Objective：This study aims to observe the effects of neutralizing interleukin-17（IL-17）on bleomycin（BLM） induced idiopathic pulmonary fibrosis and PI3K/Akt/mTOR signaling pathway. Methods：C57BL/6 mice were randomly divided into control group，BLM group，neutralizing antibody group and autophagy inhibition group，respectively. BLM group，neutralizing antibody group and autophagy inhibition group were administrated BLM（5 U/kg） through a single intratracheal injection to induce idiopathic pulmonary fibrosis，while the control group was received the equivalent sterile saline. Meanwhile，autophagy inhibition group was injected 3-methyl adenine（3-MA） via intraperitoneal injection 5 times a week for 4 weeks. Other groups were given the same amount of sterile saline. Neutralizing antibody group and autophagy inhibition group were administrated neutralizing IL-17 mAb via caudal vein every 3 days from day 3 after model made. All mice were sacrificed after 28 days. Lung tissues were used to evaluate pulmonary fibrosis by Masson staining and collagen expression changes by hydroxyproline contents measurement. Bronchoalveolar lavage fluid was collected for transform growth factor-β1（TGF-β1） measurement by ELISA. The expression of LC3Ⅱ/LC3Ⅰ，Beclin-1，p62，p-PI3K/PI3K，p-Akt/Akt and p-mTOR/mTOR proteins were all assayed by Western blot. Results：Compared with BLM group，hydroxyproline content，TGF-β1 concentration and pulmonary fibrosis in neutralizing antibody group were significantly decreased（P < 0.01），the ratio of LC3Ⅱ/LC3Ⅰ and Beclin 1 expression significantly raised（P < 0.01，P < 0.05），p62 expression reduced remarkably（P < 0.05），and the ratio of p-PI3K/PI3K，p-Akt/Akt and p-mTOR/mTOR decreased significantly（P < 0.05）. Conclusion：The mechanism of IL-17 in pulmonary fibrosis is related to inhibition of autophagy. Neutralization of endogenous IL-17 can significantly attenuate BLM-induced pulmonary fibrosis，reduce the production of TGF-β1，inhibit the PI3K/Akt/mTOR signaling pathway，and activate cell autophagy.