期刊
JOURNAL OF VIROLOGY
卷 86, 期 4, 页码 2165-2175出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.06042-11
关键词
-
类别
资金
- NIH [1R01AI083201-01]
- Croatian Science Foundation [04/16]
- Croatian Ministry of Science and Technology [0621261-1268]
- Canadian Institutes of Health Research [MOP-7781]
- Canada Research Chairs Program
- German Research Foundation [SFB490, E3, E4]
Natural killer (NK) cells and CD8(+) T cells play a prominent role in the clearance of mouse cytomegalovirus (MCMV) infection. The role of NK cells in modulating the CD8(+) T-cell response to MCMV infection is still the subject of intensive research. For analyzing the impact of NK cells on mounting of a CD8(+) T-cell response and the contribution of these cells to virus control during the first days postinfection (p.i.), we used C57BL/6 mice in which NK cells are specifically activated through the Ly49H receptor engaged by the MCMV-encoded ligand m157. Our results indicate that the requirement for CD8(+) T cells in early MCMV control inversely correlates with the engagement of Ly49H. While depletion of CD8(+) T cells has only a minor effect on the early control of wild-type MCMV, CD8(+) T cells are essential in the control of Delta m157 virus. The frequencies of virus epitope-specific CD8(+) T cells and their activation status were higher in mice infected with Delta m157 virus. In addition, these mice showed elevated levels of alpha interferon (IFN-alpha) and several other proinflammatory cytokines as early as 1.5 days p.i. Although the numbers of conventional dendritic cells (cDCs) were reduced later during infection, particularly in Delta m157-infected mice, they were not significantly affected at the peak of the cytokine response. Altogether, we concluded that increased antigen load, preservation of early cDCs' function, and higher levels of innate cytokines collectively account for an enhanced CD8(+) T-cell response in C57BL/6 mice infected with a virus unable to activate NK cells via the Ly49H m157 interaction.
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