Rouvier E, Luciani M F, Golstein P
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. 1993 Jan 1;177(1):195-200. doi: 10.1084/jem.177.1.195.
Mechanisms of T cell-mediated cytotoxicity remain poorly defined at the molecular level. To investigate some of these mechanisms, we used as target cells, on the one hand, thymocytes from lpr and gld mouse mutants, and on the other hand, L1210 cells transfected or not with the apoptosis-inducing Fas molecule. These independent mutant or transfectant-based approaches both led to the conclusion that Fas was involved in the Ca(2+)-independent component of cytotoxicity mediated by at least two sources of T cells, namely nonantigen-specific in vitro activated hybridoma cells, and antigen-specific in vivo raised peritoneal exudate lymphocytes. Thus, in these cases, T cell-mediated cytotoxicity involved transduction via Fas of the target cell death signal.
T细胞介导的细胞毒性机制在分子水平上仍未得到很好的界定。为了研究其中一些机制,一方面,我们使用lpr和gld小鼠突变体的胸腺细胞作为靶细胞,另一方面,使用转染或未转染凋亡诱导性Fas分子的L1210细胞。这些基于独立突变体或转染体的方法均得出结论,Fas参与了至少两种T细胞来源介导的细胞毒性的非钙依赖性成分,即体外活化的非抗原特异性杂交瘤细胞和体内产生的抗原特异性腹腔渗出淋巴细胞。因此,在这些情况下,T细胞介导的细胞毒性涉及通过Fas转导靶细胞死亡信号。