FOXP3 and experimental autoimmune encephalomyelitis: According to one report, in the experimental autoimmune encephalomyelitis (EAE) model in which the Th17 immune response is pathogenic, pre-treatment with CAPE inhibited the translocation of NF-κB in T cells and further increased the expression of Foxp3 in T cells, which promoted the differentiation of regulatory T cells in tissues, leading to the inhibition of EAE development [56].