Male Rag1 鈭?鈭?mice and wild type mice were subjected to partial hepatic IRI. Anti-NK1.1 (300 渭g/mouse, ip) was used to deplete NK cells. Liver injury was evaluated by level of serum alanine aminotransferase (ALT). Hepatic inflammatory cytokines, neutrophils and CXCL-2 expression were measured following ischemia and reperfusion. Additionally, NK cells were cultured with or without IL-6, IL-21, IL-23 and IL-10 for 24 h, then IL-17A level in the supernatants was analyzed by ELISA. Production of IL-17A was increased in NK cells after reperfusion. Various cytokines such as, IL-6, IL-21 and IL-23, which also elevated after IRI, can promote IL-17A production and up-regulate the phosphorylation of STAT3 in NK cells, while the increase was repressed in the presence of IL-10. Depletion of NK cells decreased IL-17A level in Rag1 鈭?鈭?mice ischemic lobes. Meanwhile, hepatic infiltration of neutrophils and CXCL-2 level were reduced and liver injury was ameliorated. Neutralization of IL-17A was used to confirm the role of this cytokine produced by NK cells in Rag1 鈭?鈭?mice. In conclusion, at initial stage of liver IRI, NK cells increase IL-17A production and promote liver injury.