The notion that Graves' ophthalmopathy is an autoimmune disease has been based primarily on the clinical associations between it and Graves' hyperthyroidism, and on the frequently beneficial response of the disease to immunosuppressive therapy. Recent advances in molecular biology have led to new insights into the pathogenesis that support an autoimmune basis for this condition. In particular, there is now compelling - although not definitive - evidence that, if verified, would represent disease transfer by thyroid- secreting hormone receptor-sensitized T cells. Future studies using animal models and in vitro systems will allow definitive identification of the immune cell types, autoantigens, and autoantibodies involved in the pathogenesis of Graves' ophthalmopathy.
|Number of pages
|Endocrinology and Metabolism Clinics of North America
|Published - 2000
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism