Graves’ disease is caused by autoantibodies that bind thyroid-stimulating hormone receptors (TSHR) in the thyroid gland, causing the production and release of excess thyroid hormone and accelerating metabolic activity. These autoantibodies also lead to Graves’ orbitopathy (thyroid eye disease) in about half of patients with Graves’ disease, causing ocular inflammation, pain, bulging of the eyes and double vision.
Current treatments for Graves’ disease can be highly intrusive and burdensome. Radioactive iodine treatment or thyroidectomy are often used to shrink or remove the thyroid, and require lifelong hormone replacement. Our goal is to develop a first-of-its-kind treatment to directly target the autoantibodies that cause this difficult-to-manage disease, while sparing healthy thyroid signaling.