〔Abstract〕 Objective To investigate the effects of metformin on the immune functions of immature dendritic cells （imDCs）and the underlying mechanisms. Methods Mouse bone marrow-derived imDCs were treated with differ⁃ ent concentrations of metformin. The working concentration and treatment time of metformin in this study were determined based on the results of cell apoptosis and cell viability assays. The effects of metformin on the phagocytic capacity of imDCs was evaluated using an antigen endocytosis assay. The expression of cluster of differentiation 205（CD205），the polymerization of filamentous actin（F-actin），and the underlying regulatory mechanisms were investigated through flow cytometry，laser confocal fluorescence microscopy，and Western blot. Results The working concentrations of metformin were 1，2，4 mmol/L for 24 h determined by the apoptosis and cell viability assays.Metformin significantly suppressed the phagocytic capacity of imDCs，down-regulated the expression of the man ⁃ nose receptor CD205 on the cell surface，which was closely associated with phagocytic function；Metformin inhib⁃ ited the RhoA-ROCK 1-LIMK 1-Cofilin signaling pathway，which inhibited the polymerization of F-actin and dis⁃ turbed its dynamic remodeling of imDCs. Conclusion Metformin can inhibit the expression of CD205 and disrupt the remodeling of F-actin，thereby suppressing the antigen-capturing capacity of imDCs.