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PMID |
Sentence |
1 |
11675375
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Here, in the course of trying to understand the mechanism for synergy between IL-12 and TNF-alpha in up-regulating IFN-gamma production, we find that when the stimulus through the TCR is too weak to induce cell proliferation, which would be needed for selection, IL-12 and TNF-alpha synergize to up-regulate not only IFN-gamma, but also the IL-12Rbeta2 chain, which triggers IFN-gamma production.
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2 |
15731046
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Moreover, the production of IFN-gamma by NK cells was greatly enhanced when a small amount of interleukin-12 (IL-12) was added, and this synergistic effect was associated with increased expression of the IL-12 receptor beta2.
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3 |
15731046
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In conclusion, we demonstrated that NK cells are present in the gastroduodenal mucosa of humans and that NK cells produce high levels of IFN-gamma when stimulated with a combination of H. pylori antigen and IL-12.
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4 |
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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5 |
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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6 |
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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7 |
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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8 |
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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9 |
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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10 |
16704888
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The adjuvant effects of the toll-like receptor 3 ligand polyinosinic-cytidylic acid poly (I:C) on antigen-specific CD8+ T cell responses are partially dependent on NK cells with the induction of a beneficial cytokine milieu.
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11 |
16704888
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Poly (I:C), a TLR3 ligand, has shown promise as a vaccine adjuvant to CD8(+) T cell responses.
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12 |
16704888
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Poly (I:C) treatment was associated with a rapid induction of inflammatory cytokines in the serum, including IL-6, IL-10, MCP-1, TNF-alpha, IFN-alpha, and IFN-gamma, and selective increases in the numbers of NK (NK1.1(+)CD11b(+)) cells and Mvarphi (NK1.1(-)CD11b(+)), but not NK T (CD3(+)NK1.1(+)) cells.
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13 |
16704888
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Poly (I:C) treatment in TNF-alpha, type I IFNR, IFN-gamma, IL-6, IL-12Rbeta2, or IL-15 gene-deficient mice revealed a reciprocal interaction and interdependence in the induction of these cytokines, where the absence of one cytokine impacted on the production of others.
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14 |
16704888
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Further, the adjuvant effects of poly (I:C) were dependent on the endogenous levels of type I IFNs, TNF-alpha, IFN-gamma, IL-12, and IL-15.
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15 |
16704888
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IFN-alpha and IFN-beta, but not TNF-alpha or IL-6, were able to mimic the adjuvant effects of poly (I:C).
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16 |
17184756
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However, by the third week of infection we found decreased IL-12Rbeta2 expression by BABL/c splenocytes, corresponding to their inability to produce interferon-gamma in Brucella recall responses at this time as reported previously.
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17 |
18490715
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IL-12p40 is a natural antagonist which inhibits IL-12- and IL-23-mediated biological activity by blocking the binding of IL-12/23 to their receptors.
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18 |
18490715
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Moreover, the differential CD8(+) T cell response by IL-12p40 was still observed in IL-12Rbeta2 knockout (IL-12Rbeta2KO), but not in IL-12Rbeta1 knockout (IL-12Rbeta1KO) mice, indicating that IL-12p40 is a cytokine which can modulate Ag-specific T cell responses depending on IL-12Rbeta1.
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19 |
19519403
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In this view, new therapeutic approaches may be planned including: i) pre-screening of melanoma patients for IL-12Rbeta2 expression to identify potential responders, ii) administration of small and less frequent doses of IL-12 to avoid toxicity and iii) targeting of IL-12 to IL-12R(+) tumor cells, such as local administration in patients with skin tumors or injection of IL-12 fused to an antibody specific to tumor cells.
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20 |
19915058
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Surprisingly, DC.Tbets were impaired in their production of IL-12 family member cytokines (IL-12p70, IL-23, and IL-27) when compared with control DC, and the capacity of DC.Tbet to preferentially prime type 1 T cell responses was only minimally inhibited by cytokine (IL-12p70, IL-23, IFN-gamma) neutralization or receptor (IL-12Rbeta2, IL-27R) blockade during T cell priming.
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