Proc Natl Acad Sci U S A 2012,
PMID: 22665768
Wu, Tuoqi; Wieland, Andreas; Araki, Koichi; Davis, Carl W; Ye, Lilin; Hale, J Scott; Ahmed, Rafi
MicroRNAs are important regulators of various developmental and physiological processes. However, their roles in the CD8(+) T-cell response are not well understood. Using an acute viral infection model, we show that microRNAs of the miR-17-92 cluster are strongly induced after T-cell activation, down-regulated after clonal expansion, and further silenced during memory development. miR-17-92 promotes cell-cycle progression of effector CD8(+) T cells, and its expression is critical to the rapid expansion of these cells. However, excessive miR-17-92 expression enhances mammalian target of rapamycin (mTOR) signaling and strongly skews the differentiation toward short-lived terminal effector cells. Failure to down-regulate miR-17-92 leads to a gradual loss of memory cells and defective central memory cell development. Therefore, our results reveal a temporal expression pattern of miR-17-92 by antigen-specific CD8(+) T cells during viral infection, the precise control of which is critical to the effector expansion and memory differentiation of CD8(+) T cells.
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Text Mining Data
(mTOR) signaling → miR-17-92: "
However, excessive
miR-17-92 expression
enhances mammalian target of rapamycin
(mTOR) signaling and strongly skews the differentiation toward short lived terminal effector cells
"
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