ABSTRACT
Objective To analyze the changes of PAIgG, CD62P, CD4+CD25+ Foxp3+Tr,and IL-18 before and after treatment in peripheral blood of children with acute idiopathic thrombocytopenic purpura(ITP) and investigate the function of these factors in the pathogenesis of ITP.Methods Forty-one cases of acute ITP children were divided into the effective group(35cases) and the ineffective group (6cases) according to the clinical treatment. To detect PAIgG,CD62P,and the number of Tr cells by using flow cytometry ,IL-18 plasma levels by ELISA assay,and analyze the variations of these indicators before and after treatment in children with acute ITP. Results In the effective treatment group, PAIgG, CD62P before treatment were 53.05%,(14.18±5.04 )%, which were significantly higher than that after treatment [18.62%, ( 8.36±1.95 )%] and control group[5.26%,(2.65±0.59) %,all P<0.01],and PAIgG,CD62P after treatment were also higher than that in control group [all P<0.05].IL-18,CD4 + T lymphocytes, Tr/CD4+T-lymphocyte ratios before treatment [415.47 ±38.92 ) ng/L,( 25.64 ± 5.81 )%,( 2.67 ± 0.14 )%]were significantly lower than that after treatment [(512.85±42. 17)ng/L,(35.08±6.07)% ,(4.76±0.58)%] and control group[(506. 39±32.28) ng/L,(35.32±2.27)% ,(5.37 ±0.69)% ,all P<0.01]. IL-18, CD4 +T lymphocytes, Tr/CD4 +T-lymphocyte ratios after treatmenthad no statistically significant difference compared with control group( all P<0.05 ). In ineffective group, the test results of PAIgG, CD62P, IL-18, CD4 +T lymphocytes, Tr/CD4+ T-lymphocyte ratios showed no significant change before and after treatment( all P<0.05 ).IL-18 had negative correlations with PAIgG,CD62P respectively before and after treatment(all P<0.05 ). Tr cells / CD4 + T had negative correlations with PAIgG,CD62P respectively (all P<0.05). Conclusions The amount of Tr, IL-18 were reduced, while CD62P and PAIgG increased in peripheral blood of children with acute ITP. IL-18, Tr , CD62P and PAIgG play important roles in the pathogenesis of acute ITP.
ABSTRACT
Objective To investigate the role of PPAR-γ in the gene expression of T-bet/GATA-3 in Jurkat T cells,and to explore the mechanisms underling this sensitizing effect of the change of TH cell subpopulation group.Methods Jurkat T cells were stimulated with PPAR-γ agonist pioglitazone.TH cell related cytokine IFN-γ and IL-10 was detected by ELISA,and the expression of transcription factors(T-bet and GATA-3)mRNA was detected by RT-PCR.To prove the PPAR-γ-dependent effect.the PPAR-γ-specific antagonist GW9662 was used.Results Stimulated with agonist PPAR-γpioglitazone.the concentration of IFN-γ and IL-10 and the expression of transcription factor T-bet and GATA-3 mRNA were both significantlY decreased in Jurkat T cells obviously,and these actions were dependent on the time and the concentrations of pioglitazone.Added with antagonist GW9662 at the same time,such inhibitory actions of IFN-γ and T-bet expression were recovered.but not IL-10 and GATA-3.Conclusion Pioglitazone can inhibite T cells proliferation and their secretion of cytokines.Pioglitazone can inhibit TH1 cells from secreting cytokines,and it is a PPAR-γ-dependent effect related to T-bet.The inhibition on TH2 is not a PPAR-γ-dependent effect and it is GATA-3 related.
ABSTRACT
Carcino-embryonic antigen related cellular adhesion molecule 1(CEACAM1),used to be called CD66a, biliar glyeoprotein(BGP) or C-CAM,is a glucoprotein expressed on the surface of cells, a member of the carcino-embryonic antigen family(CEA) and an adhesion molecule of immunoglobulin superfamily. It is widely expressed on the epithelial cells and vascular endothelial cells.CEACAM1 inhibits tumor growth and epithelial cell proliferation, induces apoptosis of epithelial cells, inhibits activation and proliferation of T lymphocytes, stimulates proliferation of B lymphocytes, inhibits the cytotoxic effects of T cells and NK cells, delays apoptosis of granulocytes and monocytes, inhibits the activity of tumor-infiltrating lymphocytes, stimulates invasion of tumor cells and motility of endothelial cells, promotes blood vessel angiogenesis, and modulates vascular remodeling, so it has many important biological functions.