Thyroid eye disease (TED) is an autoimmune disorder that manifests in the orbit. In TED, the connective tissue behind the eye becomes inflamed and remodels with increased fat accumulation and/or increased muscle and scar tissue. As orbital tissue expands, patients develop edema, exophthalmos, diplopia, and optic neuropathy. In severe cases vision loss may occur secondary to corneal scarring from exposure or optic nerve compression. Currently there is no cure for TED, and treatments are limited. A major breakthrough in TED therapy occurred with the FDA approval of teprotumumab, a monoclonal insulin-like growth factor 1 receptor (IGF1R) blocking antibody. Yet, teprotumumab therapy has limitations, including cost, infusion method of drug delivery, variable response, and relapse. We describe approaches to target orbital fibroblasts and the complex pathophysiology that underlies tissue remodeling and inflammation driving TED. Further advances in the elucidation of the mechanisms of TED may lead to prophylaxis based upon early biomarkers as well as lead to more convenient, less expensive therapies.

甲状腺眼病 (TED) 是一种发生在眼眶的自身免疫性疾病。在 TED 中，眼睛后面的结缔组织发炎并重塑，脂肪堆积增加和/或肌肉和疤痕组织增加。随着眼眶组织扩张，患者会出现水肿、眼球突出、复视和视神经病变。在严重的情况下，继发于暴露或视神经受压的角膜瘢痕可能会导致视力丧失。目前没有治愈 TED 的方法，治疗方法也很有限。TED 疗法的重大突破发生在 FDA 批准 teprotumumab 之后，teprotumumab 是一种单克隆胰岛素样生长因子 1 受体 (IGF1R) 阻断抗体。然而，teprotumumab 疗法具有局限性，包括成本、药物输送的输注方法、可变反应和复发。我们描述了靶向眼眶成纤维细胞的方法以及构成组织重塑和炎症驱动 TED 基础的复杂病理生理学。在阐明 TED 机制方面的进一步进展可能会导致基于早期生物标志物的预防以及更方便、更便宜的治疗。