MOLECULAR PATHWAYS INVOLVED IN THE PROGRAMMED DEATH OF LYMPHOCYTES

在这个项目中，我们采取了多方面的方法来研究 淋巴细胞程序性死亡的分子基础。 我们的攻击是 基于这样的假设，即主要有两种机制， T细胞的程序性死亡：i）淋巴因子剥夺性死亡（LDD）和 ii）由于活化T细胞的抗原刺激导致的杀本体死亡（PD） 细胞 关于LDD，我们正在努力了解如何退出 在T细胞的情况下，营养刺激，IL-2，可以启动 死亡程序 我们发现淋巴因子的退出导致 激活c-jun N-末端激酶（JNK）通路， 推测这会导致基因激活事件， 死亡程序 在研究PD时，我们专注于激活一种 称为Flice/Mach 1（半胱天冬酶8）的蛋白酶，其可以直接进行 死亡程序

In this project we are taking a multifaceted approach to studying molecular basis of programmed cell death in lymphocytes. Our attack is based on the hypothesis that there are principally two mechanisms of programmed death of T cells: i) lymphokine deprivation death (LDD) and ii) propriocidal death (PD) due to antigen stimulation of activated T cells. With regard to LDD, we are trying to understand how withdrawal of a trophic stimulus, IL-2 in the case of T cells, can initiate the death program. We have found that lymphokine withdrawal leads to the activation of the c-jun N-terminal kinase (JNK) pathway and we conjecture that this leads to a gene activation event that initiates the death program. In studying PD, we have focused on the activation of a protease termed Flice/Mach1 (caspase 8) which can directly carry out the death program.