Autoimmune thyroiditis research at Johns Hopkins University

Autoimmune thyroiditis is an organ-specific autoimmune disorder characterized by infiltration of the thyroid gland by lymphocytic inflammatory cells, often followed by hypothyroidism due to destruction and replacement of the follicular tissue. Dr. Noel Rose and members of his laboratory at Johns Hop...

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Bibliographic Details
Published in:Immunologic research 2010-07, Vol.47 (1-3), p.207-215
Main Author: Lynne Burek, C.
Format: Article
Language:English
Subjects:
Allergology
Animals
Autoantibodies - immunology
Autoimmune diseases
Baltimore
Biomedical and Life Sciences
Biomedical Research
Biomedicine
Disease Models, Animal
Humans
Immunology
Internal Medicine
Iodine - immunology
Medicine/Public Health
Mice
Mice, Inbred NOD
Molecular biology
Thymus Gland - immunology
Thymus Gland - pathology
Thyroglobulin - immunology
Thyroid diseases
Thyroiditis, Autoimmune - genetics
Thyroiditis, Autoimmune - immunology
Universities
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Summary:Autoimmune thyroiditis is an organ-specific autoimmune disorder characterized by infiltration of the thyroid gland by lymphocytic inflammatory cells, often followed by hypothyroidism due to destruction and replacement of the follicular tissue. Dr. Noel Rose and members of his laboratory at Johns Hopkins University have continued to study autoimmunity using autoimmune thyroiditis as a model. Autoimmune thyroiditis is multifactorial, with both genetic and environmental factors involved. We have studied familial association of thyroid antibodies in juveniles with either autoimmune thyroiditis or Graves’ disease. Epitope analysis of thyroglobulin autoantibodies showed that autoantibodies from unrelated patients with disease had greater similarity of epitope binding than members of their own family. Subclass analysis of thyroglobulin autoantibodies indicated that IgG2 was dominant in autoimmune thyroiditis. Much of our work focused around iodine as an environmental trigger of autoimmune thyroiditis. We showed that iodination of the human thyroglobulin molecule alters its immunoreactivity. We explored the role of excess iodine ingestion in exacerbating thyroiditis using the NOD.H2h4 mouse as a model. We found multiple effects of excess iodine, including changing the immunogenicity of the thyroglobulin molecule and the upregulation of ICAM-1 and ROS in the thyrocyte itself. These observations may help to delineate the mechanisms by which iodine exacerbates thyroiditis and to explain differences in the host response of genetically susceptible individuals compared to those who are resistant to disease.
ISSN:0257-277X
1559-0755
DOI:10.1007/s12026-009-8151-4