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PMID |
Sentence |
1 |
23845179
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IL4 and IFNalpha generation of dendritic cells reveals great migratory potential and NFkB and cJun expression in IL4DCs.
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2 |
23845179
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Dendritic cells (DCs) recently revealed as a potent tumor vaccine component, are commonly differentiated from monocytes by cultivation with IL-4 and GM-CSF.
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3 |
23845179
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The aim of this study was to compare the functionality and phenotypic characterization of monocyte-derived DC generated by IL-4 (IL4DC) and IFNalpha (IFNalphaDC) modified protocols.
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4 |
23845179
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We herein investigated the molecular mechanism underlying the parameters previously described, as the relative expression of NF-kB p65, c-fos and c-jun, transcription factors.
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5 |
23845179
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Our results demonstrated that IL4DC presented a stable phenotype, an increase in migratory capacity and NF-KB activation, in addition to lower levels of miR-146 a and miR-221.
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6 |
26090579
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IFN-α-Induced Downregulation of miR-221 in Dendritic Cells: Implications for HCV Pathogenesis and Treatment.
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7 |
26090579
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We report that IFN-α downregulates miR-221 in both DC subsets via inhibition of STAT3.
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8 |
26090579
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We validated proapoptotic proteins BCL2L11 and CDKN1C as miR-221 targets suggesting that IFN-α can induce DC apoptosis via miR-221 downregulation.
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9 |
26090579
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In addition, we validated another miR-221 target, SOCS1, which is known to be a negative regulator of JAK/STAT signaling.
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10 |
26090579
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Consistent with this, miR-221 overexpression in mDCs enhanced the secretion of proinflammatory cytokines IL-6 and TNF-α.
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11 |
26090579
|
In peripheral blood mononuclear cells (PBMCs) of HIV-1/HCV co-infected individuals undergoing IFN-α-based treatment the baseline miR-221 expression was lower in non-responders compared with responders; and miR-221 expression directly correlated with DC frequency and IL-6/TNF-α secretion.
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12 |
26090579
|
IFN-α-Induced Downregulation of miR-221 in Dendritic Cells: Implications for HCV Pathogenesis and Treatment.
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13 |
26090579
|
We report that IFN-α downregulates miR-221 in both DC subsets via inhibition of STAT3.
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14 |
26090579
|
We validated proapoptotic proteins BCL2L11 and CDKN1C as miR-221 targets suggesting that IFN-α can induce DC apoptosis via miR-221 downregulation.
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15 |
26090579
|
In addition, we validated another miR-221 target, SOCS1, which is known to be a negative regulator of JAK/STAT signaling.
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16 |
26090579
|
Consistent with this, miR-221 overexpression in mDCs enhanced the secretion of proinflammatory cytokines IL-6 and TNF-α.
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17 |
26090579
|
In peripheral blood mononuclear cells (PBMCs) of HIV-1/HCV co-infected individuals undergoing IFN-α-based treatment the baseline miR-221 expression was lower in non-responders compared with responders; and miR-221 expression directly correlated with DC frequency and IL-6/TNF-α secretion.
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18 |
26090579
|
IFN-α-Induced Downregulation of miR-221 in Dendritic Cells: Implications for HCV Pathogenesis and Treatment.
|
19 |
26090579
|
We report that IFN-α downregulates miR-221 in both DC subsets via inhibition of STAT3.
|
20 |
26090579
|
We validated proapoptotic proteins BCL2L11 and CDKN1C as miR-221 targets suggesting that IFN-α can induce DC apoptosis via miR-221 downregulation.
|
21 |
26090579
|
In addition, we validated another miR-221 target, SOCS1, which is known to be a negative regulator of JAK/STAT signaling.
|
22 |
26090579
|
Consistent with this, miR-221 overexpression in mDCs enhanced the secretion of proinflammatory cytokines IL-6 and TNF-α.
|
23 |
26090579
|
In peripheral blood mononuclear cells (PBMCs) of HIV-1/HCV co-infected individuals undergoing IFN-α-based treatment the baseline miR-221 expression was lower in non-responders compared with responders; and miR-221 expression directly correlated with DC frequency and IL-6/TNF-α secretion.
|
24 |
26090579
|
IFN-α-Induced Downregulation of miR-221 in Dendritic Cells: Implications for HCV Pathogenesis and Treatment.
|
25 |
26090579
|
We report that IFN-α downregulates miR-221 in both DC subsets via inhibition of STAT3.
|
26 |
26090579
|
We validated proapoptotic proteins BCL2L11 and CDKN1C as miR-221 targets suggesting that IFN-α can induce DC apoptosis via miR-221 downregulation.
|
27 |
26090579
|
In addition, we validated another miR-221 target, SOCS1, which is known to be a negative regulator of JAK/STAT signaling.
|
28 |
26090579
|
Consistent with this, miR-221 overexpression in mDCs enhanced the secretion of proinflammatory cytokines IL-6 and TNF-α.
|
29 |
26090579
|
In peripheral blood mononuclear cells (PBMCs) of HIV-1/HCV co-infected individuals undergoing IFN-α-based treatment the baseline miR-221 expression was lower in non-responders compared with responders; and miR-221 expression directly correlated with DC frequency and IL-6/TNF-α secretion.
|
30 |
26090579
|
IFN-α-Induced Downregulation of miR-221 in Dendritic Cells: Implications for HCV Pathogenesis and Treatment.
|
31 |
26090579
|
We report that IFN-α downregulates miR-221 in both DC subsets via inhibition of STAT3.
|
32 |
26090579
|
We validated proapoptotic proteins BCL2L11 and CDKN1C as miR-221 targets suggesting that IFN-α can induce DC apoptosis via miR-221 downregulation.
|
33 |
26090579
|
In addition, we validated another miR-221 target, SOCS1, which is known to be a negative regulator of JAK/STAT signaling.
|
34 |
26090579
|
Consistent with this, miR-221 overexpression in mDCs enhanced the secretion of proinflammatory cytokines IL-6 and TNF-α.
|
35 |
26090579
|
In peripheral blood mononuclear cells (PBMCs) of HIV-1/HCV co-infected individuals undergoing IFN-α-based treatment the baseline miR-221 expression was lower in non-responders compared with responders; and miR-221 expression directly correlated with DC frequency and IL-6/TNF-α secretion.
|
36 |
26090579
|
IFN-α-Induced Downregulation of miR-221 in Dendritic Cells: Implications for HCV Pathogenesis and Treatment.
|
37 |
26090579
|
We report that IFN-α downregulates miR-221 in both DC subsets via inhibition of STAT3.
|
38 |
26090579
|
We validated proapoptotic proteins BCL2L11 and CDKN1C as miR-221 targets suggesting that IFN-α can induce DC apoptosis via miR-221 downregulation.
|
39 |
26090579
|
In addition, we validated another miR-221 target, SOCS1, which is known to be a negative regulator of JAK/STAT signaling.
|
40 |
26090579
|
Consistent with this, miR-221 overexpression in mDCs enhanced the secretion of proinflammatory cytokines IL-6 and TNF-α.
|
41 |
26090579
|
In peripheral blood mononuclear cells (PBMCs) of HIV-1/HCV co-infected individuals undergoing IFN-α-based treatment the baseline miR-221 expression was lower in non-responders compared with responders; and miR-221 expression directly correlated with DC frequency and IL-6/TNF-α secretion.
|