OBJECTIVE： To study the regulatory effect of lentinan （LTN） on immune function in ulcerative colitis （UC） rats and its mechanism. METHODS： 64 SD rats were randomly divided into normal group （12 rats） and modeling group （52 rats）. UC model was induced in modeling group by a compound method of 2，4-dinitrochlorobenzene （DNCB） acetone and 2，4-DNCB ethanol. After modeling， rats were randomly divided into model group， positive group （sulfasalazine tablet， 300 mg/kg）， LTN low-dose， medium-dose and high-dose groups （0.2， 0.4， 0.8 mg/kg）， with 10 rats in each group. Treatment groups were given relevant medicine intragastrically， and normal group and model group were given normal saline intragastrically， once a day， for consecutive 15 d. The levels of CD3+，CD4+，CD8+ in peripheral blood lymphocytes （PBMC） and the levels of TNF-α， IL-2， IL-4 and IL-10 in colon were all determined， and the pathological changes of colon tissue were observed. RESULTS： Compared with normal group， the levels of CD3+，CD4+，CD8+， the ratio of CD4+/CD8+， and the levels of IL-4 and IL-10 decreased significantly， while the levels of TNF-α and IL-2 in colon tissue significantly increased （P＜0.05）； obvious ulcerative lesion was observed in colon tissue （concentrated in grade Ⅱ and Ⅲ）. Compared with model group， the levels of CD3+，CD4+，CD8+， the ratio of CD4+/CD8+， and the levels of IL-4， IL-10 increased significantly， while the levels of TNF-α， IL-2 in colon tissue significantly decreased （P＜0.05）； the inflammation of colon tissue was significantly reduced， and the ulcer formation was significantly improved. CONCLUSIONS： LTN has a certain improvement effect on UC model rats， and its mechanism may be related to enhancing the immune function.