Serum amyloid A (SAA) is an acute phase protein with pro-inflammatory cytokine-like properties. Recent studies have revealed that SAA promotes γδT cell to produce IL-17 and T helper 17 (Th17) cells differentiation and function. In this study, we established the hepatic SAA1 overexpressed transgenic mice (TG). In this mouse, IL-17 was significantly increased in conditional state by γδT cell. We revealed that SAA1 mediated IL-17 producing from γδT cell is dependent on TLR2. Moreover we immunized SAA1 TG mice with Complete Freund’s adjuvant (CFA), which is well-known inducer of Th1 response and IFN-γ. We observed increased IL-17 secretion with increased Th17 cells and decreased IFN-γ, which is contrast to wild type mice (WT). In addition, we showed that locally increased transforming growth factor- β (TGF-β) followed by Th17 cells polarization might involve in Th17 cell maintenance by suppressing the expression of T-bet, a key transcription factor for the differentiation of T helper 1 (Th1) cells. These data demonstrate that SAA1 represent potent endogenous protein that drives IL-17 induced inflammation by γδT cell partially through TLR2 and by Th17 cell. Also these increased IL-17 response maintained by TGF-β Smad2/3 signaling. Therefore we could say that SAA is central player in IL-17 related inflammatory response.