An In Vitro Model for Thyroid Autoimmunity
Clinical observations have suggested an association between iodine intake and the occurance of autoimmune thyroiditis in man (1,2), while in areas with endemic goiter prevalence due to iodine deficiency a lower incident of Hashimoto’s thyroditis was found (3), Others, however, have contested these claims (4,5). Experimentally, this association has been demonstrated with genetically susceptible chicken (6), rats (7) and dogs (8) on a high iodized diet. In the present study, we were interested in the effect iodine would have on the functional immune response of human Tlymphocytes in co-cultures with autologous thyroid epithilial cells (TECs). Classically, only immunocompetent cells, namely macrophages are able to present antigen together with the immunregulatory class-II surface antigen(9)•These class-II antigens (in man HLA-D locii) can also be found in vivo (10) and induced by various agents in vitro(11) on TECs. With this background our in vitro model system was designed to i) modulate HLA-D expression on TECs and ii) to investigate,if a potential iodide induced autoantigen on TECs would be presented through HLA-D to autologous T-lymphocytes and thus initiate a proliferative cellular immunresponse. In order to modulate the hypothetical iodine induced autoantigen the influence of Methimazole (MMI) and perchlorate (PC) on the co-culture system was to be studied. MMI has been suspected to act immune suppressively during suppression therapy of Graves’ disease (GD) in vivo and on antibody synthesis in vitro (12). Interestingly, when MMI therapy in GD hyperthyroidism was compared to PC treatment, which clearly is no immuno suppressive agent, both drugs had the same effect on the production of thyroid stimulating antibodies (TSab) (13).
KeywordsIodine Deficiency Endemic Goiter Thyroid Epithelial Cell Thyroid Stimulate Antibody Autologous Mixed Lymphocyte Reaction
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