Department of Immunology, Imperial College London, London, United Kingdom.
PLoS Comput Biol. 2011 Sep;7(9):e1002200. doi: 10.1371/journal.pcbi.1002200. Epub 2011 Sep 29.
In January 2010 two groups independently published the observation that the depletion of CD8+ cells in SIV-infected macaques had no detectable impact on the lifespan of productively infected cells. This unexpected observation led the authors to suggest that CD8+ T cells control SIV viraemia via non-lytic mechanisms. However, a number of alternative plausible explanations, compatible with a lytic model of CD8+ T cell control, were proposed. This left the field with no consensus on how to interpret these experiments and no clear indication whether CD8+ T cells operated primarily via a lytic or a non-lytic mechanism. The aim of this work was to investigate why CD8+ T cells do not appear to reduce the lifespan of SIV-infected cells in vivo.
2010 年 1 月,两个独立的研究小组发表了观察结果,表明在 SIV 感染的猕猴中耗尽 CD8+细胞对感染细胞的寿命没有明显影响。这一意外观察结果促使作者提出,CD8+T 细胞通过非裂解机制控制 SIV 病毒血症。然而,也提出了一些与 CD8+T 细胞控制的裂解模型兼容的替代合理的解释。这使得该领域对如何解释这些实验没有达成共识,也没有明确表明 CD8+T 细胞主要通过裂解还是非裂解机制起作用。这项工作的目的是研究为什么 CD8+T 细胞在体内似乎不会缩短 SIV 感染细胞的寿命。