Comparison of ECV-304 cells injured by the sera from patients with hypertension and type 2 diabetes mellitus

AIM: To compare the cellular injury model of ECV-304 induced by the sera from patients with the same blood stasis syndrome (BSS) in hypertension and type 2 diabetes mellitus (T2DM). METHODS: Studies were conducted in ECV-304 cell line, which was treated with different sera during growing, named as sera from patients with T2DM (with the sera from patients with BSS associated with T2DM), sera from patients with hypertension (with the sera from patients with BSS associated with hypertension) and control groups. The cell viability was measured by MTT colorimetry, and the morphological changes were identified by light microscopy and electron microscopy. The level of nitric oxide (NO) and endothelin (ET) in the cells was detected by nitric acid deoxidizing enzyme and non-balance method,respectively. Enzyme-linked immunosorbent assay (ELISA) was applied to assay von Willabrand factor (vWF), thrombomodulin (sTM) and endothelial cell protein C (EPCR) content in the cell culture supernatants. Intracellular free calcium ( _i) and cytoskeleton of the model cells were measured by laser scanning confocal microscopy (LSCM). RESULTS: The cells were damaged when treated with 100 mL/L sera for 24h. Compared with the control group, the level of NO, vWF, sTM, EPCR and intracellular calcium concentration in the damaged cells markedly increase while cell viability and the level of ET significantly decreased (P<0.05). Compared with the sera from patients with T2DM group, the excretion of NO and intracellular calcium concentration markedly increased while ET level, EPCR and cytoskeleton significantly decreased (P<0.05) in the cells induced by the sera from patients with hypertension. CONCLUSION: These results suggest that the sera of patients with BSS associated with T2DM or hypertension reduce cell viability and the level of ET, increase the level of NO, vWF, sTM, EPCR and intracellular free calcium ( _i) and damage cell shape and cytoskeleton. The results also clearly show that the changes of ET, NO, EPCR, _i and cytoskeleton in the cells between the sera from patients with the same BSS syndrome associate with T2DM and hypertension, which may partially explain the pathophysiology mechanism of "different disease and identical syndrome" in traditional Chinese medicine.     

Effects of IL-6 and IL-11 on differentiation of cord blood CD34+ cells towards megakaryocytes

AIM: To investigate the effects of interleukin-6 (IL-6) and interleukin-11 (IL-11) on differentiation of cord blood CD34+ cells towards megakaryocytes and platelet production in vitro.METHODS: The CD34+ cells from fresh umbilical cord blood samples were cultured in serum-free culture medium with thrombopoietin (TPO) 50 μg/L,IL-3 10 μg/L,stem cell factor (SCF) 50 μg/L as control groups,then 10 μg/L IL-6 or IL-11 or IL-6＋IL-11 respectively was added as treatment groups.Mononuclear cells (MNCs) in cultured cells were detected by cell counter,megakaryocytes (CD41+ cells) and platelets were measured by flow cytometry,respectively.Platelet agglutination after thrombin induced was observed by microscopy and flow cytometry.RESULTS: Compared with the control group,the number of MNCs was not significantly different（P>0.05）,but the numbers of CD41+ cells and platelets were increased significantly (P<0.05) in treatment groups.There were more platelet particles in treatment groups than those in control group by microscopy and the results also showed that the cytoplasmic fragments from the cultures responded to thrombin induction.CONCLUSION: It is concluded that both IL-6 and IL-11 induce the cord blood CD34+ cells to differentiate towards megakaryocytes and produce platelets.     

Expression of Th cytokines in peripheral blood before and after splenectomy in immune thrombocytopenia patients

AIM: To investigate the changes of Th cytokines before and after splenectomy in immune thrombocytopenia (ITP) patients. METHODS: The QuantiGene Plex method was used to measure the mRNA expression of Th1, Th2 (IL-4, IL-5, IL-6 and IL-10), Th3 (transforming growth factor β₁,TGF-β₁), and Th17 (IL-17) cytokines in peripheral blood of ITP patients before and after laparoscopic splenectomy and those in peripheral blood of healthy controls. RESULTS: The mRNA level of IL-2 was significantly decreased in ITP patients before operation compared with the healthy controls, whereas IL-17 was obviously over-expressed. No significant difference of the other cytokines between preoperative group and the normal controls was found. After splenectomy, the expression levels of both IL-2 and TGF-β₁ were significantly higher than those in preoperative group and the normal controls. IL-2 was also significantly increased after operation, but was still lower than that in the normal controls. No significant difference of other cytokines between postoperative group and healthy controls was observed. In addition, The Th1 cytokines (IL-2 and IFN-γ) were found to be positively correlated (r=0.647, P<0.01) in preoperative patients, while no correlation was found between the other cytokines. There was a positive correlation between IL-2 and IFN-γ (r=0.787, P<0.01) in postoperative patients. IL-17 also had positive correlations with IL-2 (r=0.554,P<0.01) and IFN-γ (r=0.461,P<0.05) in ITP patients after operation, respectively. CONCLUSION: There is an imbalance of Th cytokines in ITP patients. The mechanism of splenectomy for treating ITP may be associated with the balance regulation of Th cytokines.     

Detection and enrichment of T lymphocytes based on cytokine secretion in human mixed lymphocyte reaction

AIM: Detection and enrichment of T lymphocytes after allogeneic PBMNC stimulation according to secreted cytokine were performed in order to explore a new approach for studying allogeneic reactive T lymphocytes. METHODS: The novel cytokine secretion assay (CKSA) was applied to detect T lymphocyte secreting IFN-γ, IL-4 and IL-10 at single cell level in human mixed lymphocyte reaction. IFN-γ secreting T cells were enriched by means of magnetic sorting system. RESULTS: Allogeneic PBMNC stimulation didn't alter the proportion of IL-4 and IL-10 secreting T lymphocytes (which were 0.12%±0.03% and 0.10%±0.03%, respectively), but increased proportion of IFN-γ secreting T lymphocytes (1.12%±0.13%). These IFN-γ- secreting T lymphocytes could be further enriched to 67.3%±10.5% . CONCLUSION: It is feasible to detect significantly increased IFN-γ-secreting T cells after allogeneic PBMNC stimulation based on the novel CKSA technique, and these cells could be efficiently enriched for further use.     

Effects of glucosidorum tripterygii tororum on cytokine productions in graft-versus-host disease mice

AIM:To observe the effect of glucosidorum tripterygii tororum (GTT) on cytokine productions in acute graft-versus-host disease (aGVHD) mice. METHODS: C₅₇BL/6 mice were exposed to radiation delivered by a linear accelerator. To establish a aGVHD model, the cell suspensions, which were obtained from bone marrow and spleen of the BALB/C mice, were transplanted to the radiated C₅₇BL/6 mice. The recipients were treated with GTT, GTT+CsA and CsA+MTX. The serum concentrations of IL-2, TNF-α, IL-4 and IL-10 were determined by ELISA. RESULTS:The survival rate on day 11 in GTT group (9/10) was higher than in allogeneic bone marrow transplatation (allo-BMT) group (8/19). The concentrations of IL-2 and TNF-α in GTT group were significantly lower, but the concentration of IL-10 was remarkably higher than that in allo-BMT group (P＜0.05). However, the concentration of IL-4 showed no changed in all groups (P＞0.05). CONCLUSION:GTT inhibited aGVHD development by regulating the production of cytokines in the host.     

Changes of IL-4, IL-10, IL-12 levels in rat serum and lung during acute respiratory distress syndrome induced by oleic acid

AIM:To observe the dynamic changes of interleukin-4(IL-4), IL-10, IL-12 in rat serum and lung tissues during acute respiratory distress syndrome (ARDS).METHODS:The ARDS model of rats was induced by intravenous injection of oleic acid. The levels of IL-4, IL-10, IL-12 in serum and the supernatant of lung tissues were measured by enzyme linked immunosorbent assay (ELISA).RESULTS:The Levels of serum and lung IL-10, IL-12 in ARDS rats were increased in 4 h, 8 h, 16 h group compared with control group. The levels in IL-10 in serum in 16 h group and IL-10 in lung tissues of 8 h group were lower than that in 4 h group. The Levels of IL-4 in serum in 4 h, 8 h group were higher than that in control group, while IL-4 in 16 h group was lower than that in 8 h group. IL-4 of lung tissues in 4 h, 8 h, 16 h group were increased significantly, but in 16 h group were lower than that in 8 h group. The biggest changes of pulmonary coefficient and histopathology were observed at 4 h after injection of oleic acid.CONCLUSIONS:IL-4, IL-10 and IL-12 might play important roles in inflammatory reaction induced by oleic acid. The pro-and anti-inflammatory cytokines produced successively during ARDS.The relationship between unbalanced cytokines and lung injury in ARDS needs to be further studied.     

Palmitate triggers inflammatory response by upregulating fatty acid translocase in THP-1 macrophages

AIM: To investigate the role of fatty acid translocase (FAT/CD36) on palmitate-induced inflammation in human monocyte-derived macrophage THP-1.METHODS: THP-1 cells were treated with palmitate (0, 0.1 and 0.2 mmol/L) for 24 h. Transwell chamber assay was used to examine the migration ability of THP-1 cells. The mRNA expression of CD36, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and monocyte chemotactic protein 1 (MCP-1) was measured by real-time PCR. The protein levels of TNF-α and IL-6 in the supernatant of cultured cells were measured by ELISA. The protein level of CD36 was examined by Western blot. Small interfering RNA (siRNA) targeting CD36 (siCD36) was used to inhibit the expression of CD36 in the THP-1 cells, and the changes of the cell migration and inflammatory response were monitored as mentioned above. RESULTS: Palmitate increased the expression of CD36 in the THP-1 cells (P<0.05). Palmitate also up-regulated inflammatory cytokine and chemokine levels, and the differences were statistically significant (P<0.05). Compared with control group, palmitate promoted migration of THP-1 cells. siCD36 was transfected into the THP-1 cells and the silencing efficiency was approximately 54%. The protein levels of TNF-α and IL-6 were also decreased in siCD36 group compared with scrambled RNA (scrRNA) group, and the differences were statistically significant (P<0.05). The migrated cells in siCD36 group were significantly less than those in scrRNA group (P<0.05).CONCLUSION: Palmitate promotes migration ability and triggers inflammatory response in the THP-1 macrophages by upregulating CD36 expression.     

Oxidized α1-antitrypsin induces IL-8 and MCP-1 production in HBE cells

AIM:To investigate the effect of oxidized α1-antitrypsin (Ox-AT) on interleukin 8 (IL-8) and monocyte chemotactic protein 1(MCP-1) production in cultured human bronchial epithelial (HBE) cells. METHODS:Plasma native α1-antitrypsin (N-AT) was purified from human plasma by 50% and 75% ammonium sulfate fractionation followed by glutathione and anion exchange chromatography. Ox-AT was prepared by incubating N-AT (0.5 g/L) with N-chlorosuccinimide in a 25-fold molar excess to N-AT in PBS at room temperature for 30 min. HBE cells were cultured in the presence of Ox-AT (0.5 g/L) for 4 h, 10 h and 24 h, and the levels of IL-8 and MCP-1 in the supernatant were assayed using respective DuoSet kits. The effect of NF-κB inhibitor Bay11-7082 on the inflammatory cytokine release induced by Ox-AT was also evaluated. RESULTS:Ox-AT concentration-dependently and time-dependently increased the production of IL-8 and MCP-1 in HBE cells. The concentrations of IL-8 and MCP-1 in HBE cells induced by 0.5 g/L Ox-AT at 4 h, 10 h and 24 h were significantly higher than those in blank control and N-AT groups. Ox-AT increased the activity of NF-κB in a dose-dependent manner. The proinflammatory effect of by Ox-AT was inhibited by NF-κB inhibitor Bay11-7082. CONCLUSION: Ox-AT is a strong proinflammatory factor for HBE cells. The mechanism is related to NF-κB signaling pathway activation.     

Effect of heat shock protein 70 expression induced by glutamine on vascular hyporeactivity in rats caused by LPS

AIM: To observe the effect of heat shock protein 70(HSP70) expression induced by glutamine on Escherichia coli lipopolysaccharides(LPS)-induced vascular hyporeactivity in rats.METHODS: Twenty four healthy male Sprague-Dawley rats were randomly divided into: the control group (n=8);LPS shock group (n=8);glutamine(Gln) treated group (Gln 0.75 g·kg-1 iv,n=8).6 h after LPS shock,phenylephrine (PE,0.5-2.5 μg·kg-1 ) was applied intravenously to all groups and the percentage increase in mean arterial pressure(MAP) was detected,respectively.The concentration-response curves of aorta rings were obtained by cumulative addition of phenylephrine (PE),and PE Emax,EC50 were calculated.The blood concentration of malondialdehyde (MDA),TNF-α and IL-6 were assayed in all groups 30 min and 360 min after LPS shock,respectively.The expressions of HSP70 from heart and aorta were also assayed after 6 h LPS shock.RESULTS: The MAP level induced by PE significantly decreased by 51.4% in LPS shock group compared with the control (P<0.05).However,PE induced MAP level increased by 17.5% in Gln group compared with LPS shock group (P<0.05).Emax and EC50 to PE were significant reduced in LPS shock group compared with control group (P<0.05),but significantly improved in Gln group (P<0.05).The expressions of HSP70 from heart and aorta were much higher in Gln group than those in LPS shock group (P<0.05).The blood concentrations of TNF-α,IL-6 and MDA were much lower in Gln group than those in LPS shock group.CONCLUSION: Glutamine effectively improves α-adrenergic receptor-mediated vascular reactivity through inducing the expression of HSP 70,reducing inflammatory cytokine release and peroxide biosynthesis in LPS shock.These results suggest that glutamine have potential beneficial therapeutic effect for septic shock patients.     

Effects of diosmin on changes of TNF-α, IL-1β, IL-6, IL-8 and IL-10 in serum and kidney tissues of rats with kidney ischemia and reperfusion

AIM: To observe the effects of diosmin on the production of tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), IL-6, IL-8 and IL-10 in serum and kidney tissues of rats with kidney ischemia and reperfusion (I/R). METHODS: Sprague-Dawley rats (180 in total) were randomly divided into 3 groups including sham operation group (sham),I/R group and diosmin+I/R group (diosmin+I/R). At the end of the experiment, the blood and kidney tissues were obtained and TNF-α, IL-1β, IL-6, IL-8 and IL-10 were detected by ELISA. RESULTS: The levels of TNF-α, IL-1β, IL-6, IL-8 and IL-10 in serum and kidney tissues in I/R group and diosmin+I/R group were significantly higher than those in sham group (P<0.01 or P<0.05). Following the development of the pathologic process, the level of TNF-α, IL-1β, IL-6 and IL-8 was significantly increased in I/R group and diosmin+I/R groups, but the level of IL-10 was significantly decreased in I/R group and significantly increased in diosmin+I/R group. The levels of TNF-α, IL-1β, IL-6 and IL-8 in I/R group was significantly higher than those in diosmin+I/R group (except TNF-α at 1 h in diosmin+I/R group). The level of IL-10 in diosmin+I/R group was significantly higher than that in I/R group (P<0.01 or P<0.05). CONCLUSION: Diosmin not only decreases the production of TNF-α, IL-1β, IL-6 and IL-8, but also promotes the production of anti-inflammatory cytokine IL-10, suggesting that the protective effect of diosmin on kidney I/R injury was associated with anti-inflammatory mechanism.     

Correlation between Toll-like receptor 4 on peripheral blood monocytes and serum IL-6 in patients with chronic severe hepatitis B

AIM:To study the change of Toll like receptor 4(TLR4) on peripheral blood monocytes (PBMCs) and its role in the pathogenesis of chronic severe hepatitis B.METHODS:The expression of TLR4 on CD14+ PBMCs was determined by flow cytometry in 30 healthy control,31 patients with chronic hepatitis B and 30 patients with chronic severe hepatitis B. The level of serum interleukin-6 (IL-6) was detected by ELISA. RESULTS:The expressions of TLR4 on PBMCs and serum IL-6 in the groups of healthy control,patients with chronic hepatitis B and patients with chronic severe hepatitis B were 2.3±1.1,3.7±2.3,6.9±4.1 mean fluorescence intensity (MFI) and （11.5±7.2) ng/L,(40.8±31.2) ng/L,(77.6±33.3） ng/L. The TLR4 value in the group of patients with chronic severe hepatitis B was significant higher than that in the group of healthy control and the group of patients with chronic hepatitis B (P<0.05). However,there was no significant difference between the group of patients with chronic hepatitis B and the group of healthy control (P>0.05). Serum IL-6 increased gradually and significantly between the group of healthy control and the groups of patients with chronic hepatitis B and patients with chronic severe hepatitis B. There was a significant positive correlation between the expression of TLR4 and the content of serum IL-6 in the group of chronic severe hepatitis B. CONCLUSION:TLR4 may play a role in the pathogenesis of chronic severe hepatitis B.     

Renal tumor cell lysate antigen induces the activation of dendritic cells

AIM:To investigate the effects of renal tumor cell lysates and other cytokines on the activation of immature dendritic cells (iDCs), and to develop DCs vaccines for stimulation of renal tumour-specific immunity.METHODS:DCs induced from peripheral blood mononuclear cells of healthy volunteers were cultured and propagated in vitro using rhGM-CSF and rhIL-4, and then were cocultured with renal tumor cell lysates and different cytokines. A group: only with renal tumor cell lysates; B group: with renal tumor cell lysates and TNF-α; C group: with renal tumor cell lysates and IL-1β; D group: renal tumor cell lysates and TNF-α+IL-1β. RESULTS:iDCs were induced to mature in all four groups, and high level expressions of CD86, CD80 and HLA-DR were observed. Compared to other groups, DCs in D group expressed CD83 and CD54 at higher level (P<0.05), secreted higher quantity of IL-12 (P<0.01). Moreover, mDCs in D group induced multiplication of lymphopoiesis more effectively (P<0.05).CONCLUSION:Renal tumor cell lysates and TNF-α+IL-1β induce the mature phenotype and IL-12 production in DCs and synergistically promote the stimulatory effects of lymphopoiesis.     

Angiotensin Ⅱ stimulates TNF-α and NO production in peripheral blood mononuclear cells in heart failure patients

AIM: To examine the change of serum tumor necrosis factor-α (TNF-α), nitric oxide (NO) in patient with congestive heart failure (CHF) and the effect of angiotensin Ⅱ (AngⅡ), valsartan on TNF-α and NO production in culture peripheral blood mononuclear cells (PBMC), to assess the relationship between the renin-angiotensin system and cytokines. METHODS: Venous blood of both healthy volunteers (n=12) and patients with CHF (n=16) were collected. Serum TNF-α and NO were examined. Peripheral blood mononuclear cells (PBMC) were obtained from both the control and the patients groups and cultured with AngⅡ at concentrations of 0, 0.01, 0.1, 1 μmol/L, respectively. AngⅡ at concentration of 0.1 μmol/L combined with 0.1 μmol/L of valsartan was also used. After 24 h incubation, the contents of TNF-α and NO in the culture supernatants were measured. RESULTS: Serum TNF-α and NO production in CHF group were significantly higher than that in control group (P<0.01). The higher the heart failure degree, the higher the levels of TNF-α and NO (P<0.01), and no significant among different etiologies of CHF (P＞0.05) were observed. AngⅡ stimulated TNF-α and NO release from PBMC of patients with CHF and normal person, which was inhibited by valsartan. CONCLUSIONS: AngⅡ obviously increases TNF-α and NO production from PBMC, which indicates there is relationship between the renin-angiotensin system and TNF-α, NO. The fact that valsartan inhibits TNF-α production may be one of the mechanisms in treating CHF.     

Effects of lipopolysaccharide,IL-6 and TNFα on the tissue factor expression of astrocytes

AIM:To study the effects of lipopolysaccharide(LPS), interleukin-6(IL-6)and tumor necrosis factor α (TNFα) on tissue factor(TF) expression of astrocytes. METHODS:Astrocytes were identified with anti-glial fibrillary acidic protein antibody. The TF activity of cell lysate was measured with one stage clotting assay. RESULTS:TF activity of astrocytes of LPS,IL-6,TNFα groups were obviously higher than that of the control group(P <0.05); While LPS,IL-6 and TNFα were combined with trifluoperazine or H₇, their inductive effects were inhibited. CONCLUSION:LPS,IL-6 and TNFα promoted the TF expression of astrocytes and its mechanisms may connected with Calcium/Camodulin and protein kinase C pathway.     

Elevated levels of serum IL-6, ICAM-1 and P-selectin in stable survivors with liver transplantation

AIM: To study the profile of serum IL-6， ICAM-1 and P-selectin in stable survivors with clinical liver transplantation (LTx). METHODS: Flow cytometric analysis was used to determine the phenotype of T cell subsets in peripheral blood mononuclear cells （PBMCs） from stable survivors with liver transplantation (n=22), and healthy volunteers (n=12). Serum levels of the pro-inflammatory cytokines, tumor necrosis factor (TNF-α) and interleukin (IL-6), intercellular adhesion molecules (ICAM-1) and P-selectin in stable survivors with liver transplantation and healthy volunteers were assessed by enzyme-linked immunoabsordent assay (ELISA). Recently performed 6 cases of liver transplantation were also dynamically observed in this study. RESULTS: Percentage of CD4+ T cells， CD8+ T cells and CD3+ T cells, as well as ratio of CD4 to CD8 were no difference between two groups (P>0.05). However, a significant higher percentage of CD3+CD25+ T cells was found in stable liver transplantation group as compared to healthy group (P<0.05). Significantly increased concentrations of IL-6, ICAM-1 and P-selectin were found in stable liver transplantation group as compared to healthy group (P<0.05). A high TNF-α level was detected in stable liver transplantation group while no significant difference was found as compared to healthy volunteers group (P>0.05). There was not found no regular change of serum cytokines (IL-6, TNF-α) and adhesion molecules (ICAM-1, P-selectin) in 6 liver transplanted patients during post-operation from day 1 to day 30, indicating that was associated with the different status of patients before or after transplantation. CONCLUSIONS: Our data suggesting that increased levels of ICAM-1 and P-selectin, appears to participate in the processing of immunoregulation to transplanted livers, whereas elevated concentrations of IL-6 appear to be involved in the repair of the injury induced by TNF-α in allo-transplanted livers.     

Effects of antioxidant and NF-κB on the induction of IL-8 in human colon cancer cell line HT-29 cells in vitro

AIM: To investigate the role of nuclear factor κB (NF-κB) in the induction of IL-8 gene by TNF-α in colon cancer cells and the effect of antioxidant on the induction of IL-8. METHODS: ELISA was used to detect the concentrations of IL-8. IL-8 mRNA was analyzed by using RT-PCR. NF-κB in the cell nuclei was detected with electrophoretic mobility shift assay. RESULTS: (1) IL-8 production and IL-8 mRNA expression induced by TNF-α was blocked by pyrrolidine dithiocarbamate (PDTC). (2) TNF-α triggered the activation and translocation of NF-κB and PDTC inhibited the activation of NF-κB induced by TNF-α. CONCLUSION: The induction of IL-8 gene and protein by TNF-α is dependent on the activation of NF-κB. Antioxidants may inhibit the induction of IL-8 gene and protein through inhibiting NF-κB activation.     

The effects of rhIL-1β on human fetal islets function and IL-6 production

AIM: To study rhIL-1β effects on fetal islet function and IL-6 production in vitro METHODS: Islets from fetal pancreas was separated by collagenase type V (0.5 mg/mL) and cultured in vitro The islets were exposed to culture medium alone for 48 h or with different concentration of rhIL-1β The supernatants of culture of human fetal islets were assayed for IL-6, insulin and glucagon RESULTS:(1) IL-6 activity was increased 4 0 folds (74-294 mU/islet) when islets were exposed to rhIL-1β(20U/mL); (2) IL-6 McAb significantly reduced IL-6 activity in islet supernatants from control group or islet exposed to rhIL-1β treated group; (3)IL-6 mRNA in human fetal islet exposed to rhIL-1β is higher than control in dot hybridization; (4) Soluble insulin and cellular insulin within islet released to supernatants was slightly decreased (0.48～0.78 IU/islet and 0.65～0.79 IU/islet); (5) Glucagon secretion was significantly increased 3.2 folds (1.0～3.2 pg/islet) CONCLUSION: Pancreatic islets produce IL-6 is up-regulated by rhIL-1β On the other hand, Il-6 produced by the islet may act as a costimulator for autoreactive B and T lymphocytes in autoimmune diabetes.     

Function of dendritic cells in cord blood

AIM: To explore the function of dendritic cells in cord blood.METHODS: Dendritic cell precursor subsets pDC/pDC(CD11c+CD123- /CD11c-CD123+) in cord blood and adult peripheral blood were analyzed gated by CD34-Lin- HLA-DR+ cells and the levels of IL-12p40,IL-10,IFN-γ,IL-4 in the serums were tested by ELISA.RESULTS: The level of IL-12p40 in cord blood serum was higher than that in peripheral blood.pDC1/pDC2,IL-10,IFN-γ,IL-4 in cord blood were similar to that in peripheral blood.CONCLUSION: Function development of dendritic cells in cord blood may be consummate.