Aim To investigate the effect of heat shock protein 65 （HSP65） as the important inflammatory substances in atherosclerosis on cellular immune function and properties of high density lipoprotein in apoptotic human T cell lymphoma Jurkat cells in vitro and explore the possible molecular mechanisms of immune system and lipid metabolism. Methods Jurkat cells activated by 5 mg/L concanavalin A （ConA） were treated with different concentrations of HSP65, and the cell proliferation were detected by CCK-8 assay. The concentration of cytokines interferon-γ （IFN-γ） and interleukin-10 （IL-10） were measured by ELISA. Cholesterol efflux was assayed by liquid scintillation spectrometry. Expression of ABCA1, ABCG1, SR-BⅠ, PPARγ and LXRα mRNA were detected by RT-PCR, respectively. Results ConA enhanced the activity of Jurkat cells after 48 h incubation. HSP65 increased the proliferation activity of Jurkat cells gradually （P<0.001）. The cholesterol efflux and IL-10 level were significantly lower, whereas IFN-γ level elevated in 0.5 mg/L group and 1 mg/L group than those in control group （P<0.01）. Compared with control group, the treatment of Jurkat cells with 0.5 mg/L and 1 mg/L HSP65 resulted in a concentration-dependent decrease of ABCG1, ABCG1, SR-BⅠ, PPARγ, LXRα mRNA expression （P<0.01）. Conclusions HSP65 within the concentration range of 0.5～1 mg/L can promote the proliferation and intensify the cellular immune response, which may attenuate cholesterol efflux by down-regulating ABCG1, ABCG1, SR-BⅠ, PPARγ, LXRα mRNA expression in T cells.