Berke G
Department of Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Cell. 1995 Apr 7;81(1):9-12. doi: 10.1016/0092-8674(95)90365-8.
The potent and specific lytic activity of CTLs can occur by at least two distinct pathways. In the secretion and perforin-mediated pathway, the direct effect(s) on the target cell membrane of the pore-forming agent perforin, probably in conjunction with granzymes, also secreted from the CTLs, causes the target's demise. Intercytoplasmic transfer of granzymes is believed to be involved in inducing target apoptosis. In the Fas-mediated pathway, engagement of a CTL membrane ligand with an apoptosis-inducing target cell surface receptor, such as the FasL with Fas, triggers programmed disintegration of the CTL-bound target; secretion of granzymes and pore formation by perforin are not involved in this receptor-mediated mechanism. Despite the fundamental differences in their onset for both pathways, the downstream sequence of events that culminate in target cell apoptosis appears to be similar. Further studies will resolve this enigma.
细胞毒性T淋巴细胞（CTL）强大而特异的裂解活性至少可通过两种不同途径发生。在分泌及穿孔素介导的途径中，成孔剂穿孔素（可能与同样由CTL分泌的颗粒酶协同作用）对靶细胞膜产生直接作用，导致靶细胞死亡。颗粒酶的胞质间转移被认为参与诱导靶细胞凋亡。在Fas介导的途径中，CTL膜配体与凋亡诱导性靶细胞表面受体（如Fas配体与Fas）结合，触发与CTL结合的靶细胞程序性解体；颗粒酶的分泌及穿孔素形成孔道不参与此受体介导机制。尽管这两种途径起始阶段存在根本差异，但最终导致靶细胞凋亡的下游事件序列似乎相似。进一步研究将解开这一谜团。
