Abstract
Like most cancers, autoimmune diseases generally are due to the interaction of a number of genetic traits with an environmental trigger. Autoimmune thyroiditis, a model of organ-specific autoimmune disease, is associated with iodine as a precipitating environmental factor. T cells from patients with chronic thyroiditis proliferate in response to normal human thyroglobulin, but fail to react with non-iodinated thyroglobulin. Using a selected monoclonal antibody, we were able to identify a binding site on thyroglobulin containing iodinated thyronine. The greatest affinity was for tetraiodothyronine and binding depended upon the number as well as the positions of iodines. We have also studied an inbred strain of mice, NOD- H2(b4), that developed thyroiditis spontaneously. The onset of disease was hastened in a dose-dependent manner by adding iodine to the drinking water. The occurrence of disease was greater in conventional than in specific pathogen-free mice and correlated with T-cell proliferation and IgG(2b), antibody to thyroglobulin.
Original language | English (US) |
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Pages (from-to) | 511-517 |
Number of pages | 7 |
Journal | Critical reviews in immunology |
Volume | 17 |
Issue number | 5-6 |
State | Published - 1997 |
Keywords
- Autoimmune disease
- Environmental trigger
- Iodine
- Thyroiditis
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology