We synthesized the AP-conjugated cytoplasmic domain of CTLA-4, AP-ctCTLA-4, which showed significant suppression of IL-17A and induction of Foxp3 in vitro as well as the alleviation of experimental autoimmune encephalomyelitis (EAE), with reduced levels of pathogenic IL-17A+GM-CSF+ CD4 T cells. The gene discussed is CD4; the disease is experimental autoimmune encephalomyelitis.