期刊
SCIENCE
卷 343, 期 6169, 页码 428-432出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1243640
关键词
-
资金
- University of California San Francisco-Gladstone Center for AIDS Research (CFAR)
- NIH [P30 AI027763, R21 AI102782, U19 AI096113, 1DP1036502, P50 GM082250, P01 AI090935, P50 GM081879]
- Gladstone Institutes
- A. P. Giannini Foundation
The progressive depletion of quiescent bystander CD4 T cells, which are nonpermissive to HIV infection, is a principal driver of the acquired immunodeficiency syndrome (AIDS). These cells undergo abortive infection characterized by the cytosolic accumulation of incomplete HIV reverse transcripts. These viral DNAs are sensed by an unidentified host sensor that triggers an innate immune response, leading to caspase-1 activation and pyroptosis. Using unbiased proteomic and targeted biochemical approaches, as well as two independent methods of lentiviral short hairpin RNA-mediated gene knockdown in primary CD4 T cells, we identify interferon-gamma-inducible protein 16 (IFI16) as a host DNA sensor required for CD4 T cell death due to abortive HIV infection. These findings provide insights into a key host pathway that plays a central role in CD4 T cell depletion during disease progression to AIDS.
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