期刊
JOURNAL OF IMMUNOLOGY
卷 193, 期 1, 页码 306-316出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1400490
关键词
-
类别
资金
- National Institutes of Health [R01 AI090795]
- Colorado Clinical and Translational Sciences Institute [TL1 TR000155]
- Molecular Pathogenesis of Infectious Disease [T32 AI052066]
- Howard Hughes Medical Institute
- National Institutes of Health Division of Intramural Research
- University of Colorado, Denver, Department of Medicine Early Career Scholar Program
- MRC [MC_U117581330] Funding Source: UKRI
- Medical Research Council [MC_U117581330] Funding Source: researchfish
Tetherin/BST-2 is a host restriction factor that could directly inhibit retroviral particle release by tethering nascent virions to the plasma membrane. However, the immunological impact of Tetherin during retrovirus infection remains unknown. We now show that Tetherin influences antiretroviral cell-mediated immune responses. In contrast to the direct antiviral effects of Tetherin, which are dependent on cell surface expression, the immunomodulatory effects are linked to the endocytosis of the molecule. Mice encoding endocytosis-competent C57BL/6 Tetherin exhibited lower viremia and pathology at 7 d postinfection with Friend retrovirus (FV) compared with mice encoding endocytosis-defective NZW/LacJ Tetherin. Notably, antiretroviral protection correlated with stronger NK cell responses. In addition, Friend retrovirus infection levels were significantly lower in wild-type C57BL/6 mice than in Tetherin knockout mice at 2 wk postinfection, and antiretroviral protection correlated with stronger NK cell and virus-specific CD8(+) T cell responses. The results demonstrate that Tetherin acts as a modulator of the cell-mediated immune response against retrovirus infection in vivo.
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