Aim To study the effects of visfatin on the maturity of DC2.4 cells and the mechanism of visfatin in the pathogenesis of atherosclerosis. Methods The DC2.4 cells were divided into four groups: normal control group, LPS group （LPS, 1 mg/L）, low-dose visfatin group （100 μg/L） and high-dose visfatin dose group （200 μg/L）. MHC-II, CD86 and CD80 expression were detected by flow cytometry. Tumor necrosis factor-α （TNF-α） and interleukin-12 （IL-12） levels in cell culture supernatant were measured by enzyme-linked immunosorbent assay. The ability of visfatin to stimulate allogeneic T lymphocytes was measured by mixed lymphocyte reaction assay. Results Compared with the control group, the synaptic of cells enlarged and cell volume increased in low-dose visfatin group, high dose visfatin group and LPS group. The levels of MHC-Ⅱ, CD80 and CD86 molecule expression increased, the supernatant TNF-α, IL-12 levels were significantly increased （P<0.05）. Compared with the control group, when stimulating cell∶effector cell ratio was 1∶10 and 1∶25, visfatin low dose group and high dose group and visfatin stimulation index LPS group was significantly higher （P<0.05）. Conclusion The results suggested that visfatin could participate in the development of atherosclerosis by activating T lymphocytes and initiating the immune inflammation response.