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体外激活诱导的人巨噬细胞对HIV-1感染的抗性

Activation-induced resistance of human macrophages to HIV-1 infection in vitro.

作者信息

Zybarth G, Reiling N, Schmidtmayerova H, Sherry B, Bukrinsky M

机构信息

The Picower Institute for Medical Research, Manhasset, NY 11030, USA.

出版信息

J Immunol. 1999 Jan 1;162(1):400-6.

PMID:9886413
Abstract

Cells of the monocyte/macrophage lineage are the first targets of HIV-1 in patients and also serve as reservoirs for the virus during the course of infection. We investigated the effects of cell activation on early events of HIV-1 infection of monocyte-derived macrophages. Addition of LPS, a potent stimulator of macrophages, at the time of infection stimulated entry of HIV-1 into monocyte-derived macrophages, as judged by accumulation of early products of RT, but inhibited the synthesis of late RT products and strongly repressed nuclear import of the viral DNA, resulting in protection from infection. This effect was mediated by the CD14 receptor and involved activation of the p38 mitogen-activated protein kinase pathway. Disruption of this signaling pathway using a specific inhibitor of the p38 mitogen-activated protein kinase (SB203580) restored HIV-1 infection in the presence of LPS. These results suggest a novel view of the role of macrophage activation in anti-HIV responses of the immune system.

摘要

在患者体内,单核细胞/巨噬细胞谱系的细胞是HIV-1的首要靶标,并且在感染过程中也充当该病毒的储存库。我们研究了细胞活化对单核细胞衍生巨噬细胞感染HIV-1早期事件的影响。在感染时添加脂多糖(一种强效的巨噬细胞刺激剂),通过逆转录酶早期产物的积累判断,刺激了HIV-1进入单核细胞衍生巨噬细胞,但抑制了逆转录酶晚期产物的合成,并强烈抑制了病毒DNA的核输入,从而防止感染。这种效应由CD14受体介导,并涉及p38丝裂原活化蛋白激酶途径的激活。使用p38丝裂原活化蛋白激酶的特异性抑制剂(SB203580)破坏该信号通路,可在存在脂多糖的情况下恢复HIV-1感染。这些结果提示了巨噬细胞活化在免疫系统抗HIV反应中作用的新观点。

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