Radiation kills human peripheral T cells by a Fas-independent mechanism.

Radiation kills human peripheral T cells by a Fas-independent mechanism.
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辐射通过不依赖 Fas 的机制杀死人类外周 T 细胞。

DOI:
10.3892/ijmm.2.4.403
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发表时间:
1998
影响因子:
5.4
通讯作者:
S. Kataoka
S. Kataoka
中科院分区:
医学3区
文献类型:
--
作者:
Y. Ogawa;A. Nishioka;T. Inomata;S. Yoshida;K. Nakayama;S. Kataoka

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辐射诱导人外周T细胞凋亡的机制尚不清楚。我们利用流式细胞仪和抗cd3单克隆抗体、膜联蛋白V、碘化丙啶、抗fas抗体和抗fas配体抗体检测了正常志愿者辐照后外周血单核细胞(PBMC(S))的序列变化。60Co放射治疗单元辐照5或10 Gy后,大部分人外周血T细胞在辐照后15 h对膜联蛋白V呈阳性,23 h对碘化丙啶呈阳性。在显微镜-视频系统上,约80%的单核细胞在照射后24小时出现凋亡改变。由于其在活化诱导细胞毒性中的作用,我们还研究了Fas (CD95/Apo-1)途径在照射杀死T细胞中的作用。与未辐照细胞相比,辐照后的PBMC表面Fas表达和caspase-3活性均未增加。此外,抗fas配体未能消除照射后PBMC的凋亡性死亡。这些结果表明辐照通过一种不依赖于fas的机制直接诱导T细胞凋亡。
The mechanism by which radiation induces human peripheral T cell apoptosis is not known. We examined sequential changes in post-irradiated peripheral blood mononuclear cells (PBMC(S)) taken from normal volunteers, by using flow-cytometer and an anti-CD3 monoclonal antibody, annexin V, propidium iodide, anti-Fas antibody, and anti-Fas ligand antibody. After 5 or 10 Gy of irradiation with a 60Co radiation therapy unit, most of the human peripheral T cells showed positivity against annexin V in 15 h, and positivity against propidium iodide in 23 h after irradiation. On a microscopy-video system, approximately 80% of mononuclear cells revealed apoptotic changes in 24 h after irradiation. Because of its proposed role in activation-induced cytotoxicity, we also examined the Fas (CD95/Apo-1) pathway in killing T cells by irradiation. Irradiated PBMC, displayed no increase in surface Fas expression and caspase-3 activity relative to non-irradiated cells. In addition, the anti-Fas ligand failed to eliminate the apoptotic death of PBMC, after irradiation. These results suggest that irradiation induces direct apoptosis of T cells by a Fas-independent mechanism.