Abstract: The aim of present study was to explore the effect of triptolide derivative LB-1 on imiquimod (IMQ) induced psoriasiform inflammation in BALB/c mice, and to investigate the immune mechanism of LB-1 in the prevention and treatment of psoriasis. In the present study, topical application of IMQ for seven days induced the psoriasiform inflammation in BALB/c mice. This is a promising mouse model of psoriasis for the natural immune reaction compared to those induced by xenograft, trangenic or gene knockout. psoriasis area and severity index (PASI) score, hematoxylin-eosin (HE) staining and flowcytometry were employed to investigate the changes of psoriasiform inflammation, histopathological response and percentage of T cells, respectively. The result showed that LB-1 significantly attenuated the psoriasiform inflammation. Com-pared with model group, PASI score were decreased in the LB-1 group. In the isolated immunocytes of spleen, LB-1 decreased percentage of CD8⁺ (P < 0.01) T cells and increased the ratio of CD4⁺/CD8⁺ T cells at the dosage of 2 mg·kg^-1 (P < 0.01), whereas LB-1 raised percentage of CD4⁺ T cells and CD3⁺ T cells at the dosage of 4 mg·kg^-1. In conclusion, the present study demonstrated that LB-1 attenuated psoriasiform inflammation induced by imiquimod in BALB/c mice. The mechanism of LB-1 action may be related to change percentage of CD4⁺ T, CD8⁺ T cells in the spleen. These results provide a basis for LB-1 or other triptolide derivative in the intervention of psoriasis in the future.