Acacetin regulated the reciprocal differentiation of Th17 cells and Treg cells and mitigated the symptoms of collagen-induced arthritis in mice.

BACKGROUND AND AIM: The immune-regulative effect of acacetin on the development of autoimmune arthritis remains unexplored. This study aims to investigate the potential effect of acacetin on the treatment of collagen-induced arthritis (CIA) in mice and clarify its underlying mechanism. METHODS AND RESULTS: In a type II collagen (CII)-induced autoimmune arthritis model, acacetin significantly repressed the incidence of CIA, prevented the pathological alteration, and reduced CII-specific IgG and IgG1 levels. Flow cytometry assay suggested that the recipients of acacetin showed the expansion of Treg cells and the decreasing Th17 cells in spleen and inguinal lymph nodes after the initiation of CIA. In vitro experiment suggested that in addition to altering the pro-inflammatory production in dendritic cells, engagement of acacetin relieved the generation of Th17 cells and maintained the ratio of Treg cells under Th17-polarized condition. The addition of acacetin inhibited the T cell proliferation, as well as the expression of the transcriptional coactivator TAZ, which regulated the balance of Treg/Th17 immunity, in a dose-dependent manner. CONCLUSION: Our data demonstrated that acacetin mitigated the development of CIA and might be a potential agent for the treatment of autoimmune arthritis.