期刊
CELL HOST & MICROBE
卷 12, 期 4, 页码 571-584出版社
CELL PRESS
DOI: 10.1016/j.chom.2012.09.002
关键词
-
资金
- CNRS
- Inserm
- Agence Nationale de la Recherche (ANR) (pDCphysiology) [ANR-07-MIME-018-01]
- Agence Nationale de la Recherche (ANR) (EMICIF) [ANR-08-MIEN-008-02]
- Agence Nationale de la Recherche (ANR) (PhyloGenDC) [ANR-09-BLAN-0073-02]
- I2HD collaborative project
- SANOFI
- Agence Nationale de la Recherche (ANR) [ANR-09-BLAN-0073] Funding Source: Agence Nationale de la Recherche (ANR)
Type I interferons (IFNs) are central to antiviral defense, but how they orchestrate immune cell function is incompletely understood. We determined that IFNs produced during murine cytomegalovirus (MCMV) infection differentially affect dendritic cells (DCs) and natural killer (NK) cells. IFNs induce cell-intrinsic responses in DCs, activating antiproliferative, antiviral, and lymphocyte-activating gene networks, consistent with high activity of the transcription factor STAT1 in these cells. By comparison, NK cells exhibit lower STAT1 expression and reduced IFN responsiveness. Rather, IFNs indirectly affect NK cells by inducing IL-15, which activates the transcription factor E2F and stimulates genes promoting cell expansion. IFN cell-intrinsic responses are necessary in DCs, but not NK cells, for MCMV resistance. Thus, sensitivity to IFN-induced cytokines and differences in IFN receptor signaling program immune cells to mount distinct responses that promote viral control.
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