Figure 1.

Schematic representation of thyroid eye disease pathophysiology. The backbone of TED pathogenesis involves the uncontrolled activation of orbital fibroblasts by thyroid-stimulating autoantibodies, IGF-1R autoantibodies, and through the proinflammatory microenvironment created by T- and B-cells. Activated orbital fibroblasts lead to adipogenesis, which is involved in proptosis and orbital fat expansion, as well as glycosaminoglycan, hyaluronan, and proteoglycan production, markers involved in scar formation. The figure was created with BioRender.com.