Zagury D
Adv Exp Med Biol. 1982;146:149-69. doi: 10.1007/978-1-4684-8959-0_10.
Direct identification, enumeration and biological characterization of cytolytic T lymphocytes (CTL) complementing the chromium release test had allowed us to propose a mechanism for T-cell mediated cytotoxicity (T-CMC). One CTL without accessory cells is able to lyse a specific target. Binding which allows cell contact (E-T doublets), should activate effector CTLs and render target cells susceptible to lysis. Secretion of hydrolytic enzymes localized at the CTL-target junction accounts for the lethal hit given by CTLs to susceptible targets. This hypothesis that the resulting cell lesion is identified with an alteration of the lipid bilayer membrane had been confirmed by single killer cell study. Furthermore, we have proposed that phospholipase enzymes are involved in the membrane alterations, since susceptible targets bound to effector cells (conjugates) were lysed in a much higher yield in the presence of phospholipase. Membrane cell lesion determined by hydrolytic enzyme (phospholipase) could represent a basic general mechanism for other cellular or molecular mediated processes.
对细胞毒性T淋巴细胞(CTL)进行直接鉴定、计数和生物学特性分析,并结合铬释放试验,使我们能够提出一种T细胞介导的细胞毒性(T-CMC)机制。一个没有辅助细胞的CTL能够裂解特定靶细胞。允许细胞接触的结合(E-T双联体)应激活效应CTL,并使靶细胞易于裂解。位于CTL-靶细胞交界处的水解酶分泌是CTL对易感靶细胞造成致命打击的原因。通过单个杀伤细胞研究证实了这样一种假说,即由此产生的细胞损伤与脂质双分子层膜的改变有关。此外,我们提出磷脂酶参与了膜的改变,因为在磷脂酶存在的情况下,与效应细胞结合的易感靶细胞(结合物)裂解率更高。由水解酶(磷脂酶)决定的膜细胞损伤可能代表其他细胞或分子介导过程的基本通用机制。