CD80
CD86
细胞凋亡
分子生物学
CTL公司*
A组
免疫学
生物
男科
细胞毒性T细胞
CD40
内科学
医学
免疫系统
T细胞
生物化学
体外
CD8型
作者
Jie Yin,Guoqiang Li,Yue Yu,Yi Shi,Beicheng Sun,Feng Cheng,Wen-Gang Ge,Xuehao Wang
摘要
Objective To study the mechanism of enhancement of the CTL activity in mice coexpressing of CD80, CD86 and CD137L genes. Methods The mice were randomly divided into five groups, named A, B, C, D and E. The group A and B were control groups (CG). H22-BAL B/c HCC mouse model was established by subcutaneous injection with hepatocellular carcinoma cells of cell line H22- Wt (group A), H22-neo (group B), H22-CD80/CD86 (group C), H22-CD137L (group D) and H22- CD80/CD86/CD137L(group E), respectively. On the 14th, 35th, 56th and 84th day after the first inoculation of tumor cells, TUNEL staining and DNA ladder examination were used to detect apoptosis of splenic T lymphocytes in all groups at each post-inoculation time point. Electrophoretie mobility-shift assay (EMSA) method was used to detect the activity of nuclear factor κB (NF-κB) in splenic T lymphocytes in each group at each time point post-inoculation. Results Apoptosis was found in a great number of T lymphocytes in CG on the 14th day, much more than that in group C and E. The number of apoptotic T cells in group C had a significant difference compared with that in the group E from 14th to 84th day (P = 0. 003). DNA ladder analysis showed typical positive results in group C and E. The significant apoptosis fragments were found in group C on 21st, 35th and 84th days. NF-KB activity of T cells in groups C and E was remarkably higher than that of groups CG and D, with higher in group D than that of CG ( P =0. 002), and with no significant difference between group C and E on 14th day. The activity in group E was stable andremarkably higher than that of group C on 56th and 84th days after the first inoculation. Conclusion H22- CD80/CD86/CD137L induces higher NF-KB activity of the host T cells by synergistic action of CD28 and CD137, which may be one of the mechanisms of enhancement of the host CTL activity induced by coexpression of CD80, CD86 and CD137L genes.
Key words:
CD80 ; CD86 ; CD137L; Hepatocellular carcinoma; NF-κB ; Apoptosis
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