| Literature DB >> 23084923 |
Thomas Baranek1, Thien-Phong Vu Manh, Yannick Alexandre, Muhammad Ahmad Maqbool, Joaquin Zacarias Cabeza, Elena Tomasello, Karine Crozat, Gilles Bessou, Nicolas Zucchini, Scott H Robbins, Eric Vivier, Ulrich Kalinke, Pierre Ferrier, Marc Dalod.
Abstract
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.Entities:
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Year: 2012 PMID： 23084923 DOI： 10.1016/j.chom.2012.09.002
Source DB: PubMed Journal: Cell Host Microbe ISSN： 1931-3128 Impact factor: 21.023