Abstracts of the EUGOGO Global TED Forum 2025

highly express thyroid-stimulating hormone receptor (TSHR) and insulinlike growth factor-1 receptor (IGF-1R) on their surface, represent the core link in the immune imbalance of TED.Recent studies have demonstrated that, in addition to the classic T helper (Th) 1-and Th2-mediated inflammatory responses, Th17 cells can further induce orbital tissue remodeling, while cytotoxic T cells may be a critical factor contributing to tissue damage.TED-associated autoantibodies target the tightly bound "functional unit" of TSHR and IGF-1R, activate downstream signaling, promote OFs to release hyaluronic acid and inflammatory mediators, and induce their differentiation into orbital adipocytes, thereby forming a positive feedback loop.With the clinical application of biological agents targeting the neonatal Fc receptor (FcRN), interleukin (IL)-6R, and IGF-1R, it has become particularly important to clarify the mechanisms underlying the interaction between T cells and B cells via autoantibodies, cytokines, and co-stimulatory molecules.Myeloid cells secrete cytokines such as IL-6, tumor necrosis factor-α (TNF-α), and IL-23, which amplify the "crosstalk" between T cells and B cells and sustain the activation of OFs.Elucidating this complex immune-inflammatory network is expected to pave the way for novel approaches to the precise treatment of TED.