Abstract
Clinical observations, including the close temporal relationship between the diagnoses of Graves’ hyperthyroidism and Graves’ orbitopathy (GO), have long suggested that these two autoimmune conditions may share pathophysiologic features. The demonstration of TSHR expression in orbital fibroblasts, the target cells in GO, supported the notion of a common autoantigen. Subsequent studies from several laboratories measured elevated TSHR expression in GO orbital fibroblasts and described associations between levels of circulating TSHR autoantibodies (TRAb) and disease activity or poor prognosis. Using monoclonal stimulatory TRAb, TSH, an activating mutant TSHR, or purified IgG from patients with Graves’ disease (GD-IgG), several research groups demonstrated direct effects of TSHR or IGF-1R activation on GO orbital fibroblast functions relevant to disease development. Additional studies suggested that physical and/or functional relationships may exist between TSHR and IGF-1R in GO. A current concept integrating these findings is that activation of both receptors within the orbit, perhaps by TRAb as well as locally produced IGF-1, may be involved in the development of the ocular manifestations of Graves’ disease.
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Bahn, R.S. (2015). Pathogenesis of Graves’ Orbitopathy. In: Bahn, R. (eds) Graves' Disease. Springer, New York, NY. https://doi.org/10.1007/978-1-4939-2534-6_13
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DOI: https://doi.org/10.1007/978-1-4939-2534-6_13
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