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 Experiment Videos

Autoimmunity causing thyroid dysfunction.

R Volpé1

  • 1Department of Medicine, University of Toronto, Ontario, Canada.

Endocrinology and Metabolism Clinics of North America
|September 1, 1991
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Search for Leptonic Decays of Dark Photons at NA62.

Physical review letters·2024
Same author

Search for Rare b→dℓ^{+}ℓ^{-} Transitions at Belle.

Physical review letters·2024
Same author

First Measurement of R(X_{τ/ℓ}) as an Inclusive Test of the b→cτν Anomaly.

Physical review letters·2024
Same author

Tests of Light-Lepton Universality in Angular Asymmetries of B^{0}→D^{*-}ℓν Decays.

Physical review letters·2023
Same author

Precise Measurement of the D_{s}^{+} Lifetime at Belle II.

Physical review letters·2023
Same author

Search for a τ^{+}τ^{-} Resonance in e^{+}e^{-}→μ^{+}μ^{-}τ^{+}τ^{-} Events with the Belle II Experiment.

Physical review letters·2023
Same journal

Navigating Adrenal Disease: A Comprehensive, Practical Guide for the Clinician.

Endocrinology and metabolism clinics of North America·2026
Same journal

Adrenal Disorders in Pregnancy.

Endocrinology and metabolism clinics of North America·2026
Same journal

Diagnosis and Management of Adrenocortical Carcinoma.

Endocrinology and metabolism clinics of North America·2026
Same journal

Pheochromocytomas and Paragangliomas.

Endocrinology and metabolism clinics of North America·2026
Same journal

Hereditary Conditions Associated with Adrenocortical Carcinoma, Pheochromocytoma, and Other Adrenal Tumors: Genetic Testing and Management Recommendations.

Endocrinology and metabolism clinics of North America·2026
Same journal

Primary Bilateral Macronodular Adrenal Hyperplasia.

Endocrinology and metabolism clinics of North America·2026
See all related articles

Autoimmune thyroid disease (AITD) likely stems from a genetic defect in suppressor T lymphocytes, potentially worsened by environmental factors. This immune dysregulation, not an antigen abnormality, initiates and perpetuates thyroid disease.

Area of Science:

  • Immunology
  • Endocrinology
  • Genetics

Background:

  • Autoimmune thyroid disease (AITD) is characterized by immune system dysfunction targeting the thyroid gland.
  • Existing theories suggest a genetically induced, antigen-specific defect in suppressor T lymphocytes plays a key role in AITD pathogenesis.
  • Environmental factors and hyperthyroidism itself may exacerbate this underlying defect.

Purpose of the Study:

  • To investigate the underlying mechanisms of autoimmune thyroid disease (AITD).
  • To explore the roles of genetic defects, antigen presentation, and environmental factors in AITD.
  • To understand the factors contributing to disease initiation, perpetuation, and clinical variability.

Main Methods:

  • Review of existing evidence from multiple laboratories and experimental techniques.

Related Experiment Videos

  • Analysis of the role of HLA-related genes in antigen presentation.
  • Assessment of environmental and disease-specific factors influencing T lymphocyte function.

    • Main Results:

    • Evidence points to a genetically determined, antigen-specific defect in suppressor T lymphocytes as the primary cause of AITD.
    • Abnormal antigen presentation via HLA-related genes may contribute to the defect.
    • Environmental factors and hyperthyroidism can reduce suppressor T lymphocyte numbers and function, acting as precipitating factors.

    Conclusions:

    • The initiating event in AITD appears to be a perturbation of the generalized immune system superimposed on an organ-specific immunoregulatory abnormality.
    • Antigen presentation by thyroid cells is a secondary event, not the primary cause.
    • Disease expression varies based on the severity of the suppressor T lymphocyte defect and environmental influences.