Objective：To investigate the effect and mechanism of narrow-band ultraviolet B（NB-UVB）in promoting vitamin D（VD） metabolism and alleviating imiquimod（IMQ）induced psoriasis -like dermatitis in mice. Methods：C57BL/6 mice were treated with IMQ cream on the back skin to induce psoriasis-like dermatitis. The levels of VD metabolites 25（OH）D₃ and 1，25（OH）₂D₃ in serum were detected，as well as the expression of VD receptor（VDR）mRNA in the skin lesions. After determining the irradiation energy of NB-UVB irradiated mice，the model group combined with NB-UVB irradiation was performed to observe mouse skin lesions. The levels of 25（OH）D3，1，25（OH）₂D₃ in serum，VDR and inflammatory factors[interleukin（IL）-17A，IL-23，tumor necrosis factor（TNF）-α，IL-1β] mRNA expression and inflammatory factors protein contents in skin lesions，and the proportion of CD3 + CD4 + IL -17A+ T cells were detected. After pretreatment with the specific inhibitor Dafadine - A to block cytochrome P450 family 27 subfamily A member 1 （CYP27A1，a key enzyme in vitamin D metabolism）activity，the mice underwent psoriasiform dermatitis induction followed by NB -UVB irradiation. Skin lesions were observed，the proportion of CD3 + CD4 + IL - 17A+ T cells，inflammatory factors and VDR mRNA expression in the skin lesions，and serum levels of 25（OH）D₃ and 1，25（OH）2D3 were detected. Results：The levels of 25（OH）D3 and 1，25（OH）2D3 in the serum of psoriasis - like mouse models and the mRNA expression of VDR in skin lesions were significantly reduced. After NB-UVB irradiation on psoriasis-like mouse model，compared to the model group，the levels of 25（OH）D3，1，25（OH）₂D₃ in the serum of the irradiated mice and the mRNA expression of VDR in the skin lesions were upregulated. The mRNA expression and content of inflammatory factors IL -17A，IL -23，TNF - α and IL -1β in the skin lesions were downregulated，and the proportion of CD3 + CD4 + IL -17A+ T cells was significantly reduced. Compared to the IMQ+NB -UVB group，Dafadine -A pretreated mice showed significantly decreased serum levels of 25（OH）D3 and 1，25（OH）2D3，reduced VDR mRNA expression in skin lesions，along with significantly increased proportions of CD3+ CD4+ IL-17A+ T cells and elevated inflammatory cytokine levels of IL-17A，IL-23，TNF-α and IL -1β in lesions. Conclusion：NB UVB irradiation ameliorates psoriasiform dermatitis and cutaneous inflammation in mice by promoting VD metabolism. Importantly，specific inhibition of CYP27A1 markedly attenuates the therapeutic effects of NB-UVB on both psoriatic skin lesions and associated inflammatory responses.