期刊
FRONTIERS IN IMMUNOLOGY
卷 8, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2017.01696
关键词
MicroRNAs; CD8(+) T cells; T-bet; influenza; Src homology 2-containing inositol phosphatase-1; miR-155
类别
资金
- NIH [R01 AI117718, AI105343, P01 AI108545, U19 AI082630, U19 AI117950]
- Parker Institute
- Worldwide Cancer Research
- Erasmus University Medical Center
We report here that the expression of the transcription factor T-bet, which is known to be required for effector cytotoxic CD8(+) T lymphocytes (CTL) generation and effector memory cell formation, is regulated in CTL by microRNA-155 (miR-155). Importantly, we show that the proliferative effect of miR-155 on CD8(+) T cells is mediated by T-bet. T-bet levels in CTL were controlled in vivo by miR-155 via SH2 (Src homology 2)-containing inositol phosphatase-1 (SHIP-1), a known direct target of miR-155, and SHIP-1 directly downregulated T-bet. Our studies reveal an important and unexpected signaling axis between miR-155, T-bet, and SHIP-1 in in vivo CTL responses and suggest an important signaling module that regulates effector CTL immunity.
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