p19, a novel cytokine heavy-chain homologue of the IL6 subfamily, was discovered as a computational sequence [27] . When the p19 chain is linked to the p40 chain, a subunit of IL12 (another subunit of the IL12 heterodimers is the p35 chain), it forms a novel cytokine designated IL23. Therefore, the deletion of IL12p40 will affect the functions of both IL12 and IL23. Cua and colleagues verified that Il23 but not Il12 is essential for the induction of EAE by generating Il23p19 knockout (KO) mice and comparing them with IL12p35 KO mice [28] . Furthermore, an IL17-producing Tcell subset, driven and expanded by IL23, can pathogenically induce EAE when adoptively transferred into naïve wildtype mice [29, 30] . These IL17-producing T cells were dramatically reduced in the CNS of IL23p19-deficient mice. Based on these studies, researchers confidently suggested that IL17-producing CD4 + T cells are a distinct and novel Th subset that exacerbates autoimmunity, and designated them Th17 cells [31, 32] . Th17 cells are a Th-cell subset distinct from Th1 and Th2 cells in terms of their differentiation, expansion, and effector functions [33, 34] . The discovery of Th17 cells further clarifies the cytokine profile of MS [35] .