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首页> 外文期刊>Nature >Peak SIV replication in resting memory CD4(+) T cells depletes gut lamina propria CD4(+) T cells
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Peak SIV replication in resting memory CD4(+) T cells depletes gut lamina propria CD4(+) T cells

机译：静息记忆CD4（+）T细胞中的高峰SIV复制耗尽肠道固有层CD4（+）T细胞

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摘要

In early simian immunodeficiency virus (SIV) and human immunodeficiency virus-1 (HIV-1) infections, gut-associated lymphatic tissue (GALT), the largest component of the lymphoid organ system(1), is a principal site of both virus production and depletion of primarily lamina propria memory CD4(+) T cells; that is, CD4-expressing T cells that previously encountered antigens and microbes and homed to the lamina propria of GALT(2-9). Here, we show that peak virus production in gut tissues of SIV-infected rhesus macaques coincides with peak numbers of infected memory CD4(+) T cells. Surprisingly, most of the initially infected memory cells were not, as expected(10,11), activated but were instead immunophenotypically 'resting' cells that, unlike truly resting cells, but like the first cells mainly infected at other mucosal sites and peripheral lymph nodes(12,13), are capable of supporting virus production. In addition to inducing immune activation and thereby providing activated CD4(+) T-cell targets to sustain infection, virus production also triggered(14) an immunopathologically limiting Fas-Fas-ligand-mediated apoptotic pathway(15,16) in lamina propria CD4(+) T cells, resulting in their preferential ablation. Thus, SIV exploits a large, resident population of resting memory CD4(+) T cells in GALT to produce peak levels of virus that directly (through lytic infection) and indirectly ( through apoptosis of infected and uninfected cells) deplete CD4(+) T cells in the effector arm of GALT. The scale of this CD4(+) T-cell depletion has adverse effects on the immune system of the host, underscoring the importance of developing countermeasures to SIV that are effective before infection of GALT.
机译：在早期猿猴免疫缺陷病毒（SIV）和人类免疫缺陷病毒1（HIV-1）感染中，肠相关淋巴组织（GALT）是淋巴器官系统的最大组成部分（1），是这两种病毒产生的主要部位和主要的固有层记忆CD4（+）T细胞的耗竭；也就是说，以前遇到抗原和微生物并归巢到GALT（2-9）固有层的CD4表达T细胞。在这里，我们显示SIV感染的恒河猴猕猴的肠道组织中的峰值病毒生产与感染的记忆CD4（+）T细胞的峰值数量一致。出乎意料的是，大多数最初感染的记忆细胞未如预期的那样被激活（10,11），而是被免疫表型上的``静止''细胞，与真正的静止细胞不同，但与最初感染其他黏膜部位和外周淋巴的细胞一样节点（12,13）能够支持病毒生产。除了诱导免疫活化从而提供活化的CD4（+）T细胞靶标以维持感染外，病毒的产生还触发了固有固有层CD4中Fas-Fas-配体介导的凋亡途径的免疫病理学限制（14,15）。 （+）T细胞，导致其优先消融。因此，SIV利用GALT中大量驻留的静息记忆CD4（+）T细胞来产生峰值水平的病毒，该病毒水平直接（通过裂解感染）和间接（通过感染和未感染细胞的凋亡）耗尽CD4（+）T GALT效应臂中的细胞。这种CD4（+）T细胞耗竭的规模对宿主的免疫系统有不利影响，从而强调了在感染GALT之前制定有效的SIV对策的重要性。

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