The notion that Craves' ophthalmopathy is an autoimmune disease has been ba
sed primarily on the clinical associations between it and Graves' hyperthyr
oidism, and on the frequently beneficial response of the disease to immunos
uppressive therapy. Recent advances in molecular biology have led to new in
sights into the pathogenesis that support an autoimmune basis for this cond
ition. In particular, there is now compelling-although not definitive-evide
nce that, if verified, would represent disease transfer by thyroid-secretin
g hormone receptor-sensitized T cells. Future studies using animal models a
nd in vitro systems will allow definitive identification of the immune cell
types, autoantigens, and autoantibodies involved in the pathogenesis of Gr
aves' ophthalmopathy.