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It is clear that there would be great advantage in having a reasonably exact experimental model for Graves' disease, since no spontaneous animal model has (at least yet) presented itself. Of course, spontaneous hyperthyroidism has appeared in animals, particularly cats (1), but these cases have had the characteristics of toxic nodular goitre, with no evidence of thyroid-stimulating antibody (TSAb) (2, 3). One might reasonably expect that an appropriate natural animal model would eventually appear but, so far, Graves' disease has been a uniquely human disorder, characterized by antibodies and T lymphocytes directed against the thyrotrophin receptor (TSHR), and by extrathyroidal features such as ophthalmopathy (4). Thus studies of the pathogenesis and experimental treatment of Graves' disease have had to be performed on the patients themselves, or in vitro (on the patients' thyrocytes and/or peripheral blood mononuclear cells), while an in vivo experimental model has long continued to be awaited.
Autoimmune
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