ObjectiveTo observe the therapeutic effect of resiquimod on atopic dermatitis model mice and explore its mechanisms.MethodsThirty BALB/c mice were randomly divided into blank group, model group, and treatment group, with 10 mice in each group. The atopic dermatitis model was induced by calcipotriol liniment (2 nmol daily for 14 d) on the ear in the model group and treatment group. At the same time, the model group was intraperitoneally injected with 200 μL phosphate-buffered saline (PBS) every day, and the treatment group was intraperitoneally injected with 50 nmol resiquimod (dissolved in 200 μL PBS) every day. The mice in the blank group was not given any treatment. On the 15^th day, the erythema, swelling and scale of the ear lesions of mice in each group were observed. The infiltration of inflammatory cells in skin lesions was observed by hematoxylin-eosin staining and toluidine blue staining. The levels of serum immunoglobulin E (IgE), interleukin (IL)-4 and IL-13 were detected by enzyme-linked immunosorbent assay. The expression of thymic stromal lymphopoietin (TSLP) and interferon γ mRNA in the skin lesions was detected by quantitative polymerase chain reaction.ResultsCompared with the blank group, erythema, swelling and scale appeared on the ear skin of mice in the model group, and the levels of serum IgE, IL-4 and IL-13 were significantly increased (all P < 0.01), indicating that the atopic dermatitis model was successfully constructed. Compared with the model group, the erythema, swelling, scale and infiltration of inflammatory cells of the ear lesions in the treatment group were improved, the levels of serum IgE, IL-4 and IL-13 were significantly decreased (all P < 0.05), and the mRNA expression of interferon γ was significantly increased (P < 0.05). The mRNA expression of TSLP in skin lesions was not significantly different between the model group and treatment group (P > 0.05).ConclusionResiquimod can improve the symptoms of atopic dermatitis mice, and its mechanism may be related to regulating helper T cell (Th)1/Th2 immune response and affecting the expression of related cytokines.