School of Cancer Sciences and MRC Centre for Immune Regulation, College of Medicine, University of Birmingham, Birmingham, United Kingdom.
PLoS Pathog. 2009 Dec;5(12):e1000699. doi: 10.1371/journal.ppat.1000699. Epub 2009 Dec 18.
Viruses that naturally infect cells expressing both MHC I and MHC II molecules render themselves potentially visible to both CD8+ and CD4+ T cells through the de novo expression of viral antigens. Here we use one such pathogen, the B-lymphotropic Epstein-Barr virus (EBV), to examine the kinetics of these processes in the virally-infected cell, comparing newly synthesised polypeptides versus the mature protein pool as viral antigen sources for MHC I- and MHC II-restricted presentation. EBV-transformed B cell lines were established in which the expression of two cognate EBV antigens, EBNA1 and EBNA3B, could be induced and then completely suppressed by doxycycline-regulation. These cells were used as targets for CD8+ and CD4+ T cell clones to a range of EBNA1 and EBNA3B epitopes. For both antigens, when synthesis was induced, CD8 epitope display rose quickly to near maximum within 24 h, well before steady state levels of mature protein had been reached, whereas CD4 epitope presentation was delayed by 36-48 h and rose only slowly thereafter. When antigen expression was suppressed, despite the persistence of mature protein, CD8 epitope display fell rapidly at rates similar to that seen for the MHC I/epitope half-life in peptide pulse-chase experiments. By contrast, CD4 epitope display persisted for many days and, following peptide stripping, recovered well on cells in the absence of new antigen synthesis. We infer that, in virally-infected MHC I/II-positive cells, newly-synthesised polypeptides are the dominant source of antigen feeding the MHC I pathway, whereas the MHC II pathway is fed by the mature protein pool. Hence, newly-infected cells are rapidly visible only to the CD8 response; by contrast, latent infections, in which viral gene expression has been extinguished yet viral proteins persist, will remain visible to CD4+ T cells.
天然感染同时表达 MHC I 和 MHC II 分子的细胞的病毒通过新表达病毒抗原,使自身能够被 CD8+和 CD4+T 细胞潜在地识别。在这里,我们使用一种这样的病原体,即 B 淋巴细胞嗜性 Epstein-Barr 病毒 (EBV),来检查病毒感染细胞中这些过程的动力学,将新合成的多肽与成熟蛋白池作为 MHC I 和 MHC II 限制性呈递的病毒抗原来源进行比较。我们建立了 EBV 转化的 B 细胞系,其中可以诱导两种同源 EBV 抗原 EBNA1 和 EBNA3B 的表达,然后通过强力霉素调控完全抑制其表达。这些细胞被用作针对一系列 EBNA1 和 EBNA3B 表位的 CD8+和 CD4+T 细胞克隆的靶标。对于两种抗原,当合成被诱导时,CD8 表位的展示迅速上升到接近最大值,在达到成熟蛋白的稳定状态水平之前,在 24 小时内,而 CD4 表位的呈递被延迟 36-48 小时,此后才缓慢上升。当抗原表达被抑制时,尽管成熟蛋白持续存在,CD8 表位的展示迅速下降,下降速度与肽脉冲追踪实验中 MHC I/表位半衰期相似。相比之下,CD4 表位的展示持续了许多天,并且在肽洗脱后,在没有新抗原合成的情况下,细胞上的恢复情况良好。我们推断,在感染病毒的 MHC I/II 阳性细胞中,新合成的多肽是主要的抗原来源,为 MHC I 途径提供抗原,而 MHC II 途径则由成熟蛋白池提供抗原。因此,新感染的细胞仅迅速对 CD8 反应可见;相比之下,潜伏感染,即病毒基因表达已被消除但病毒蛋白仍存在,将对 CD4+T 细胞可见。