Iodine: An environmental trigger of thyroiditis

Noel R. Rose, Raphael Bonita, C. Lynne Burek

Research output: Contribution to journalReview articlepeer-review

Abstract

Like most autoimmune diseases of humans, chronic lymphocytic (Hashimoto's) thyroiditis results from the combination of a genetic predisposition and an environmental trigger. A body of clinical and epidemiologic evidence points to excessive ingestion of iodine as an environmental agent. In genetically determined thyroiditis in animals, iodine enrichment has been shown to increase the incidence and severity of disease. Its mechanism of action is still uncertain. Using a new animal model of autoimmune thyroiditis, the NOD.H2 h4 mouse, we have been able to show that iodine enhances disease in a dose-dependent manner. Immunochemical studies suggest that iodine incorporation in the thyroglobulin may augment the antigenicity of this molecule by increasing the affinity of its determinants for the T-cell receptor or the MHC-presenting molecule either altering antigen processing or by affecting antigen presentation.

Original languageEnglish (US)
Pages (from-to)97-103
Number of pages7
JournalAutoimmunity Reviews
Volume1
Issue number1-2
DOIs
StatePublished - Feb 1 2002

Keywords

  • CLT: chronic lymphocytic thyroiditis
  • Hashimoto's disease
  • Iodine
  • MHC: major histocompatibility complex
  • NOD.H2
  • RFLP: restriction fragment length polymorphism
  • TPO: thyroid peroxidase
  • Tg: thyroglobulin
  • Thyroglobulin
  • Thyroiditis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Fingerprint Dive into the research topics of 'Iodine: An environmental trigger of thyroiditis'. Together they form a unique fingerprint.

Cite this