Defective activation induced cell death of CD4+ T cells in primary biliary cirrhosis murine model
- VernacularTitle:CD4+T细胞活化诱导细胞凋亡在原发性胆汁性肝硬化小鼠模型中的作用研究
- Author:
Tingwang JIANG
;
Anmei DENG
;
Chuanyong WU
;
Bo CHEN
;
Ye ZHOU
;
Cheng QIAN
;
Mingli GU
;
Yan CHEN
;
Renqian ZHONG
- Publication Type:Journal Article
- Keywords:
Poly I∶C;
Liver cirrhosis,biliary;
Apoptosis;
Model,murine
- From:
Chinese Journal of Microbiology and Immunology
2008;28(5):431-434
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the activation induced cell death (AICD) of CD4+ T cells in primary biliary cirrhosis(PBC)murine model induced by poly I∶C. Methods Thirty female C57BL/6 mice were divided into model and control group randomly, and the former were injected with 5 mg/kg of poly I∶C, the later with PBS. PBC mice were detected 16 weeks after injection. CD4+ T cells isolated from spleen were stimulated in vitro by Con A and anti-CD3, and the apoptosis were determined by Annexin-V and PI staining. The expression of Fas, FasL and TRAIL were assayed by relative quantitative real-time PCR. Bcl-2 was detected by Western blot. Results Compared with control group, the portal areas of mice in model group were infiltrated with mononuclear cells obviously. The positive rate of serum antimitochondrial antibody(AMA) and the level of alkali phosphatase (ALP) were higher than that in control group (P<0.001). AICD of splenic CD4+ T cells in model group was lower than that of control group (P<0.001). The mRNA of FasL and TRAIL in model mice was down-regulated. Simultaneously, the anti-apoptosis protein Bcl-2 was up-regulated in model group. Conclusion These observations suggest that a defect in AICD of auto-reactive TH1 cells may contribute to the pathogenesis of PBC model. Furthermore, this defect in AICD may results from the change of Fas/FasL, TRAIL pathway and the up-regulation of Bcl-2.
