Colston Julia M, Bolinger Beatrice, Cottingham Matthew G, Gilbert Sarah, Klenerman Paul
Nuffield Department of Medicine, Peter Medawar Building for Pathogen Research, University of Oxford, Oxford OX1 3SY, United Kingdom; and
Nuffield Department of Medicine, Peter Medawar Building for Pathogen Research, University of Oxford, Oxford OX1 3SY, United Kingdom; and.
J Immunol. 2016 Apr 15;196(8):3354-63. doi: 10.4049/jimmunol.1502687. Epub 2016 Mar 4.
The establishment of robust T cell memory is critical for the development of novel vaccines for infections and cancers. Classical memory generated by CD8(+)T cells is characterized by contracted populations homing to lymphoid organs. T cell memory inflation, as seen for example after CMV infection, is the maintenance of expanded, functional, tissue-associated effector memory cell pools. Such memory pools may also be induced after adenovirus vaccination, and we recently defined common transcriptional and phenotypic features of these populations in mice and humans. However, the rules that govern which epitopes drive memory inflation compared with classical memory are not fully defined, and thus it is not currently possible to direct this process. We used our adenoviral model of memory inflation to first investigate the role of the promoter and then the role of the epitope context in determining memory formation. Specifically, we tested the hypothesis that conventional memory could be converted to inflationary memory by simple presentation of the Ag in the form of minigene vectors. When epitopes from LacZ and murine CMV that normally induce classical memory responses were presented as minigenes, they induced clear memory inflation. These data demonstrate that, regardless of the transgene promoter, the polypeptide context of a CD8(+)T cell epitope may determine whether classical or inflating memory responses are induced. The ability to direct this process by the use of minigenes is relevant to the design of vaccines and understanding of immune responses to pathogens.
建立强大的T细胞记忆对于开发针对感染和癌症的新型疫苗至关重要。CD8(+)T细胞产生的经典记忆的特征是归巢至淋巴器官的收缩性群体。T细胞记忆膨胀,例如在巨细胞病毒(CMV)感染后所见,是扩大的、功能性的、组织相关效应记忆细胞池的维持。在腺病毒疫苗接种后也可能诱导出这样的记忆池,并且我们最近在小鼠和人类中定义了这些群体的共同转录和表型特征。然而,与经典记忆相比,决定哪些表位驱动记忆膨胀的规则尚未完全明确,因此目前无法指导这一过程。我们利用我们的腺病毒记忆膨胀模型首先研究启动子的作用,然后研究表位背景在决定记忆形成中的作用。具体而言,我们测试了这样的假设,即通过以小基因载体形式简单呈递抗原,可以将传统记忆转化为膨胀性记忆。当通常诱导经典记忆反应的来自LacZ和小鼠CMV的表位以小基因形式呈现时,它们诱导了明显的记忆膨胀。这些数据表明,无论转基因启动子如何,CD8(+)T细胞表位的多肽背景可能决定诱导的是经典记忆反应还是膨胀性记忆反应。利用小基因指导这一过程的能力与疫苗设计和对病原体免疫反应的理解相关。