Rahelu M, Williams G T, Kumararatne D S, Eaton G C, Gaston J S
Department of Immunology, University of Birmingham, UK.
J Immunol. 1993 Jun 1;150(11):4856-66.
Stimulation of human CD4+ T cell clones with appropriate specific peptides or with lectins in the absence of APC induces a substantial degree of cell death. We have investigated the mechanisms of induction of this cell death and show that it occurs by apoptosis, identified by morphology and the characteristic pattern of DNA degradation. We also investigated whether this T cell death was a result of a suicide process activated in the T cell after "inappropriate" recognition of Ag on the surface of another T cell clone (and in the absence of other accessory signals), or was due to a conventional lethal hit delivered by one cytolytic T cell to another "target" T cell. Our results strongly suggest that peptide-induced cell death of human CD4+ CTL is due to active killing of Ag-presenting target T cells by effector T cells of the same clone. The cell death that is induced in the target T cell occurs via apoptosis that requires de novo RNA transcription and translation in the effector T cell.
在没有抗原呈递细胞(APC)的情况下,用适当的特异性肽或凝集素刺激人CD4 + T细胞克隆会导致相当程度的细胞死亡。我们已经研究了这种细胞死亡的诱导机制,并表明它是通过凋亡发生的,通过形态学和DNA降解的特征模式得以鉴定。我们还研究了这种T细胞死亡是在T细胞对另一个T细胞克隆表面的抗原进行“不适当”识别后(且在没有其他辅助信号的情况下)激活的自杀过程的结果,还是由于一个细胞毒性T细胞对另一个“靶”T细胞施加的传统致死打击所致。我们的结果强烈表明,肽诱导的人CD4 + 细胞毒性T淋巴细胞(CTL)的细胞死亡是由于同一克隆的效应T细胞对呈递抗原的靶T细胞进行主动杀伤所致。靶T细胞中诱导的细胞死亡是通过凋亡发生的,这需要效应T细胞中从头开始的RNA转录和翻译。