Fig. 1.

Model of TSHR/IGF-1R crosstalk in TED pathogenesis. Activation of TSHR by GO-Igs in GOFs activates two signal transduction pathways − one that is independent of IGF-1R (dark gray arrow) and another that is dependent on IGF-1R (light gray arrows). TSHR and IGF-1R are in close proximity within a signalosome for which β-arrestin 1 (β-ARR) acts as a scaffold. TSHR- and IGF-1R-mediated pathways combine through crosstalk, leading to a more robust stimulation of HA secretion. Modified from Krieger et al. [7, 41].