文摘
Developmentally regulated GTP-binding protein 2 (DRG2) represents a novel subclass of GTP-binding proteins. We here report that transgenic overexpression of DRG2 in mice ameliorates experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis (MS). The protective effect of DRG2 in EAE was mediated by the inhibition of the development of Tb>Hb>17 cells. DRG2 enhanced the activity of PPAR纬, which led to an inhibition of the nuclear factor kappa B (NF-魏B) activity and IL-6 production in antigen presenting cells and an inhibition of the development of Tb>Hb>17 cells. Our results demonstrate that DRG2 is an essential modulator of EAE.