Endothelial cells enhance human immunodeficiency virus type 1 replication in macrophages through a C/EBP-dependent mechanism.
Endothelial cells enhance human immunodeficiency virus type 1 replication in macrophages through a C/EBP-dependent mechanism.
复制标题
内皮细胞通过 C/EBP 依赖性机制增强巨噬细胞中人类免疫缺陷病毒 1 型的复制。
DOI：
10.1128/jvi.75.20.9703-9712.2001
复制
发表时间：
2001
影响因子：
5.4
通讯作者：
Henderson,AJ
中科院分区：
文献类型：
--
作者：
Lee,ES;Zhou,H;Henderson,AJ
Macrophages are early targets of human immunodeficiency virus type 1 (HIV-1) infection and serve as potential reservoirs for long-term infection. Through inflammatory mediators and direct cell contact, infected macrophages interact with neighboring cell populations, such as the endothelium, which create a microenvironment favorable for HIV-1 replication. We hypothesize that the transcriptional activator C/EBPβ is critical for macrophages to respond to endothelial cell-derived signals. We show that endothelial cells significantly enhance C/EBPβ binding activity and HIV-1 replication in macrophages. This increase in HIV-1 transcription is due to cell-cell contact as well as the production of soluble factors, mediated in part by ICAM-1 and interleukin 6, respectively. Furthermore, C/EBP factors are necessary for endothelial cell-dependent activation of HIV-1 transcription in macrophages, and HIV-1 induction can be inhibited by a C/EBP dominant-negative protein. In addition, C/EBP binding sites are necessary for efficient LTR activity and HIV-1 replication in the presence of endothelial cells. Taken together, these results indicate that endothelial cells, through the activation of C/EBPβ, provide a microenvironment that supports HIV-1 replication in monocytes/macrophages.
