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在感染猿猴免疫缺陷病毒的猕猴中,CD8(+) T细胞耗竭后血浆病毒血症急剧上升。

Dramatic rise in plasma viremia after CD8(+) T cell depletion in simian immunodeficiency virus-infected macaques.

作者信息

Jin X, Bauer D E, Tuttleton S E, Lewin S, Gettie A, Blanchard J, Irwin C E, Safrit J T, Mittler J, Weinberger L, Kostrikis L G, Zhang L, Perelson A S, Ho D D

机构信息

The Aaron Diamond AIDS Research Center, The Rockefeller University, New York 10016, USA.

出版信息

J Exp Med. 1999 Mar 15;189(6):991-8. doi: 10.1084/jem.189.6.991.

Abstract

To determine the role of CD8(+) T cells in controlling simian immunodeficiency virus (SIV) replication in vivo, we examined the effect of depleting this cell population using an anti-CD8 monoclonal antibody, OKT8F. There was on average a 99.9% reduction of CD8 cells in peripheral blood in six infected Macaca mulatta treated with OKT8F. The apparent CD8 depletion started 1 h after antibody administration, and low CD8 levels were maintained until day 8. An increase in plasma viremia of one to three orders of magnitude was observed in five of the six macaques. The injection of a control antibody to an infected macaque did not induce a sustained viral load increase, nor did it significantly reduce the number of CD8(+) T cells. These results demonstrate that CD8 cells play a crucial role in suppressing SIV replication in vivo.

摘要

为了确定CD8(+) T细胞在体内控制猴免疫缺陷病毒(SIV)复制中的作用,我们使用抗CD8单克隆抗体OKT8F研究了耗尽该细胞群体的效果。在用OKT8F处理的6只感染恒河猴中,外周血中的CD8细胞平均减少了99.9%。抗体给药后1小时开始出现明显的CD8细胞耗竭,低CD8水平一直维持到第8天。6只猕猴中有5只观察到血浆病毒血症增加了1至3个数量级。向感染的猕猴注射对照抗体既未诱导病毒载量持续增加,也未显著减少CD8(+) T细胞的数量。这些结果表明,CD8细胞在体内抑制SIV复制中起着关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5978/2193038/18a1818f4ce8/JEM982254.f1.jpg

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