Thyroid-associated ophthalmopathy(TAO)is an organ-specific autoimmune disease closely associated with autoimmune thyroid diseases. It is pathologically characterized by orbital fibroblast activation, glycosaminoglycan accumulation and extraocular muscle fibrosis, which seriously impair patients' visual function and quality of life. Autoimmune response imbalance constitutes the core pathogenesis of TAO, among which the disturbance of T helper 17 cell(Th17)and regulatory T cell(Treg)homeostasis plays a pivotal role in disease progression. This paper reviews the research progress of Th17/Treg cell imbalance in TAO. It firstly summarizes the immunopathological mechanism of TAO and clarifies the roles of thyroid-stimulating hormone receptor, insulin-like growth factor-1 receptor and various orbital autoantigens. Then it elaborates the biological characteristics and functional balance mechanism of Th17 and Treg cells, covering the regulatory roles of retinoic acid-related orphan receptor γ t, the key transcription factor for Th17 cell differentiation, and forkhead box protein P3, the core functional molecule of Treg cells. Furthermore, it concludes the clinical evidence of Th17/Treg imbalance in TAO patients, as well as the specific mechanism by which Th17 cells drive intraorbital inflammation via secreting pro-inflammatory factors such as interleukin-17A, and the immune dysregulation caused by the reduced number and functional defects of Treg cells. Finally, it sorts out therapeutic strategies targeting this imbalance, including research advances in cytokine antagonism, epigenetic regulation, immune checkpoint intervention and other directions, and points out the deficiencies and future prospects of current studies. This review aims to provide references for the research on immunopathological mechanisms and precise clinical treatment of TAO.

梅州市医药卫生科研项目(No.2023-B-32)