These data raise the questions of whether MS is mediated solely by Th1 cells or solely by Th17 cells, whether it is mediated by both pathways, or whether perhaps it is mediated by neither pathway [175] . There is growing evidence that autoreactive T cells (particularly Th1 and Th17 cells) participate in the pathophysiology of MS. Although the exact roles of Th1 and Th17 cells in the development of MS lesions are not well understood, it appears that both these effector T-cell populations can cause CNS inflammation and demyelinating lesions in MS and EAE [50, 178] .