期刊
JOURNAL OF LEUKOCYTE BIOLOGY
卷 94, 期 2, 页码 337-341出版社
WILEY
DOI: 10.1189/jlb.0313158
关键词
type I interferon; interferon regulatory factors; interferon-stimulated genes; APOBEC3
资金
- U.S. National Institutes of Health [DA12815, DA22177, DA27550]
- NATIONAL INSTITUTE ON DRUG ABUSE [R01DA027550, R01DA022177, R01DA012815] Funding Source: NIH RePORTER
RIG-I signaling of macrophages against HIV can be beneficial in the treatment of HIV disease, where intracellular immune defense is compromised. The RIG-I signaling pathway is critical in the activation of the type I IFN-dependent antiviral innate-immune response. We thus examined whether RIG-I activation can inhibit HIV replication in macrophages. We showed that the stimulation of monocyte-derived macrophages with 5ppp-dsRNA, a synthetic ligand for RIG-I, induced the expression of RIG-I, IFN-/, and several IRFs, key regulators of the IFN signaling pathway. In addition, RIG-I activation induced the expression of multiple intracellular HIV-restriction factors, including ISGs, several members of the APOBEC3 family, tetherin and CC chemokines, the ligands for HIV entry coreceptor (CCR5). The inductions of these factors were associated with the inhibition of HIV replication in macrophages stimulated by 5ppp-dsRNA. These observations highlight the importance of RIG-I signaling in macrophage innate immunity against HIV, which can be beneficial for the treatment of HIV disease, where intracellular immune defense is compromised by the virus.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据