Mintern Justine D, Bedoui Sammy, Davey Gayle M, Moffat Jessica M, Doherty Peter C, Turner Stephen J
Department of Microbiology and Immunology, University of Melbourne, Parkville 3010, Australia.
Proc Natl Acad Sci U S A. 2009 Apr 21;106(16):6724-9. doi: 10.1073/pnas.0901128106. Epub 2009 Apr 3.
Antigen expressed as MHC Class I glycoprotein (pMHCI) complexes on dendritic cells is the primary driver of CD8(+) T cell clonal expansion and differentiation. As we seek to define the molecular differences between acutely stimulated cytotoxic T lymphocyte (CTL) effectors and long-lived memory T cells, it is essential that we understand the duration of in vivo pMHCI persistence. Although infectious influenza A virus is readily cleared by mammalian hosts, that does not necessarily mean that all influenza antigen is totally eliminated. An exhaustive series of carefully controlled adoptive transfer experiments using 3 different carboxy fluorescein diacetate succinimidyl ester-labeled T cell receptor-transgenic CTL populations and a spectrum of genetically engineered and wild-type influenza A viruses provided no evidence for pMHCI persistence over the 30-60-d interval after virus challenge. Molecular profiles identified in antigen-specific T cells at this time may thus be considered to reflect established immunologic memory and not recent CTL activation from a persistent pMHCI pool.
树突状细胞上作为MHC I类糖蛋白（pMHCI）复合物表达的抗原是CD8(+) T细胞克隆扩增和分化的主要驱动因素。当我们试图定义急性刺激的细胞毒性T淋巴细胞（CTL）效应器与长寿记忆T细胞之间的分子差异时，了解体内pMHCI持续存在的持续时间至关重要。虽然甲型流感病毒感染很容易被哺乳动物宿主清除，但这并不一定意味着所有流感抗原都被完全消除。一系列详尽的、经过精心控制的过继转移实验，使用3种不同的羧基荧光素二乙酸琥珀酰亚胺酯标记的T细胞受体转基因CTL群体以及一系列基因工程和野生型甲型流感病毒，没有提供病毒攻击后30 - 60天间隔内pMHCI持续存在的证据。因此，此时在抗原特异性T细胞中鉴定出的分子谱可能被认为反映了已建立的免疫记忆，而不是来自持续pMHCI库的近期CTL激活。
