Edwards K M, Davis J E, Browne K A, Sutton V R, Trapani J A
John Connell Laboratory, Austin Research Institute, Heidelberg, Victoria, Australia.
Immunol Cell Biol. 1999 Feb;77(1):76-89. doi: 10.1046/j.1440-1711.1999.00799.x.
Cytotoxic T cells and natural killer cells together constitute a major defence against virus infection, through their ability to induce apoptotic death in infected cells. These cytolytic lymphocytes kill their targets through two principal mechanisms, and one of these, granule exocytosis, is essential for an effective in vivo immune response against many viruses. In recent years, the authors and other investigators have identified several distinct mechanisms that can induce death in a targeted cell. In the present article, it is postulated that the reason for this redundancy of lethal mechanisms is to deal with the array of anti-apoptotic molecules elaborated by viruses to extend the life of infected cells. The fate of such a cell therefore reflects the balance of pro-apoptotic (immune) and anti-apoptotic (viral) strategies that have developed over eons of evolutionary time.
细胞毒性T细胞和自然杀伤细胞共同构成了抵御病毒感染的主要防线，它们能够诱导被感染细胞发生凋亡性死亡。这些细胞溶解淋巴细胞通过两种主要机制杀死靶细胞，其中一种机制即颗粒胞吐作用，对于针对多种病毒的有效体内免疫反应至关重要。近年来，作者及其他研究人员已经确定了几种可诱导靶细胞死亡的不同机制。在本文中，我们推测这种致死机制冗余的原因在于应对病毒所产生的一系列抗凋亡分子，这些分子可延长被感染细胞的存活时间。因此，此类细胞的命运反映了在漫长进化过程中形成的促凋亡（免疫）和抗凋亡（病毒）策略之间的平衡。
