Dendritic cells(DC) stimulate T-cell proliferation and activation in the course of adaptive immunity. Its role in unstable coronary plaque in humans is unknown. So we investigated the functional role of DC in patients with unstable angina pectoris(US) using human monocyte-derived DC. Twenty milliliters of blood was drawn from the femoral artery of 20 patients, who underwent coronary angiography. Ten patients with a diagnosis of US and 10 patients with normal CAG were included in the observation and control groups, respectively. The mononuclear cells were separated from the peripheral blood and cultured in RPMI1640 with supplement of rh GM-CSF and rh IL-4 to induce DC. The shape and ultrastructure of DC was analyzed with electronic microscopy. The phenotype of DC was analyzed with FACS and the alloantigen presenting capacity of DC was evaluated by mixed lymphocyte reaction (MLR). The levels of cytokines in allogenic DC/T cell cultures were assayed by ELISA. The expression rate of CD86 in patients with US was 30.8±3.3%, which was obviously higher than that of normal DC(19.4±3.0%), P< 0.001. The capacity of proliferation of patients DC to induce allogenic T cells(OD 1.82±1.29), which was obviously higher than that of the normal DC(OD 0.81±0.41), P< 0.005. TNF-α.(40.05±7.15 pg/ml),IL-1β.(19.01±1.39 pg/ml) and IL-6 (40.80±16.04 pg/ml), produced during MLR were higher in patients with US than that of normal patients 7.85±1.10, 12.18±1.93 and 19.55±0.7, respectively, P< 0.05. IL-10(10.94±0.56 pg/ml) produced during MLR was lower in patients with US than that of normal patients (16.63±3.40 pg/ml), P< 0.05. Our results suggest that the function of DC in patients with US is increased and these activated effects of DC may play a primary role in the immune process of plaque rupture. Its role in unstable coronary plaque in humans is unknown. So we investigated the functional role of DC in patients with unstable angina pectoris (US) using human monocyte -derived DC. Twenty milliliters of blood was drawn from the femoral artery of 20 patients, who underwent coronary angiography. Ten patients with a diagnosis of US and 10 patients with normal CAG were included in the observation and control groups, respectively. The mononuclear cells were separated from the peripheral blood and cultured in RPMI 1640 with supplement of rh GM-CSF and rh IL-4 to induce DC. The shape and ultrastructure of DC was analyzed with electronic microscopy. The phenotype of DC was analyzed with FACS and the alloantigen presenting capacity of DC was evaluated by mixed lymphocyte reaction (MLR). The levels of cytokines in allogenic DC / T cell cultures were assayed by ELISA. The expression rate of CD86 i The capacity of proliferation of patients DC to induce allogenic T cells (OD 1.82 ± 1.29), which was obviously higher than that of normal DC (19.4 ± 3.0%), P <0.001 was significantly higher than that of the normal DC (OD 0.81 ± 0.41), P <0.005. TNF-α (40.05 ± 7.15 pg / ml), IL- 40.80 ± 16.04 pg / ml), produced during MLR were higher in patients with US than that of normal subjects 7.85 ± 1.10, 12.18 ± 1.93 and 19.55 ± 0.7, respectively, P <0.05.IL-10 (10.94 ± 0.56 pg / ml ) produced during MLR was lower in patients with US than that of normal patients (16.63 ± 3.40 pg / ml), P <0.05. Our results suggest that the function of DC in patients with US is increased and these activated effects of DC may play a primary role in the immune process of plaque rupture.