Background: Fibrinogen-like protein 2 (FGL2),an immunosuppressive cytokine expressed by regulatory CD4+ T (Treg) cells,is identified to be important for immunomodulatory activity.However,the mechanism of FGL2 in (Inflammatory bowel disease)IBD is still unclear.We investigated expression of FGL2 and Interleukin (IL)-17 in the TNBS(trinitro-benzene-sulfonic acid)-induced colitis mice to identify the function of FGL2 based on effector CD4+ T helper (Th) 17 cells/Treg balance in the IBD.Methods: Clinical manifestation,colon macroscopic and histopathological score were evaluated in controls and mice with IBD.Expressions of FGL2,IL-17,and Tumor Necrosis Factor-a (TNF-a) protein in colon were detected by western blot and immunohistochemistry.Levels of those factors in plasma were measured by ELISA.The mRNA expressions of Forkhead boxp3 (Foxp3),retinoic acid related rphan receptor-gt (ROR-gt) and above-mentioned factors in colon and spleen mononuclear cells were examined by Real-time PCR.The differentiation of Th17/Treg cells in splenocytes was studied by flow cytometry.Results: Compared with control mice,TNBS-induced mice showed significant improvements of clinical manifestation,macroscopic and histopathological damage.The percentage of Treg cells was reduced,but Th17 cells were enhanced after TNBS challenge.Intestinal and peripheral expression of FGL2 were unexpectedly up-regulated in TNBS-induced mice,while that was decreased in spleen.Expression of IL-17 were higher in TNBS-induced mice.Conclusions: FGL2 and IL-17 levels were significantly higher,and the balance between Th17 and Treg cells was broken in the TNBS-induced colitis.Our data indicated that FGL2 was involved in the immunopathogenesis of IBD via Th17/Treg balance.