Galgano Alessia, Barinov Aleksandr, Vasseur Florence, de Villartay Jean-Pierre, Rocha Benedita
INSERM, U1020, CNRS, UMR 8253, Medical Faculty Paris Descartes, Université Paris Descartes Sorbonne Paris Cité, Paris, France.
INSERM, UMR 1163, Institut Imagine, Hôpital Necker-Enfants Malades, Paris, France.
PLoS One. 2015 Oct 20;10(10):e0140849. doi: 10.1371/journal.pone.0140849. eCollection 2015.
Immune responses are efficient because the rare antigen-specific naïve cells are able to proliferate extensively and accumulate upon antigen stimulation. Moreover, differentiation into memory cells actually increases T cell accumulation, indicating improved productive division in secondary immune responses. These properties raise an important paradox: how T cells may survive the DNA lesions necessarily induced during their extensive division without undergoing transformation. We here present the first data addressing the DNA damage responses (DDRs) of CD8 T cells in vivo during exponential expansion in primary and secondary responses in mice. We show that during exponential division CD8 T cells engage unique DDRs, which are not present in other exponentially dividing cells, in T lymphocytes after UV or X irradiation or in non-metastatic tumor cells. While in other cell types a single DDR pathway is affected, all DDR pathways and cell cycle checkpoints are affected in dividing CD8 T cells. All DDR pathways collapse in secondary responses in the absence of CD4 help. CD8 T cells are driven to compulsive suicidal divisions preventing the propagation of DNA lesions. In contrast, in the presence of CD4 help all the DDR pathways are up regulated, resembling those present in metastatic tumors. However, this up regulation is present only during the expansion phase; i.e., their dependence on antigen stimulation prevents CD8 transformation. These results explain how CD8 T cells maintain genome integrity in spite of their extensive division, and highlight the fundamental role of DDRs in the efficiency of CD8 immune responses.
免疫反应之所以高效,是因为罕见的抗原特异性幼稚细胞能够在抗原刺激下广泛增殖并积累。此外,分化为记忆细胞实际上会增加T细胞的积累,这表明在二次免疫反应中生产性分裂得到改善。这些特性引发了一个重要的悖论:T细胞如何在其广泛分裂过程中必然诱导产生的DNA损伤中存活而不发生转化。我们在此展示了首批数据,这些数据涉及小鼠初次和二次反应指数扩增期间体内CD8 T细胞的DNA损伤反应(DDRs)。我们发现,在指数分裂期间,CD8 T细胞会启动独特的DDRs,这些DDRs在其他指数分裂细胞、紫外线或X射线照射后的T淋巴细胞或非转移性肿瘤细胞中并不存在。在其他细胞类型中,单一的DDR途径会受到影响,而在分裂的CD8 T细胞中,所有的DDR途径和细胞周期检查点都会受到影响。在没有CD4辅助的情况下,所有DDR途径在二次反应中都会崩溃。CD8 T细胞被迫进行自杀性分裂,以防止DNA损伤的传播。相反,在有CD4辅助的情况下,所有DDR途径都会上调,类似于转移性肿瘤中的情况。然而,这种上调仅在扩增阶段存在;也就是说,它们对抗原刺激的依赖性可防止CD8细胞发生转化。这些结果解释了CD8 T细胞如何在广泛分裂的情况下维持基因组完整性,并突出了DDRs在CD8免疫反应效率中的基本作用。