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Recent data suggests that the immune system is involved in atherogenesis. It is essential to adaptive immunity that antigen-presenting cells (APCs) such as dendritic cells (DCs) and monocytes present antigens to T cells to make proliferation and activation. Thus, interest has been raised as to the possible antigens that could serve as the adaptive immunity initiators to atherosclerosis. In the current work, murine heat shock protein 60(mHSP60) induced DC expression of costimulatory molecules (i.e., CD80, CD86). Moreover, mHSP60 boosts in secretion of the proinflammatory TH1 cytokine Interferon-y(IFN-y) by murine DCs; however TIC cytokine interleukin-10 (IL-10) no significance. mHSP60-stimulated APCs had a greater capacity to stimulate T-cell proliferation and cytokine secretion, as documented by mixed lymphocyte reactions and ELISA assays. To form murine model of atherosclerosis, we sequentia immunized with mHSP60-plused DCs (mHSP60-DC) to ApoE-/- mice fed by high-cholesterol diet (HCD). It indicated that mHSP60 significantly enhanced the recruitment of DCs to atherosclerotic lesions in vivo and reinforced the inflammatory of lesions to result in lesions unstable, however LPS-pulsed DC (LPS-DC) could not elicit these effects. mHSP60 activates DCs and augments their capacity to stimulate T-cell proliferation and cytokine secretion, Moreover these effects of mHSP60 contribute to its influence on the progression of atherosclerotic lesions.