Hueber A O, Raposo G, Pierres M, He H T
Centre d'Immunologie Institut National de la Santé et de la Recherche Médicale-Centre National de la Recherche Scientifique de Marseille Luminy, France.
J Exp Med. 1994 Mar 1;179(3):785-96. doi: 10.1084/jem.179.3.785.
Programmed cell death plays an important role during thymocyte development, since a vast majority (97%) of mouse cortical thymocytes die in thymus, whereas only 3% of these cells are rescued from cell death and positively selected. Although it seems well established that thymocyte fate depends upon appropriate surface-expressed T cell receptor, little is known about the molecular mechanism(s) responsible for the massive thymocyte elimination that occurs in the thymus. We report here that Thy-1 is capable of triggering mouse thymocyte death in vitro through a bcl-2-resistant mechanism. We have previously shown that Thy-1 is involved in mouse thymocyte adhesion to thymic stroma through interaction with an epithelial cell ligand. To examine the Thy-1 signaling function in thymocytes, we have mimicked its interaction with stromal cells by culturing mouse thymocytes onto tissue culture plates coated with monoclonal antibodies (mAb) directed at distinct Thy-1 epitope regions. mAb recognizing determinants in a defined Thy-1 structural domain, but not others, were found to induce marked thymocyte apoptosis as evidenced by morphological and biochemical data. Use of a quantitative DNA dot blot assay indicated that Thy-1-mediated thymocyte apoptosis was not blocked by RNA or protein synthesis inhibitors, EGTA, or by cyclosporin A, and differed, therefore, from "activation-driven cell death". Moreover, Thy-1(+)-transfected, but not wild-type AKR1 (Thy-1-d) thymoma cells underwent apoptosis after ligation with apoptosis-inducing, Thy-1-specific mAb. In contrast to thymocytes, the latter event was inhibitable by RNA and protein synthesis inhibitors, an indication that thymocytes, but not thymoma cells, contain the molecular components necessary for Thy-1-driven apoptosis. We further showed that Thy-1-triggered thymocyte death is a developmentally regulated process operative in fetal thymocytes from day 17 of gestation, but not in peripheral T cells. Indeed, the target of apoptosis by anti-Thy-1 was found to reside mainly within the CD4+8+3- and CD4+8+3lo double positive immature thymocyte subsets. Finally, it is of major interest that Thy-1-mediated apoptosis, which was found to be readily detectable in thymocytes from bcl-2-transgenic mice, represents a thus far unique experimental system for studying bcl-2-resistant thymocyte death mechanism(s).
程序性细胞死亡在胸腺细胞发育过程中起着重要作用,因为绝大多数(97%)的小鼠皮质胸腺细胞在胸腺中死亡,而这些细胞中只有3%能从细胞死亡中被挽救并得到阳性选择。尽管胸腺细胞的命运似乎很大程度上取决于适当的表面表达的T细胞受体,但对于胸腺中发生的大量胸腺细胞清除的分子机制却知之甚少。我们在此报告,Thy-1能够通过一种抗bcl-2的机制在体外触发小鼠胸腺细胞死亡。我们之前已经表明,Thy-1通过与上皮细胞配体相互作用参与小鼠胸腺细胞与胸腺基质的黏附。为了研究Thy-1在胸腺细胞中的信号功能,我们通过将小鼠胸腺细胞培养在包被有针对不同Thy-1表位区域的单克隆抗体(mAb)的组织培养板上,模拟了其与基质细胞的相互作用。发现识别特定Thy-1结构域中决定簇的mAb,而不是其他mAb,能诱导明显的胸腺细胞凋亡,形态学和生化数据都证明了这一点。使用定量DNA斑点印迹分析表明,Thy-1介导的胸腺细胞凋亡不受RNA或蛋白质合成抑制剂、EGTA或环孢素A的阻断,因此与“激活驱动的细胞死亡”不同。此外,用诱导凋亡的、Thy-1特异性mAb连接后,Thy-1(+)转染的,但不是野生型AKR1(Thy-1 - d)的胸腺瘤细胞发生凋亡。与胸腺细胞相反,后一事件可被RNA和蛋白质合成抑制剂抑制,这表明胸腺细胞而不是胸腺瘤细胞含有Thy-1驱动的凋亡所需的分子成分。我们进一步表明,Thy-1触发的胸腺细胞死亡是一个在妊娠第17天起在胎儿胸腺细胞中起作用的发育调控过程,但在外周T细胞中不起作用。事实上,发现抗Thy-1诱导凋亡的靶标主要存在于CD4 + 8 + 3 - 和CD4 + 8 + 3lo双阳性未成熟胸腺细胞亚群中。最后,非常有趣的是,在bcl-2转基因小鼠的胸腺细胞中很容易检测到的Thy-1介导的凋亡,代表了一个迄今为止用于研究抗bcl-2胸腺细胞死亡机制的独特实验系统。