Recently, the levels of IL17 produced by MBP-stimulated peripheral blood cells obtained from MS patients or controls were shown to correlate with the active lesions in MS patients observed with magnetic resonance imaging (MRI) [36] . Like other Th subsets, the Th17 lineage is activated by a specific cytokine milieu. However, IL23 cannot produce Th 17 cells de novo from naïve T cells, and the IL23 receptor (IL23R) is not expressed on naïve T cells [37] . Transforming growth factor β (TGFβ) upregulates IL23R expression, thereby conferring responsiveness to IL23, which confirms that TGFβ is a critical cytokine in the commitment to Th17 expansion in vitro and in vivo [38] . In mice, TGFβ together with IL6 can activate antigen-responsive naïve CD4 + T cells to develop into Th17 cells [39] . In humans, naïve CD4 + cells exposed to IL6, TGFβ, and IL21 can develop into Th17 cells, and the production of IL23 plays a role in maintaining these Th17 cells [40, 41] . Altogether, Th17 cells require IL23, TGFβ, IL6, and IL1 for their generation. Th17 cells produce IL17A and IL17F, which are upregulated in chronic lesions [42] , and IL22, which is also involved in the pathogenesis of MS. Thus, Th17 cells are a recently discovered, unique Th lineage that produces a repertoire of signature cytokines, including IL17A, IL17F, IL21, and IL22, that are essential for the development of autoimmune diseases such as MS [43] .