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PMID |
Sentence |
1 |
16275627
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Chlorophyllin attenuates IFN-gamma expression in lipopolysaccharide-stimulated murine splenic mononuclear cells via suppressing IL-12 production.
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2 |
16275627
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RT-PCR analysis showed that LPS-activated IFN-gamma expression gradually declined by CHL treatment in a dose dependent manner while mRNA production of TNF-alpha, IL-2, and FasL was not changed.
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3 |
16275627
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CHL also suppressed IL-12 production (p70, a heterodimer of p40 and p35) and the mRNA expression of IL-12 p40 and IL-12 receptors (both IL-12Rbeta1 and IL-12Rbeta2), which are involved in the induction of IFN-gamma expression.
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4 |
16275627
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Furthermore, an electrophoretic mobility shift assay showed that CHL inhibited DNA binding activity of NF-kappaB, STAT-3, and STAT-4 to their cognate DNA recognition motifs, all of which contribute to the IL-12-induced IFN-gamma transcription.
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5 |
16275627
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Exogenous addition of recombinant IL-12 abrogated the inhibitory effect of CHL on IFN-gamma and its mRNA expression in LPS-activated splenocytes.
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6 |
16275627
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Collectively, these results show that CHL inhibits IFN-gamma production by LPS-stimulated splenic mononuclear cells due to down-regulation of IL-12 production.
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7 |
19002608
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IL-10 is able to decrease the needed Th1-generated IFN-gamma and downregulates production of nitric oxide, a required effector mechanism of parasite killing.
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8 |
19002608
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We have been studying the pathways that the host uses to partially control L. mexicana infection, which include STAT4, IFN-gamma, and inducible nitric oxide synthase, but found that the IL-12 pathway is suppressed by IL-10.
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9 |
20434781
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Further studies demonstrated that CS-A up-regulated STAT4 expression and thus, induced IFN-gamma production and Th1 CD4 T cell differentiation.
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10 |
20434781
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CS-A also up-regulated STAT3 and IL-23 expression and thus increased IL-17 producing T cells.
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11 |
22154007
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T cells produce IFNγ in response to IL-12 and IL-18 secreted from Mtb infected macrophages.
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12 |
22154007
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C5(-/-) T cells produced lower levels of IFNγ upon stimulation by antigen presenting cells (APCs) infected with Mtb or when stimulated directly with a combination of IL-12 and IL-18.
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13 |
22154007
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The latter was in part due to a reduced phosphorylation of STAT4 following IL-12/IL-18 stimulation.
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14 |
22154007
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Addition of C5a peptide to IL-12/IL-18 partially restored STAT4 phosphorylation and IFNγ synthesis in C5(-/-) T cells indicating that IL-12/IL-18 mediated signaling within CD3(+) T cells involves C5a peptide.
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15 |
25336459
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CD8 T cells in innate immune responses: using STAT4-dependent but antigen-independent pathways to gamma interferon during viral infection.
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16 |
25336459
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The innate cytokines type 1 IFNs and interleukin-12 (IL-12) can also stimulate IFN-γ production by natural killer (NK) but not naive T cells.
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17 |
25336459
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High basal expression of signal transducer and activator of transcription 4 (STAT4), used by type 1 IFN and IL-12 to induce IFN-γ as well as CD25, contributes to the NK cell responses.
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18 |
25336459
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During acute viral infections, antigen-specific CD8 T cells are stimulated to express elevated STAT4 and respond to the innate factors with IFN-γ production.
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19 |
25336459
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Primary infections of mice with lymphocytic choriomeningitis virus (LCMV) demonstrated that although the elicited antigen-specific CD8 T cells acquired STAT4-dependent innate cytokine responsiveness for IFN-γ and CD25 induction ex vivo, TCR stimulation induced these through STAT4-independent pathways.
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20 |
25336459
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During secondary infections, LCMV-immune CD8 T cells had STAT4-dependent IFN-γ expression at times of innate cytokine induction but subsequently expanded through STAT4-independent pathways.
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21 |
25336459
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The T cell IFN-γ response was STAT4 and IL-12 dependent, but antigen-dependent expansion was absent.
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22 |
25336459
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Natural killer cells can also produce IFN-γ in response to the innate cytokines type 1 IFNs and/or interleukin-12.
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23 |
25336459
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CD8 T cells in innate immune responses: using STAT4-dependent but antigen-independent pathways to gamma interferon during viral infection.
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24 |
25336459
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The innate cytokines type 1 IFNs and interleukin-12 (IL-12) can also stimulate IFN-γ production by natural killer (NK) but not naive T cells.
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25 |
25336459
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High basal expression of signal transducer and activator of transcription 4 (STAT4), used by type 1 IFN and IL-12 to induce IFN-γ as well as CD25, contributes to the NK cell responses.
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26 |
25336459
|
During acute viral infections, antigen-specific CD8 T cells are stimulated to express elevated STAT4 and respond to the innate factors with IFN-γ production.
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27 |
25336459
|
Primary infections of mice with lymphocytic choriomeningitis virus (LCMV) demonstrated that although the elicited antigen-specific CD8 T cells acquired STAT4-dependent innate cytokine responsiveness for IFN-γ and CD25 induction ex vivo, TCR stimulation induced these through STAT4-independent pathways.
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28 |
25336459
|
During secondary infections, LCMV-immune CD8 T cells had STAT4-dependent IFN-γ expression at times of innate cytokine induction but subsequently expanded through STAT4-independent pathways.
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29 |
25336459
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The T cell IFN-γ response was STAT4 and IL-12 dependent, but antigen-dependent expansion was absent.
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30 |
25336459
|
Natural killer cells can also produce IFN-γ in response to the innate cytokines type 1 IFNs and/or interleukin-12.
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31 |
25336459
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CD8 T cells in innate immune responses: using STAT4-dependent but antigen-independent pathways to gamma interferon during viral infection.
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32 |
25336459
|
The innate cytokines type 1 IFNs and interleukin-12 (IL-12) can also stimulate IFN-γ production by natural killer (NK) but not naive T cells.
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33 |
25336459
|
High basal expression of signal transducer and activator of transcription 4 (STAT4), used by type 1 IFN and IL-12 to induce IFN-γ as well as CD25, contributes to the NK cell responses.
|
34 |
25336459
|
During acute viral infections, antigen-specific CD8 T cells are stimulated to express elevated STAT4 and respond to the innate factors with IFN-γ production.
|
35 |
25336459
|
Primary infections of mice with lymphocytic choriomeningitis virus (LCMV) demonstrated that although the elicited antigen-specific CD8 T cells acquired STAT4-dependent innate cytokine responsiveness for IFN-γ and CD25 induction ex vivo, TCR stimulation induced these through STAT4-independent pathways.
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36 |
25336459
|
During secondary infections, LCMV-immune CD8 T cells had STAT4-dependent IFN-γ expression at times of innate cytokine induction but subsequently expanded through STAT4-independent pathways.
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37 |
25336459
|
The T cell IFN-γ response was STAT4 and IL-12 dependent, but antigen-dependent expansion was absent.
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38 |
25336459
|
Natural killer cells can also produce IFN-γ in response to the innate cytokines type 1 IFNs and/or interleukin-12.
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39 |
25336459
|
CD8 T cells in innate immune responses: using STAT4-dependent but antigen-independent pathways to gamma interferon during viral infection.
|
40 |
25336459
|
The innate cytokines type 1 IFNs and interleukin-12 (IL-12) can also stimulate IFN-γ production by natural killer (NK) but not naive T cells.
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41 |
25336459
|
High basal expression of signal transducer and activator of transcription 4 (STAT4), used by type 1 IFN and IL-12 to induce IFN-γ as well as CD25, contributes to the NK cell responses.
|
42 |
25336459
|
During acute viral infections, antigen-specific CD8 T cells are stimulated to express elevated STAT4 and respond to the innate factors with IFN-γ production.
|
43 |
25336459
|
Primary infections of mice with lymphocytic choriomeningitis virus (LCMV) demonstrated that although the elicited antigen-specific CD8 T cells acquired STAT4-dependent innate cytokine responsiveness for IFN-γ and CD25 induction ex vivo, TCR stimulation induced these through STAT4-independent pathways.
|
44 |
25336459
|
During secondary infections, LCMV-immune CD8 T cells had STAT4-dependent IFN-γ expression at times of innate cytokine induction but subsequently expanded through STAT4-independent pathways.
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45 |
25336459
|
The T cell IFN-γ response was STAT4 and IL-12 dependent, but antigen-dependent expansion was absent.
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46 |
25336459
|
Natural killer cells can also produce IFN-γ in response to the innate cytokines type 1 IFNs and/or interleukin-12.
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47 |
25336459
|
CD8 T cells in innate immune responses: using STAT4-dependent but antigen-independent pathways to gamma interferon during viral infection.
|
48 |
25336459
|
The innate cytokines type 1 IFNs and interleukin-12 (IL-12) can also stimulate IFN-γ production by natural killer (NK) but not naive T cells.
|
49 |
25336459
|
High basal expression of signal transducer and activator of transcription 4 (STAT4), used by type 1 IFN and IL-12 to induce IFN-γ as well as CD25, contributes to the NK cell responses.
|
50 |
25336459
|
During acute viral infections, antigen-specific CD8 T cells are stimulated to express elevated STAT4 and respond to the innate factors with IFN-γ production.
|
51 |
25336459
|
Primary infections of mice with lymphocytic choriomeningitis virus (LCMV) demonstrated that although the elicited antigen-specific CD8 T cells acquired STAT4-dependent innate cytokine responsiveness for IFN-γ and CD25 induction ex vivo, TCR stimulation induced these through STAT4-independent pathways.
|
52 |
25336459
|
During secondary infections, LCMV-immune CD8 T cells had STAT4-dependent IFN-γ expression at times of innate cytokine induction but subsequently expanded through STAT4-independent pathways.
|
53 |
25336459
|
The T cell IFN-γ response was STAT4 and IL-12 dependent, but antigen-dependent expansion was absent.
|
54 |
25336459
|
Natural killer cells can also produce IFN-γ in response to the innate cytokines type 1 IFNs and/or interleukin-12.
|
55 |
25336459
|
CD8 T cells in innate immune responses: using STAT4-dependent but antigen-independent pathways to gamma interferon during viral infection.
|
56 |
25336459
|
The innate cytokines type 1 IFNs and interleukin-12 (IL-12) can also stimulate IFN-γ production by natural killer (NK) but not naive T cells.
|
57 |
25336459
|
High basal expression of signal transducer and activator of transcription 4 (STAT4), used by type 1 IFN and IL-12 to induce IFN-γ as well as CD25, contributes to the NK cell responses.
|
58 |
25336459
|
During acute viral infections, antigen-specific CD8 T cells are stimulated to express elevated STAT4 and respond to the innate factors with IFN-γ production.
|
59 |
25336459
|
Primary infections of mice with lymphocytic choriomeningitis virus (LCMV) demonstrated that although the elicited antigen-specific CD8 T cells acquired STAT4-dependent innate cytokine responsiveness for IFN-γ and CD25 induction ex vivo, TCR stimulation induced these through STAT4-independent pathways.
|
60 |
25336459
|
During secondary infections, LCMV-immune CD8 T cells had STAT4-dependent IFN-γ expression at times of innate cytokine induction but subsequently expanded through STAT4-independent pathways.
|
61 |
25336459
|
The T cell IFN-γ response was STAT4 and IL-12 dependent, but antigen-dependent expansion was absent.
|
62 |
25336459
|
Natural killer cells can also produce IFN-γ in response to the innate cytokines type 1 IFNs and/or interleukin-12.
|