Chiu V K, Walsh C M, Liu C C, Reed J C, Clark W R
Department of Biology and Molecular Biology Institute, University of California at Los Angeles 90024.
J Immunol. 1995 Mar 1;154(5):2023-32.
The ability of bcl-2 in target cells to block cell-mediated cytotoxicity by allospecific CTL was tested. The blocking effect was variable. Because killing by CTL involves two different pathways, degranulation (perforin plus granzymes) and fas, we examined the effect of bcl-2 on these pathways independently. Bcl-2 in target cells blocked apoptotic cell death induced either by cytotoxic granule extracts or by CTL killing under conditions in which the fas pathway is blocked. On the other hand, bcl-2 had no effect on target cell-killing either by Fas-specific mAb or by CTL capable of killing only via the fas pathway. These data suggest bcl-2 may block apoptotic lysis induced by perforin plus granzymes, but not apoptotic lysis induced via the fas pathway. Thus, any analysis of the effect of bcl-2 on apoptotic cell death in target cells killed by CTL must take into account the relative contributions of the degranulation vs fas pathways.
检测了靶细胞中bcl-2阻断同种特异性细胞毒性T淋巴细胞（CTL）介导的细胞毒性的能力。阻断效果存在差异。由于CTL杀伤涉及两条不同途径，即脱颗粒（穿孔素加颗粒酶）和Fas途径，我们分别研究了bcl-2对这些途径的影响。在Fas途径被阻断的条件下，靶细胞中的bcl-2可阻断由细胞毒性颗粒提取物或CTL杀伤诱导的凋亡性细胞死亡。另一方面，bcl-2对Fas特异性单克隆抗体或仅通过Fas途径杀伤的CTL介导的靶细胞杀伤没有影响。这些数据表明，bcl-2可能阻断由穿孔素加颗粒酶诱导的凋亡性裂解，但不阻断通过Fas途径诱导的凋亡性裂解。因此，在分析bcl-2对CTL杀伤的靶细胞中凋亡性细胞死亡的影响时，必须考虑脱颗粒途径与Fas途径的相对贡献。
