Chronic LCMV Infection Is Fortified with Versatile Tactics to Suppress Host T Cell Immunity and Establish Viral Persistence.
Chronic LCMV Infection Is Fortified with Versatile Tactics to Suppress Host T Cell Immunity and Establish Viral Persistence.
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DOI：
10.3390/v13101951
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发表时间：
2021-09-29
期刊：
影响因子：
--
通讯作者：
Hahm B
中科院分区：
文献类型：
--
作者：
Studstill CJ;Hahm B
自从分离出淋巴细胞脉络丛脑膜炎病毒（LCMV）的免疫调节毒株（例如克隆13）以来，小鼠的LCMV感染已成为病毒免疫抑制和病毒持久性机制研究的有价值的模型。在 LCMV 感染过程中，病毒特异性 T 细胞被耗尽，并且在小鼠模型中使用 LCMV 感染对其潜在机制进行了广泛研究。特别是，我们对分子和转录水平上 CD8+ T 细胞逐渐耗竭的机制进行了研究。这些研究揭示了抑制性受体、表面标记物、调节细胞因子和转录因子（包括 PD-1、PSGL-1、CXCR5 和 TOX）在 T 细胞调节中的关键作用。然而，CD4+ T 细胞抑制的作用模式很大程度上未知。最近，鞘氨醇激酶 2 被证明可以特异性抑制 CD4+ T 细胞增殖并导致 LCMV 持续存在。由于 CD4+ T 细胞调节也被认为对病毒的持久性很重要，因此揭示 CD4+ T 细胞抑制机制的研究可以帮助我们更好地了解病毒如何启动并延长其持久性。这篇综述总结了 LCMV 研究中关于 T 细胞抑制机制和终止病毒持续存在的方法的发现，特别强调 CD8+ T 细胞。
Ever since the immune regulatory strains of lymphocytic choriomeningitis virus (LCMV), such as Clone 13, were isolated, LCMV infection of mice has served as a valuable model for the mechanistic study of viral immune suppression and virus persistence. The exhaustion of virus-specific T cells was demonstrated during LCMV infection, and the underlying mechanisms have been extensively investigated using LCMV infection in mouse models. In particular, the mechanism for gradual CD8+ T cell exhaustion at molecular and transcriptional levels has been investigated. These studies revealed crucial roles for inhibitory receptors, surface markers, regulatory cytokines, and transcription factors, including PD-1, PSGL-1, CXCR5, and TOX in the regulation of T cells. However, the action mode for CD4+ T cell suppression is largely unknown. Recently, sphingosine kinase 2 was proven to specifically repress CD4+ T cell proliferation and lead to LCMV persistence. As CD4+ T cell regulation was also known to be important for viral persistence, research to uncover the mechanism for CD4+ T cell repression could help us better understand how viruses launch and prolong their persistence. This review summarizes discoveries derived from the study of LCMV in regard to the mechanisms for T cell suppression and approaches for the termination of viral persistence with special emphasis on CD8+ T cells.
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影响因子：
--
作者：
Arasanz H;Gato-Cañas M;Zuazo M;Ibañez-Vea M;Breckpot K;Kochan G;Escors D
通讯作者：
Escors D
影响因子：
5.4
作者：
AHMED, R;HAHN, CS;STRAUSS, JH
通讯作者：
STRAUSS, JH
影响因子：
5.4
作者：
BORROW, P;EVANS, CF;OLDSTONE, MBA
通讯作者：
OLDSTONE, MBA
DOI：
10.1073/pnas.0811139106
发表时间：
2008-12-23
影响因子：
11.1
作者：
Brooks, David G.;Ha, Sang-Jun;Oldstone, Michael B. A.
通讯作者：
Oldstone, Michael B. A.
影响因子：
30.5
作者：
Blackburn, Shawn D.;Shin, Haina;Haining, W. Nicholas;Zou, Tao;Workman, Creg J.;Polley, Antonio;Betts, Michael R.;Freeman, Gordon J.;Vignali, Dario A. A.;Wherry, E. John
通讯作者：
Wherry, E. John