MS is the most common disabling CNS disease in young adults. It is characterized by recurrent relapses and/or progression, which are attributable to multifocal inflammation, demyelination, and axonal pathology within the brain and/or spinal cord [175] . The effector Th cells play a well-recognized role in the initiation of autoimmune tissue inflammation, and these autoreactive effector CD4 + T cells have an established association with the pathogenesis of this disorder [17] . However, in models thought to be driven by Th1 cells, mice lacking the hallmark Th1 cytokine IFNγ were not protected from EAE but tended to display enhanced susceptibility to this disease [26] . The identification of Th17 cells has shed light on this apparent discrepancy. Like Th1 cells, polarized Th17 cells have the capacity to cause inflammation and autoimmune disease. A deficiency of the Th17-related cytokine IL23, but not of the Th1-related cytokine IL12, induces resistance to EAE, implying that Th17 cells are the chief contributors to EAE/MS [28] , whereas Th1 cells can consistently transfer EAE disease [16, 17] . Komiyama et al. demonstrated that EAE was significantly suppressed in Il17 −/− mice, manifested as delayed onset, reduced maximum severity, ameliorated histological changes, and early recovery [176] . However, the outcomes have varied when the differentiation and/or functions of Th17 cells have been blocked in clinical trials of human autoimmune diseases, with notable success only in psoriasis and Crohn's disease, but negative results in relapsing/remitting MS. The strategy of inhibiting the Th17 response has had even less support in preclinical studies in animal models [177] .