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Insights into CD8 T Cell Activation and Exhaustion from a Mouse Gammaherpesvirus Model.
Viral Immunology ( IF 1.5 ) Pub Date : 2020-04-01 , DOI: 10.1089/vim.2019.0183
Sally R Sarawar 1 , Jadon Shen 2 , Peter Dias 1
Affiliation  

(S.R.S.) I was introduced to viral immunology while working in Peter Doherty's laboratory in the early stages of my research career, inspiring a lifelong interest in this area. During those early years under Peter's mentorship, we studied a mouse gammaherpesvirus model (murine gammaherpesvirus-68 [MHV-68]) that provided a useful small animal model for investigating the immunological control of gammaherpesvirus infection. Interestingly, while CD4 T cells were not required for acute control of MHV-68 in the lung, CD8 T cell-mediated control was progressively lost in the absence of CD4 T cell help, leading to viral recrudescence. This was one of several early studies showing that CD8 T cell control of persistent viral infections was lost in the absence of CD4 T cell help, preceding the concept of CD8 T cell exhaustion. Further studies showed that MHV-68 infection of mice offered a unique model for comparing the mechanisms of acute and long-term control of a persistent viral infection and developing strategies for reversing T cell exhaustion. Here, we provide a brief review of the literature on CD8 T cell activation and exhaustion in this model, focusing on the role of CD40 and B7 family members and including some previously unpublished data.

中文翻译:

从小鼠 Gammaherpes 病毒模型深入了解 CD8 T 细胞激活和耗竭。

(SRS) 在我研究生涯的早期阶段,我在 Peter Doherty 的实验室工作时接触了病毒免疫学,激发了我对这一领域的终生兴趣。在 Peter 的指导下的那些早年,我们研究了小鼠 gammaherpesvirus 模型(小鼠 gammaherpesvirus-68 [MHV-68]),该模型为研究 gammaherpesvirus 感染的免疫控制提供了一个有用的小动物模型。有趣的是,虽然 CD4 T 细胞不需要急性控制肺部 MHV-68,但在没有 CD4 T 细胞帮助的情况下,CD8 T 细胞介导的控制逐渐丧失,导致病毒复发。这是几项早期研究之一,表明在 CD8 T 细胞耗竭概念出现之前,如果没有 CD4 T 细胞的帮助,CD8 T 细胞对持续性病毒感染的控制就会丧失。进一步的研究表明,小鼠的 MHV-68 感染提供了一个独特的模型,用于比较持续病毒感染的急性和长期控制机制以及制定逆转 T 细胞耗竭的策略。在这里,我们简要回顾了关于该模型中 CD8 T 细胞激活和耗竭的文献,重点关注 CD40 和 B7 家族成员的作用,并包括一些以前未发表的数据。
更新日期:2020-04-01
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