Functionally, using experimental autoimmune encephalomyelitis (EAE) as a pre-clinical mouse model for MS, we showed that Tc17 cells provided “reverse help” for the encephalogenicity of IL-17-producing CD4+ T (Th17) cells via their hallmark cytokine IL-17A12, revealing an important Tc17-dependent enhancement of Th17-mediated autoimmunity of the CNS. This evidence concerns the gene CD4 and myeloid sarcoma.