helper cells (Th1, Th2, Th17) and regulatory T cells.
  • Examination of the influence of hormonal milieu (sex steroids, glucocorticoids) and thyroid hormones on immune responses.

Main Results:

  • Thyroid self-tolerance breakdown leads to immune cell infiltration and autoantibody production.
  • Pregnancy-associated Th2 shift promotes tolerance, while postpartum Th1 shift increases postpartum thyroiditis risk.
  • Bidirectional communication exists between thyroid hormones and the immune system, with immune cells secreting TSH.

Conclusions:

  • Understanding the intricate interplay between the immune system, thyroid, and hormones is crucial.
  • Immune dysregulation, hormonal fluctuations, and thyroid cell properties contribute to autoimmune thyroid disease development.
  • Further research into these complex pathways is vital for effective prevention and therapeutic strategies.