The Mechanism Of IGF-IR In Thyroid-associated Ophthalmopathy And Progress In Its Treatment

Thyroid-associated ophthalmopathy is an autoimmune disease that is potentially blinding and disfiguring.B cells and T cells have been proved to be key participants in TAO.The orbital fibroblast represents the central target for immune reactivity.It is critical factor in the pathogenesis of thyroid ophthalmopathy.The role for TSHR and TSI is considerably less well established.Many circumstantial pieces of evidence suggest that TSHR and TSAb may be involved.The pathogenesis of TAO is not completely clear.Recent studies show that insulin-like growth factor-I receptor(IGF-IR)is also involved in the pathogenesis of TAO.It not only participates in the pathogenesis of TAO through its own pathway,but also complex with TSHR and participates in the pathogenesis of TAO.Currently available therapies for active TAO are viewed widely as inadequate and have proven to be ineffective in many patients,especially those with particularly severe disease.As insulin-like growth factor-I receptor(IGF-IR)is involved in the pathogenesis of TAO,the signal transduction initiated by any receptor can be weakened by inhibiting the activity of IGF-IR,whichlays a foundation for targeted treatment of IGF-IR in active TAO.In clinical trials,The apparent effectiveness of teprotumumab and its promising side-effect profile make IGF-IR inhibition an exciting early step on the road.