The malfunctioning of regulatory T cells (Tregs) is crucial in the development and progression of Graves’ disease (GD). Programmed cell death 1 (PD-1) induces FoxP3 expression in Tregs and increases their suppressive function. The function of thyroid hormone in the PD-1 expression of Tregs in GD and whether aberrant PD-1 expression contributes to Treg breakdown remain largely unknown. To investigate the role of PD-1 in Treg activity and triiodothyronine (T3) in PD-1 expression in GD patients and mice given T3. Researchers enlisted the help of 30 GD patients and 30 healthy donors. The expression of PD-1 in Tregs and the function of Tregs were studied. T3 was utilized to treat human peripheral blood mononuclear cells in order to assess the impact of thyroid hormone on PD-1 expression in Tregs (PBMCs). They next administered T3 to mice to establish the effect of thyroid hormone on PD-1 expression in Tregs and Treg activity in vivo. In individuals with GD, PD-1 expression in Tregs and Treg suppressive activity were dramatically reduced. T3 inhibited PD-1 expression in human Tregs in vitro in a concentration- and time-dependent manner.

Treg dysfunction in GD patients may be caused by PD-1 downregulation in Tregs caused by elevated serum T3 levels.