Journal
CELL REPORTS
Volume 20, Issue 11, Pages 2598-2611Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2017.08.065
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Funding
- National Research Foundation of Korea (NRF) - Ministry of Science, ICT & Future Planning [2015R1A2A1A10056084, 2016R1A2B4014230]
- Korean Health Technology R&D Project through the Korean Health Industry Development Institute (KHIDI) - Ministry of Health Welfare [HI14C2680, HI15C0493]
- National Research Council of Science & Technology (NST) grant [CRC-15-02-KRIBB]
- National Research Foundation of Korea [2016R1A2B4014230, 2015R1A2A1A10056084] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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MicroRNA (miR)-150 is a developmental regulator of several immune-cell types, but its role in CD8(+) T cells is largely unexplored. Here, we show that miR-150 regulates the generation of memory CD8(+) T cells. After acute virus infection, miR-150 knockout (KO) mice exhibited an accelerated differentiation of CD8(+) T cells into memory cells and improved production of effector cytokines. Additionally, miR-150 KO CD8(+) T cells displayed an enhanced recall response and improved protection against infections with another virus and bacteria. We found that forkhead box O1 (Foxo1) and T cell-specific transcription factor 1 (TCF1) are upregulated during the early activation phase in miR-150 KO CD8(+) T cells and that miR-150 directly targets and suppresses Foxo1. These results suggest that miR-150-mediated suppression of Foxo1 regulates the balance between effector and memory cell differentiation, which might aid in the development of improved vaccines and T cell therapeutics.
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