Functional role of dendritic cells in patients with unstable angina.

To investigate the function of dendritic cells (DC) in patients with unstable angina, 10 mL of blood was drawn from 30 subjects. 15 patients diagnosed as having unstable angina and 15 healthy subjects were included in an observation and a control groups respectively. The mononuclear cells were separated from the peripheral blood and cultured in RPM11640 supplemented with recombinant human granulocyte/macrophage-colony stimulating factor (rh GM-CSF) and recombinant human interleukin-4 (rh IL-4) to induce dendritic cells. The shape and ultrastructure of DC was examined with electronic microscope. The phenotype of DC was analyzed with FACS and the alloantigen presenting capacity of DC was evaluated by mixed lymphocyte reaction (MLR). The expression rate of CD86 of DC in patients with unstable angina was (40.7 +/- 3.6) %, which was obviously higher than that of normal DC (29.6 +/- 2.5%) ( P < 0.001). The capacity of the DCs in unstable angina patients to induce allogenic T cells (OD 2.73 +/- 1.10), was significantly higher than that of the normal DC (OD:0.9 +/- 0.21) (P < 0.005). It is suggested that the function of DC in patients with unstable angina is increased, which may play an important role in the initiation of immune reaction in the plaque.

Functional Role of Dendritic Cells in Patients with Unstable Angina / 华中科技大学学报（医学）（英德文版）

To investigate the function of dendritic cells (DC) in patients with unstable angina, 10 mL of blood was drawn from 30 subjects. 15 patients diagnosed as having unstable angina and 15 healthy subjects were included in an observation and a control groups respectively. The mononuclear cells were separated from the peripheral blood and cultured in RPMI1640 supplemented with recombinant human granulocyte/macrophage-colony stimulating factor (rh GM-CSF) and recombinant human interleukin-4 (rh IL-4) to induce dendritic cells. The shape and ultrastructure of DC was examined with electronic microscope. The phenotype of DC was analyzed with FACS and the alloantigen presenting capacity of DC was evaluated by mixed lymphocyte reaction (MLR). The expression rate of CD86 of DC in patients with unstable angina was (40.7±3.6) %, which was obviously higher than that of normal DC (29.6±2.5 %) (P<0.001). The capacity of the DCs in unstable angina patients to induce allogenic T cells (OD 2.73±1.10), was significantly higher than that of the normal DC (OD:0.9±0.21) (P<0.005). It is suggested that the function of DC in patients with unstable angina is increased, which may play an important role in the initiation of immune reaction in the plaque.

Effects of Ginkgo leaf extract on function of dendritic cells and Th1/Th2 cytokines in patients with unstable angina pectoris / 中国结合医学杂志

<p><b>OBJECTIVE</b>To investigate the effects of Ginkgo leaf extract (GLE) on function of dendritic cells (DC) and Th1/Th2 cytokines in patients with unstable angina pectoris (UAP).</p><p><b>METHODS</b>Fifty-four patients with UAP were equally assigned into two groups, the treated group and the control group, both treated with conventional Western medicine, but with GLE given additionally to the treated group. Blood of all patients was taken before and 4 weeks after treatment to prepare the peripheral mononuclear cells, then which were incubated in the completed medium containing granulocyte-macrophage colony stimulatory factor (GM-CSF) and interleukin-4 (IL-4) to induce mature DC. The expression of co-stimulating factor CD86 (B7-2) on the surface of DC was detected by flow cytometry, and the stimulating capacity of DC was determined by mixed lymphocyte reaction (MLR). The blood levels of cytokines, interferon-gamma (IFN-gamma), and IL-4, were analyzed by ELISA, and blood C-reactive protein (CRP) level by turbidimetry. Moreover, the direct effect of Ginkgolide B on CD86 expression on DC were also tested in vitro.</p><p><b>RESULTS</b>After treatment, CD86 expression on DC, the stimulating capacity of DC as well as levels of IFN-gamma and CRP were lowered in both groups (P < 0.05 or P < 0.01), but the changes were much more significant in the treated group than those in the control group. Ginkgolide B showed a direct inhibitory effect on the CD86 expression on DC.</p><p><b>CONCLUSION</b>The inhibition of GLE on DC and thereby the suppression on inflammatory reaction may be one of the mechanisms of GLE in treating patients with UAP.</p>

Differentiation of dendritic cells in monocyte cultures isolated from patients with unstable angina.

OBJECTIVE: 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. METHODS: 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. RESULTS: 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-alpha (40.05+/-7.15 pg/ml), IL-1beta (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. CONCLUSION: 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.

[Effects of atorvastatin on the function of dendritic cells in patients with unstable angina pectoris].

OBJECTIVE: To investigate the function of dendritic cells (DC) in patients with unstable angina pectoris (UAP) and the effects of atorvastatin on it. METHODS: 27 patients with UAP were divided into two groups treated respectively with regular pharmacotherapy and regular pharmacotherapy plus atorvastatin. PBMC from the UAP patients (before and 2 weeks after the treatment) and 11 healthy subjects were incubated and induced to mature DC in a completed medium containing GM-CSF and IL-4. Flow cytometric analysis was used to detect the expression of co-stimulating factor CD86 (B7-2) on DC. The stimulating capacity of DC was determined in allogenic mixed lymphocyte reaction (MLR). ELISA was used to analyze the level of cytokines (IL-1beta, IL-6, IL-10 and TNF-alpha) in the medium of MLR. Relationship of expression of CD86 to risk factors and blood CRP level was also analyzed. RESULTS: When compared with normal group, CD86 on DC was much more expressed in UAP patients; the stimulating capacity of DC in MLR was higher; T lymphocytes in MLR secreted higher levels of pro-inflammation cytokines (IL-1beta, IL-6 and TNF-alpha) and lower level of anti-inflammation cytokine (IL-10). Blood LDL-C before treatment was positively related to the expression of CD86. Atorvastatin inhibited the function of DC and lowered blood level of CRP and CD86, the levels of which were significantly positively correlated. CONCLUSIONS: DC in UAP are activated, which may play an important role in initiating immune reaction in the plaque. LDL-C may be one of the activators of DC; inhibitory effect of atorvastatin on inflammation in UAP may be due to its inhibition on DC.