The immune effect of CD4~+CD28~-T cells on Graves'ophthalmopathy(GO)was investigated.The expressions of interferon-γ(IFN-γ),interleukin-2(IL-2),and IL-4 in CD4~+ CD28~-T ceils were assayed by flow cytometry in GO patients,Graves'disease(GD)patients without ophthalmopathy,and healthy control subjects.The results showed that the percentage of CD4~+CD28~-T cells significantly increased in GO patients(P<0.05),with increased IFN-γ expression(P<0.05)and decreased IL-2 expression(P<0.05).These changes were closely correlated with clinical activity score(P<0.05).There were no significant differences in IL-4 expression among three groups.The resuh suggests that CIM~+ CD28~- T cells which hishly secrete IFN-γare related to the pathological lesion of GO.

Objective To investigate the effect of different gene expression levels of Syntenin on invasion and mi?gration of glioma cells and the underlying molecular mechanisms. Methods Lentiviral RNA interference was used to knockdown the expression of syntenin in U-87 cells. Real-time quantitative PCR was used to detect mRNA expression levels of syntenin . Transwell assay and adhesion assay were used to examine the invasion, migration and adhesion, re?spectively. Western-blot was used to detect the protein expression levels of Syntenin, AKT, p-AKT, and MMP-9. Re?sults The mRNA expression level of Syntenin was greatly reduced in interference group compared with empty vector group (P<0.01). The ability of invasion and migration was much lower in interference group than in empty vector group (P<0.01). However, there were no significant differences in invasion and migration between empty vector group and con?trol group. The adhesion ability of glioma U-87 cells was much higher in interference group than in empty vector group (P<0.05). However, when U-87 cells were seeded on 96-wells coated with HUVEC, the adhesion ability was much lower in interference group than in empty vector group(P<0.05). The protein expression levels of Syntenin, p-AKT, and MMP-9 in interference group were markedly decreased compared with empty vector group(P<0.05). There was no signif?icant difference in expression of AKT protein between interference group and empty vector group (P>0.05). Conclusion Syntenin may enhance the invasion and migration ability of glioma though up-regulation of p-AKT, which in turn pro?motes MMP-9 expression in a corresponding signal transduction pathway.

AIM: To prepare and characterize a novel anti-human CD83 monoclonal mAb. METHODS: Female BALB/c mice of 6-8 weeks old were immunized with CD83 transfectant (L929/CD83) as immunogen. The spleen B cells of the mice were fused with Sp2/0 myeloma cells. The hybridoma cells were screened with CD83 transfectant (L929/CD83 and 293/CD83) by FCM. The biological characteristics of antibody were investigated by rapid isotyping analysis, karyotype analysis, competitive inhibition test and Western blot. RESULTS: One hybridoma cell line named 9D8 was obtained, which had the property of secreting antihuman CD83 monoclonal antibody steadily, This mAb specifically recognized CD83 molecule expressed on human mature DC, activated T cells, and tumor cell line Daudi, myeloma cell line 8226. This mAb can recognize a distinct epitope from comercial mAb(HB15e). CONCLUSION: One hybndoma cell line has been developed successfully, which may lay a fundation for further study on the function of this molecule.

Objective: To further explore TCE-induced hepatotoxicity and its mechanisms by identification of trichloroethylene (TCE) induced abnormal histone methylation in human liver cells. Methods: L-02 cells were treated with 0 and 8 mmol/L TCE for 24 h. Histones were extracted by acid. Liquid chromatography electrospray ionization tandem mass spectrometry (ESI-LC-MS/MS) were used to identify and quantify TCE related histone methylations. TCE induced abnormal methylation of H3K79 me2 and H3K79 me3 were validated by Western blot analysis. The further analysis of the function of histone abnormal methylation modifications were done by single cell gel electrophoresis (SCGE) and Western blot analysis of p53 and ɤH2AX. Results: After treatment with TCE for 24 h in L-02 cells, the 36 TCE related histone methylation sites in 28 peptide segments were identified by MS. After treatment with TCE in concentrations of 0 and 8.0 mmol/L in L-02 cells for 24 h, the relative expression level of histone H3K79 me3 were 1.00±0.06, 0.70±0.09 (t=15.01, P=0.015); the relative expression level of histone H3K79 me2 were 1.00±0.05, 0.74±0.07 (t=16.69, P=0.018); the Olive Tail Moment about DNA damage were 1.46±0.28, 3.12± 0.68 (t=15.22, P=0.018); the relative expression levels of p53 were 1.00±0.04, 1.24±0.04 (t=18.71, P= 0.012); and the relative expression levels of ɤH2AX were 1.00 ± 0.03, 1.56 ± 0.11 (t=8.32, P=0 045). Conclusion TCE can induce changes in the relative expression level of H3K79 me2 and H3K79 me3 in L-02 cell, and induce DNA damage, suggesting that TCE may induce changes in the relative expression level of H3K79 me2 and H3K79 me3 by DNA damage.