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Linking iodine with autoimmune thyroiditis.
N R Rose1, L Rasooly, A M Saboori
1Department of Molecular Microbiology and Immunology, The Johns Hopkins Medical Institutions, Baltimore, MD 21205, USA. nrrose@jhsph.edu
Environmental Health Perspectives
|September 30, 1999
Summary
Iodine exposure directly triggers autoimmune thyroiditis by altering thyroglobulin structure and enhancing T-cell responses. This study highlights iodine
Area of Science:
- Immunology
- Endocrinology
- Autoimmunity
Background:
- Circumstantial evidence links iodine to increased autoimmune thyroiditis.
- Human T cells show specific proliferation to iodinated thyroglobulin.
Purpose of the Study:
- To investigate the direct role of iodine in inducing autoimmune thyroiditis.
- To elucidate the molecular and immunological mechanisms involved.
Main Methods:
- Human T-cell proliferation assays with iodinated/non-iodinated thyroglobulin.
- Monoclonal antibody analysis of antigenic determinants.
- Utilizing the nonobese diabetic (NOD)-H2(h4) mouse model with iodine supplementation.
- Adoptive transfer of immune cells.
Main Results:
- Iodine alters thyroglobulin conformation, creating new antigenic determinants, including one linked to thyroxine.
- Iodine supplementation markedly increases autoimmune thyroiditis prevalence and severity in NOD-H2(h4) mice.
- Immune responses are specific to thyroglobulin, with IgG2b antibody predicting lesions.
- Iodine feeding enhances T-cell responses to thyroglobulin in susceptible mice.
Conclusions:
- Iodine acts as an environmental trigger, increasing the autoantigenic potency of thyroglobulin.
- This leads to the induction of autoimmune thyroiditis in genetically susceptible individuals.
- The NOD-H2(h4) mouse model is valuable for studying iodine's role in autoimmunity.