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PMID |
Sentence |
1 |
22665768
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Temporal expression of microRNA cluster miR-17-92 regulates effector and memory CD8+ T-cell differentiation.
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2 |
22665768
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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.
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3 |
22665768
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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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4 |
22665768
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Temporal expression of microRNA cluster miR-17-92 regulates effector and memory CD8+ T-cell differentiation.
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5 |
22665768
|
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.
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6 |
22665768
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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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7 |
22665768
|
Temporal expression of microRNA cluster miR-17-92 regulates effector and memory CD8+ T-cell differentiation.
|
8 |
22665768
|
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.
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9 |
22665768
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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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10 |
24605077
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TFH cells are characterized by their expression of master regulator, Bcl-6, and chemokine receptor, CXCR5, which are essential for the migration of T cells into the B cell follicle.
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11 |
24605077
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IL-6 and IL-21 cytokine-mediated STAT signaling pathways, including STAT1 and STAT3, are crucial for inducing Bcl-6 expression and TFH cell differentiation.
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12 |
24605077
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TFH cells express important surface molecules such as ICOS, PD-1, IL-21, BTLA, SAP and CD40L for mediating the interaction between T and B cells.
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13 |
24605077
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The miR-17-92 cluster induces Bcl-6 and TFH cell differentiation, whereas miR-10a negatively regulates Bcl-6 expression in T cells.
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14 |
24605077
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In addition, follicular regulatory T (TFR) cells are studied as thymus-derived CXCR5(+)PD-1(+)Foxp3(+) Treg cells that play a significant role in limiting the GC response.
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15 |
26276869
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Cutting Edge: miR-17-92 Is Required for Both CD4 Th1 and T Follicular Helper Cell Responses during Viral Infection.
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16 |
26276869
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Two recent studies demonstrated that the microRNA cluster miR-17-92 selectively promotes CD4 TFH responses.
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17 |
26276869
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Upon viral infection, miR-17-92-deficient CD4 T cells showed impaired clonal expansion and subsequent memory formation.
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18 |
26276869
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Overexpression of miR-17-92 in CD4 T cells resulted in increased expansion of both virus-specific Th1 and TFH cells but selectively enhanced the Th1 response.
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19 |
26276869
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Cutting Edge: miR-17-92 Is Required for Both CD4 Th1 and T Follicular Helper Cell Responses during Viral Infection.
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20 |
26276869
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Two recent studies demonstrated that the microRNA cluster miR-17-92 selectively promotes CD4 TFH responses.
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21 |
26276869
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Upon viral infection, miR-17-92-deficient CD4 T cells showed impaired clonal expansion and subsequent memory formation.
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22 |
26276869
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Overexpression of miR-17-92 in CD4 T cells resulted in increased expansion of both virus-specific Th1 and TFH cells but selectively enhanced the Th1 response.
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23 |
26276869
|
Cutting Edge: miR-17-92 Is Required for Both CD4 Th1 and T Follicular Helper Cell Responses during Viral Infection.
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24 |
26276869
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Two recent studies demonstrated that the microRNA cluster miR-17-92 selectively promotes CD4 TFH responses.
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25 |
26276869
|
Upon viral infection, miR-17-92-deficient CD4 T cells showed impaired clonal expansion and subsequent memory formation.
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26 |
26276869
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Overexpression of miR-17-92 in CD4 T cells resulted in increased expansion of both virus-specific Th1 and TFH cells but selectively enhanced the Th1 response.
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27 |
26276869
|
Cutting Edge: miR-17-92 Is Required for Both CD4 Th1 and T Follicular Helper Cell Responses during Viral Infection.
|
28 |
26276869
|
Two recent studies demonstrated that the microRNA cluster miR-17-92 selectively promotes CD4 TFH responses.
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29 |
26276869
|
Upon viral infection, miR-17-92-deficient CD4 T cells showed impaired clonal expansion and subsequent memory formation.
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30 |
26276869
|
Overexpression of miR-17-92 in CD4 T cells resulted in increased expansion of both virus-specific Th1 and TFH cells but selectively enhanced the Th1 response.
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