高级检索
姚振江, 王滨有, 赵景波, 李洪源, 高桥めぐみ, 高桥秀实. SIVmac239对猕猴B淋巴细胞生长活性的抑制[J]. 中国公共卫生, 2005, 21(10): 1195-1196.
引用本文: 姚振江, 王滨有, 赵景波, 李洪源, 高桥めぐみ, 高桥秀实. SIVmac239对猕猴B淋巴细胞生长活性的抑制[J]. 中国公共卫生, 2005, 21(10): 1195-1196.
YAO Zhenjiang, WANG Binyou, ZHAO Jingbo, . Inhibition mechanism of SIVmac239 on macques B lymphocyte(MM133)proliferation in vitro[J]. Chinese Journal of Public Health, 2005, 21(10): 1195-1196.
Citation: YAO Zhenjiang, WANG Binyou, ZHAO Jingbo, . Inhibition mechanism of SIVmac239 on macques B lymphocyte(MM133)proliferation in vitro[J]. Chinese Journal of Public Health, 2005, 21(10): 1195-1196.

SIVmac239对猕猴B淋巴细胞生长活性的抑制

Inhibition mechanism of SIVmac239 on macques B lymphocyte(MM133)proliferation in vitro

  • 摘要:
      目的   探讨恒河猴免疫缺陷病毒(SIVmac239)感染CD4 +T淋巴细胞后, 可否产生某些抑制B淋巴细胞生长的活性因子, 为HIV/AIDS病原学研究提供线索。
      方法   用四甲基偶氮噻唑蓝(MTT)实验观察不同时间收集的SIV-mac239感染的CD4 +T淋巴细胞上清和未感染SIVmac239的CD4 +T淋巴细胞的上清对猕猴B淋巴细胞生长的抑制作用, 用3H thymidine uptake assay判断其是否抑制B淋巴细胞的DNA合成, 用凝胶电泳方法检测DNA合成抑制的凋亡机制, 用Western blot方法检测Cyclin D1的表达情况。
      结果   SIVmac239感染的CD4 +T淋巴细胞上清含有抑制猕猴B淋巴细胞生长的因子, 其抑制效果随作用时间的延长而增加。这些因子可较强的抑制CD4 +T淋巴细胞的DNA合成, 最高抑制率可达81%。凝胶电泳试验结果未见DNA梯状条带。Western blot试验发现Cyclin D1表达被抑制。
      结论   SIVmac239感染CD4 +T淋巴细胞可产生抑制B淋巴细胞生长的因子。此因子可较强的抑制猕猴B淋巴细胞DNA的合成, 但并不引起B淋巴细胞凋亡。其主要机制为抑制猕猴B淋巴细胞的细胞周期蛋白D1的产生, 使B淋巴细胞停止在G1期, 即抑制作用的主要机制为细胞被捕获在细胞周期的G1期。

     

    Abstract:
      Objective   To explore the inhibition factors which CD4 +T lymphocyte secreted after infection with SIVmac239, whether or not these factors Could inhibit the Blymphocyte proliferation activity and it's inhibition mechanism, some helpful clue for pathogenology research of AIDS would be supplied.
      Methods   Proliferation activity of MM133 cells treated by the supernatant of C8166 cells infected SIVmac239 tested by MTT assay. The inhibition of DNA synthesis of supernatant of C8166 cells infected by SIVmac239 on B cells estimated by 3H thymidine uptake assay. Whether or not the apoptosis happened when the DNA synthesis inhibiton judged by DNA fragmentation detection. Cyclin D1 expression was examined through western blot assay.
      Results   SIVmac239 could stimulate CD4 +T lymphocyte to secret some inhibitant factors for the macques B lymphocyte. These factors could inhibit the DNA synthesis of B cells through 3H thymidine uptake assay, electrophoresis result did not show DNA ladder, there was not Cyclin D1 bands on western blot assay for the concentration of 25% and 12.5% supernantant of C8166 infected by SIVmac239.
      Conclusion   CD4+T lymphocyte infected by SIVmac239 can produce some inhibitant factors on the macques B lymphocyte; these factors also can inhibit the DNA synthesis of B cells, but the factors do not induce the apoptosis of B cells. The major mechanism of inhibition of the factors on the B cells is to arrest the cells in G1 phase duing cell cycling. A new phenomenon has been found in this experiment, B cells can not be infected by SIVmac239, but they will be arrested in G1 phase by some factor produced by CD4 +T Lymphocyte infected with SIVmac239. Thus the function of B lymphocytes and the humoral immunity may be limited.

     

/

返回文章
返回