Objective To study the role of suppressor of cytokine signaling ( SOCS ) in the pathogenesis of primary biliary cirrhosis( PBC),the levels of SOCS protein and the changes of function of dendritic cell(DC) were respectively observed from PBC patients.MethodsThe study population consisted of 10 patients of PBC and 8 healthy controls.Phenotypic analysis of cultured peripheral blood mononuclear cells (PBMC)-derived DC was performed by flow cytometry (FCM),such as CD83,CD86 and human leukocyte antigen DR (HLA-DR).The levels of interleukin-10 (IL-10),interferon-γ( IFN-γ) and IL-12 in culture supematant of DC were measured by enzyme linked immunosorbent assay ( ELISA ).The protein levels of SOCS1 and SOCS3 were detected by Western blot ( WB ).The features of changes in these parameters were analyzed between the two groups.ResultsThe expression of CD83,CD86 and HLA-DR in PBC patients were ( 79.4 ± 4.8 ) ％,( 86.5 ± 6.3 ) ％ and (90.0 ± 3.5 ) ％,which were significantly higher than those in healthy control group[ (68.3 ±4.1 )％,(74.2 ±6.3)％ and (83.6 ±7.6)％ ],respectively (t =5.340,4.120,2.514,P ＜0.05).The levels of IL-12 and IFN-γin PBC patients were (53.5 ± 11.1)and (32.0 ±9.0) ng/L,which were significantly higher than those in healthy control group[ (32.1 ± 10.7) and (15.4 ± 8.1 ) ng/L; t =4.123,3.818,P ＜ 0.01 ].There were not any significant difference of IL-10 level between PBC patients [ (7.0 ± 4.6) ng/L ] and the healthy controls [ ( 5.8 ± 4.2) ng/L; t =0.563,P ＞ 0.05 ].The proteins levels of SOCS1 and SOCS3 in PBMC-derived DC from PBC group were decreased significantly than those in healthy control group.ConclusionsThe results suggest that the PBMC-derived DC in PBC patients has greater ability of potent maturation and antigen presentation function.The decreased expression of SOCS levels may be associated with the excessive immunological reaction and the breakdown of self-tolerance.

AIM: To investigate the expression profile of peripheral-type benzodiazepine receptor(PBR) involved in mitochondrial permeability transition(PT) regulation,and to observe the binding dynamic of the mitochondrial PBR with specificity ligand during rat live regeneration.METHODS: Liver regeneration model was produced by 70% partial hepatectomy(PH) performed in male SD rats.The animals of sham groups underwent the same surgical operations as PH groups did,but the liver lobes were not resected.The animals in the PH groups and corresponding sham groups were sacrificed at 3,6,12,24,48,72,120 and 168 hours after the operation.The livers were removed,weighted and processed for isolation of mitochondria.Semi-quantitative RT-PCR was performed to examine the expression level of PBR in 70% hepatectomized rat livers during the whole regeneration process and compared to that in the sham and normal groups.Compared with healthy rats,the kinetic parameters of PBR was evaluated by using a specific radioligand -PK11195.RESULTS: Compared with healthy rats,the expression of PBR was unchanged.Meanwhile,the results obtained in the present experiments by scatchard analysis,Bmax of PK11195 for PBR significantly decreased,returned to normal level in 168 h after PH.Kd of PK11195 for PBR significantly decreased at 72 h and 168 h after PH of rat liver regeneration(P

Objective To investigate the expression of sialic acid-binding immunoglobulin-like lectin-one (Siglec-1, also called CD169) in lymphocytes, monocytes and neutrophils in peripheral blood in patients with coronary heart disease(CHD), and explore the relationship between Siglec-1 expression and atheresclerosis. Methods CD145 CD169 positive cell proportion and CD169 mRNA levels were respectively measured by flow cytometry and real-time quantitative reverse transcription-polymerase chain reaction (FQ-RT-PCR) in 57 CHD patients and 38 healthy controls. And the levels of serum hpids were determined by automatic biochemistry analyzer. Results The flow cytometry analysis showed that CD169 protein was not found in lymphocytes and neutrophils in both CHD patients and healthy controls. The rate of CD14 CD169 double positive ceils in monocytes in CHD group was significandy higher than that in healthy controls [(12.7±2.4)% vs (1.0±0.3)% ,t =23.2,P<0.01]. And FQ-RT-PCR analysis showed that the mean CD± mRNA copy number in PBMCs in CHD group was significantly higher(3.2 fold) than that in healthy controls [t = 6. 59, P < 0.01]. However, neither differences of CD169 protein positivities [[(12. 2 ± 2. 3) %vs (13.4±2.5)% ,t = 1.87,P >0.05] nor mRNA levels [3.64 fold vs 2.79 fold when compared with healthy controls,t =0. 98, P > 0. 05] were found between CHD patients with normal and abnormal levels of serum Lipids. Conclusions CD169 is mainly expressed in human tissue-resident macrophages but not expressed in peripheral blood monecytes. And when the monocytes is stimulated by inflammation, the expression of CD169 is increased. In patients with CHD, the increased expression of CD169 protein and mRNA level has demonstrated the activation of monocytes in peripheral blood. CD169 and CD169-mediated monocytes activation may play an important role in the development and progression of atherosclerosis.