Abstract
The immunopathogenesis of Graves' ophthalmopathy (GO) is still incompletely understood. Attention has shifted from the TSH receptor (TSHR) to the IGF-I receptor (IGF-1R) as a major autoantigen. This review on the pathophysiology of GO focused on orbital fibroblasts and the question whether autoimmunity against TSHR or IGF-1R is primarily involved.