In mice, TGFβ and IL-6 have been the standard for Th17 cell differentiation. Recently, variations for Th17 development have been found by using assorted combinations of Th17-related cytokines, including IL-21 and IL-1β. In humans, the role of TGFβ is slightly more controversial, as multiple reports have pleaded both the case for and against its role in Th17 differentiation. IL-17, one of the major products of Th17 cells, induces inflammation by recruiting and activating neutrophils and granulocytes through CXCL8 induction.

Murine naïve T cells do not express IL-23R or RORγt. IL-6, like many Th17 cytokines, signals through STAT3, which leads to production of IL-21. IL-21 works in a positive feedback fashion to promote a Th17 bias. Upon activation, Th17 cells can express IL-23R. IL-23 is required for the expansion and maintenance of Th17 populations. It should be noted that human, naïve CD161+, CD4+ Th17 precursor cells express IL-23R and RORγt even without activation.

References: 
Annunziato F, et al. 2008. Int. Immunol. 20:1361.
Awasthi A, et al. 2009. Int. Immunol. 21:489.