IL6 and experimental autoimmune encephalomyelitis: Heink et al. have reported that the IL-6 cluster signaling transmitting by Sirpα+ DCs promotes the differentiation of pathogenic Th17 cells by inducing earlier activation of STAT3 signaling and more robust expression of IL-23R, while the classical IL-6 signaling suppresses the differentiation of Foxp3+ Treg cells in experimental autoimmune encephalomyelitis (EAE) [22].