Abstract
Background: The pathogenesis of Graves’ ophthalmopathy (GO) and the mechanism for its link to thyroid autoimmunity is poorly understood. Our present research focuses on the role of the skeletal muscle calcium binding protein calsequestrin (CASQ1). Earlier studies showed that the CASQ1 gene was up-regulated in thyroid tissue from patients with GO compared to those with Graves’ hyperthyroidism (GH) without eye signs, however, the protein levels remained the same in both groups, raising the possibility that the orbital autoimmune reaction begins in the thyroid gland. Here, we measured the concentration of the CASQ1 protein in normal and Graves’ thyroid tissue, correlating levels with parameters of the eye signs, CASQ1 antibody levels and the CASQ1 gene polymorphism rs3838216, shown previously to be a risk factor for ophthalmopathy.
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