SIRT1-Regulated Abnormal Acetylation of FOXP3 Induces Regulatory T-Cell Function Defect in Hashimoto's Thyroiditis

Abstract

The findings demonstrate that the reduced FOXP3 expression level and Treg function defect in HT patients are regulated by SIRT1-mediated abnormal FOXP3 acetylation. Ex-527 may upregulate the FOXP3 acetylation level and subsequently increase the number and suppressive function of Treg cells.