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Gene Information
Gene symbol: IFNA1
Gene name: interferon, alpha 1
HGNC ID: 5417
Synonyms: IFNA@, IFL, IFN, IFN-ALPHA, IFNA13, IFN-alphaD
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 1373261 | In the present study, primary antibody responses were assessed in cattle immunized with either 2 or 50 micrograms of gIV, and treated with multiple doses of IL-2 or combinations of IL-2 and IFN-alpha or IL-2 and IFN-gamma. |
| 2 | 1373261 | Addition of IFN-alpha or IFN-gamma to the IL-2/gIV/Avridine formulation did not affect any of the immune parameters tested. |
| 3 | 1373261 | As IFN-alpha is an effective immunoprophylactic agent for infectious bovine rhinotracheitis (IBR), combination vaccine-immunoprophylaxis may become feasible using IL-2 as a co-adjuvant. |
| 4 | 1373261 | In the present study, primary antibody responses were assessed in cattle immunized with either 2 or 50 micrograms of gIV, and treated with multiple doses of IL-2 or combinations of IL-2 and IFN-alpha or IL-2 and IFN-gamma. |
| 5 | 1373261 | Addition of IFN-alpha or IFN-gamma to the IL-2/gIV/Avridine formulation did not affect any of the immune parameters tested. |
| 6 | 1373261 | As IFN-alpha is an effective immunoprophylactic agent for infectious bovine rhinotracheitis (IBR), combination vaccine-immunoprophylaxis may become feasible using IL-2 as a co-adjuvant. |
| 7 | 1373261 | In the present study, primary antibody responses were assessed in cattle immunized with either 2 or 50 micrograms of gIV, and treated with multiple doses of IL-2 or combinations of IL-2 and IFN-alpha or IL-2 and IFN-gamma. |
| 8 | 1373261 | Addition of IFN-alpha or IFN-gamma to the IL-2/gIV/Avridine formulation did not affect any of the immune parameters tested. |
| 9 | 1373261 | As IFN-alpha is an effective immunoprophylactic agent for infectious bovine rhinotracheitis (IBR), combination vaccine-immunoprophylaxis may become feasible using IL-2 as a co-adjuvant. |
| 10 | 1701805 | The empirical evidence that IFN alpha exerts clinically significant anti-tumor effects against melanoma is reviewed, and evolving status of adjuvant trials of IFN alpha and gamma is noted. |
| 11 | 1701805 | Regional therapy by the intralesional route has yielded enhanced activity for a range of biologics, including bacillus Calmette-Guerin (BCG), IL-2, and tumor necrosis factor (TNF). |
| 12 | 1728399 | We have administered the cytokines interleukin 2 (IL-2), alpha-interferon (IFN-alpha), and gamma-interferon (IFN-gamma) to mice and measured the alterations in hepatic drug-metabolizing enzyme activities. |
| 13 | 1728399 | The administration of IL-2 alone or in combination with IFN-alpha or IFN-gamma causes dose-dependent increases in hexobarbital-induced sleep times. |
| 14 | 1728399 | Sublethally irradiated mice and athymic nude mice receiving injections of IL-2 or IL-2 plus IFN-alpha do not show the inhibition of drug metabolism seen in normal mice. |
| 15 | 1728399 | We have administered the cytokines interleukin 2 (IL-2), alpha-interferon (IFN-alpha), and gamma-interferon (IFN-gamma) to mice and measured the alterations in hepatic drug-metabolizing enzyme activities. |
| 16 | 1728399 | The administration of IL-2 alone or in combination with IFN-alpha or IFN-gamma causes dose-dependent increases in hexobarbital-induced sleep times. |
| 17 | 1728399 | Sublethally irradiated mice and athymic nude mice receiving injections of IL-2 or IL-2 plus IFN-alpha do not show the inhibition of drug metabolism seen in normal mice. |
| 18 | 1728399 | We have administered the cytokines interleukin 2 (IL-2), alpha-interferon (IFN-alpha), and gamma-interferon (IFN-gamma) to mice and measured the alterations in hepatic drug-metabolizing enzyme activities. |
| 19 | 1728399 | The administration of IL-2 alone or in combination with IFN-alpha or IFN-gamma causes dose-dependent increases in hexobarbital-induced sleep times. |
| 20 | 1728399 | Sublethally irradiated mice and athymic nude mice receiving injections of IL-2 or IL-2 plus IFN-alpha do not show the inhibition of drug metabolism seen in normal mice. |
| 21 | 2128947 | The production of mumps ELISA antibodies was closely related to IFN-gamma production (r = 0.326, p less than 0.01) but not to IFN-alpha production (r = 0.084, p greater than 0.05). |
| 22 | 2411662 | In freshly prepared whole-spleen cultures and in 2-h adherent cultures, F-1 induced predominantly IFN-alpha/beta. |
| 23 | 2411662 | In whole-spleen cultures that were allowed to age for 24 to 48 h before stimulation, F-1 was seen to induce mostly IFN-gamma, with low levels of IFN-alpha/beta present. |
| 24 | 2411662 | Since only IFN-alpha/beta was produced in T-cell-depleted populations (at 2 h or at 48 h), it is suggested that T cells are responsible for IFN-gamma production in aged cultures. |
| 25 | 2411662 | In freshly prepared whole-spleen cultures and in 2-h adherent cultures, F-1 induced predominantly IFN-alpha/beta. |
| 26 | 2411662 | In whole-spleen cultures that were allowed to age for 24 to 48 h before stimulation, F-1 was seen to induce mostly IFN-gamma, with low levels of IFN-alpha/beta present. |
| 27 | 2411662 | Since only IFN-alpha/beta was produced in T-cell-depleted populations (at 2 h or at 48 h), it is suggested that T cells are responsible for IFN-gamma production in aged cultures. |
| 28 | 2411662 | In freshly prepared whole-spleen cultures and in 2-h adherent cultures, F-1 induced predominantly IFN-alpha/beta. |
| 29 | 2411662 | In whole-spleen cultures that were allowed to age for 24 to 48 h before stimulation, F-1 was seen to induce mostly IFN-gamma, with low levels of IFN-alpha/beta present. |
| 30 | 2411662 | Since only IFN-alpha/beta was produced in T-cell-depleted populations (at 2 h or at 48 h), it is suggested that T cells are responsible for IFN-gamma production in aged cultures. |
| 31 | 2494319 | The effect of treating cultured Madin-Darby bovine kidney cells (MDBK) with recombinant bovine interferon-alpha 1 (IFN-alpha 1) or recombinant bovine interferon-gamma (IFN-gamma) on the intracellular development of Eimeria tenella was studied. |
| 32 | 2494319 | Treatment of the MDBK cells with IFN alpha-1 for 24 hr before infection and for 48 hr after infection had no effect on the development of E. tenella. |
| 33 | 2494319 | The effect of treating cultured Madin-Darby bovine kidney cells (MDBK) with recombinant bovine interferon-alpha 1 (IFN-alpha 1) or recombinant bovine interferon-gamma (IFN-gamma) on the intracellular development of Eimeria tenella was studied. |
| 34 | 2494319 | Treatment of the MDBK cells with IFN alpha-1 for 24 hr before infection and for 48 hr after infection had no effect on the development of E. tenella. |
| 35 | 2509777 | The SEA-induced IFN was inactivated by treatment with 0.2M glycine-HCl (pH 2.0) but not by heating at 56 degrees C for 30 min. nor by treatment with anti-IFN alpha/beta antibodies, and the fact suggest that the IFN belonged to the gamma type. 2. |
| 36 | 2509777 | Treatment of the BCG-sensitized mice with silica and 2-chloroadenosine (2CA), specific lethal agents for macrophages, reduced the SEA-induced IFN production. 3. |
| 37 | 2509777 | The SEA-induced IFN production occurred in mice immunized with BCG either intravenously or intraperitoneally, although they showed weak or no footpad reaction to purified protein derivatives (PPD). |
| 38 | 2509777 | In contrast, mice sensitized subcutaneously with BCG showed strong foodpad reaction to PPD but not the SEA-induced IFN production. |
| 39 | 2509777 | Thus, the mere presence of BCG-sensitized T cells does not appear to result in the SEA-induced IFN production. 4. |
| 40 | 2509777 | In vitro experiments, in which SEA-induced IFN production was determined in the culture of BCG-sensitized spleen cells, showed that principal IFN-producing cells were Lyt-1+ T cells. 5. |
| 41 | 2509777 | Deprivation of macrophages from BCG-sensitized spleen cell population by passing through Sephadex G-10 column reduced the SEA-induced IFN production in the culture. |
| 42 | 2509777 | Addition of 2CA to the culture medium also reduced the SEA-induced IFN production by the BCG-sensitized spleen cells. 6. |
| 43 | 2509777 | The SEA-induced IFN production in the culture of the BCG-sensitized spleen cells was suppressed in the presence of lipoxygenase inhibitor, i.e., caffeic acid or nordihydroguaiaretic acid. 7. |
| 44 | 2509777 | The suppression of the SEA-induced IFN production of BCG-sensitized spleen cells in the presence of the lipoxygenase inhibitor was prevented by addition of synthetic LTC4. |
| 45 | 2837507 | Other cytokines including IFN-alpha, IL-1, and commercially available low m.w. |
| 46 | 2848301 | In the presence of inactivated antigen, PBMC from both BHV1-infected and control calves produced interferon (IFN)-alpha in 24 hour cultures. |
| 47 | 2848301 | Mononuclear cells from control animals failed to produce either IFN-alpha or -gamma when cultured with inactivated PI3 virus. |
| 48 | 2848301 | In the presence of inactivated antigen, PBMC from both BHV1-infected and control calves produced interferon (IFN)-alpha in 24 hour cultures. |
| 49 | 2848301 | Mononuclear cells from control animals failed to produce either IFN-alpha or -gamma when cultured with inactivated PI3 virus. |
| 50 | 3541131 | Ribavirin and recombinant interferon alpha-A (IFN-alpha-A) also inhibit HIV replication, although their mechanisms of action are less clear. |
| 51 | 3805784 | The IFN produced was neutralized by an antibody against IFN-alpha/beta. |
| 52 | 6187478 | On the other hand, production of IFN-alpha/beta was demonstrated in spleen cell cultures obtained from one of four nude mice (BALB/c, nu/nu). |
| 53 | 6187478 | Therefore, it is important to know the reason why the spleen cells of mice other than nude mice did produce only IFN-gamma, but did not produce IFN-alpha/beta in response to HK-LM. |
| 54 | 6187478 | Spleen cells obtained from ddY mice were fractionated, and the cellular source for IFN production of either IFN-alpha/beta or IFN-gamma induced by HK-LM was investigated. |
| 55 | 6187478 | Macrophage-depleted spleen cells produced neither IFN-gamma nor IFN-alpha/beta, but these cells acquired the ability to produce IFN-alpha/beta, not IFN-gamma, only when they had been treated with IFN-alpha/beta. |
| 56 | 6187478 | A possible mechanism of both IFN-gamma and IFN-alpha/beta induction by Listeria in mouse spleen cell cultures is discussed. |
| 57 | 6187478 | On the other hand, production of IFN-alpha/beta was demonstrated in spleen cell cultures obtained from one of four nude mice (BALB/c, nu/nu). |
| 58 | 6187478 | Therefore, it is important to know the reason why the spleen cells of mice other than nude mice did produce only IFN-gamma, but did not produce IFN-alpha/beta in response to HK-LM. |
| 59 | 6187478 | Spleen cells obtained from ddY mice were fractionated, and the cellular source for IFN production of either IFN-alpha/beta or IFN-gamma induced by HK-LM was investigated. |
| 60 | 6187478 | Macrophage-depleted spleen cells produced neither IFN-gamma nor IFN-alpha/beta, but these cells acquired the ability to produce IFN-alpha/beta, not IFN-gamma, only when they had been treated with IFN-alpha/beta. |
| 61 | 6187478 | A possible mechanism of both IFN-gamma and IFN-alpha/beta induction by Listeria in mouse spleen cell cultures is discussed. |
| 62 | 6187478 | On the other hand, production of IFN-alpha/beta was demonstrated in spleen cell cultures obtained from one of four nude mice (BALB/c, nu/nu). |
| 63 | 6187478 | Therefore, it is important to know the reason why the spleen cells of mice other than nude mice did produce only IFN-gamma, but did not produce IFN-alpha/beta in response to HK-LM. |
| 64 | 6187478 | Spleen cells obtained from ddY mice were fractionated, and the cellular source for IFN production of either IFN-alpha/beta or IFN-gamma induced by HK-LM was investigated. |
| 65 | 6187478 | Macrophage-depleted spleen cells produced neither IFN-gamma nor IFN-alpha/beta, but these cells acquired the ability to produce IFN-alpha/beta, not IFN-gamma, only when they had been treated with IFN-alpha/beta. |
| 66 | 6187478 | A possible mechanism of both IFN-gamma and IFN-alpha/beta induction by Listeria in mouse spleen cell cultures is discussed. |
| 67 | 6187478 | On the other hand, production of IFN-alpha/beta was demonstrated in spleen cell cultures obtained from one of four nude mice (BALB/c, nu/nu). |
| 68 | 6187478 | Therefore, it is important to know the reason why the spleen cells of mice other than nude mice did produce only IFN-gamma, but did not produce IFN-alpha/beta in response to HK-LM. |
| 69 | 6187478 | Spleen cells obtained from ddY mice were fractionated, and the cellular source for IFN production of either IFN-alpha/beta or IFN-gamma induced by HK-LM was investigated. |
| 70 | 6187478 | Macrophage-depleted spleen cells produced neither IFN-gamma nor IFN-alpha/beta, but these cells acquired the ability to produce IFN-alpha/beta, not IFN-gamma, only when they had been treated with IFN-alpha/beta. |
| 71 | 6187478 | A possible mechanism of both IFN-gamma and IFN-alpha/beta induction by Listeria in mouse spleen cell cultures is discussed. |
| 72 | 6187478 | On the other hand, production of IFN-alpha/beta was demonstrated in spleen cell cultures obtained from one of four nude mice (BALB/c, nu/nu). |
| 73 | 6187478 | Therefore, it is important to know the reason why the spleen cells of mice other than nude mice did produce only IFN-gamma, but did not produce IFN-alpha/beta in response to HK-LM. |
| 74 | 6187478 | Spleen cells obtained from ddY mice were fractionated, and the cellular source for IFN production of either IFN-alpha/beta or IFN-gamma induced by HK-LM was investigated. |
| 75 | 6187478 | Macrophage-depleted spleen cells produced neither IFN-gamma nor IFN-alpha/beta, but these cells acquired the ability to produce IFN-alpha/beta, not IFN-gamma, only when they had been treated with IFN-alpha/beta. |
| 76 | 6187478 | A possible mechanism of both IFN-gamma and IFN-alpha/beta induction by Listeria in mouse spleen cell cultures is discussed. |
| 77 | 7502485 | Additionally, supernatants derived from human PBML were screened for interferons (IFN) alpha and gamma as well as for tumor necrosis factor by enzyme-linked immunosorbent assay. |
| 78 | 7502485 | IFN alpha/beta was found to be responsible for the antiviral effect. |
| 79 | 7502485 | Supernatants derived from human, porcine and ovine PBML stimulated with replicable PPV, native VV MVA and MVA lacZ recombinant or native APV and APV lacZ recombinant virus regularly contained IFN alpha. |
| 80 | 7502485 | Additionally, supernatants derived from human PBML were screened for interferons (IFN) alpha and gamma as well as for tumor necrosis factor by enzyme-linked immunosorbent assay. |
| 81 | 7502485 | IFN alpha/beta was found to be responsible for the antiviral effect. |
| 82 | 7502485 | Supernatants derived from human, porcine and ovine PBML stimulated with replicable PPV, native VV MVA and MVA lacZ recombinant or native APV and APV lacZ recombinant virus regularly contained IFN alpha. |
| 83 | 7502485 | Additionally, supernatants derived from human PBML were screened for interferons (IFN) alpha and gamma as well as for tumor necrosis factor by enzyme-linked immunosorbent assay. |
| 84 | 7502485 | IFN alpha/beta was found to be responsible for the antiviral effect. |
| 85 | 7502485 | Supernatants derived from human, porcine and ovine PBML stimulated with replicable PPV, native VV MVA and MVA lacZ recombinant or native APV and APV lacZ recombinant virus regularly contained IFN alpha. |
| 86 | 7551237 | Induction of enhanced cytokine secretion has been found to involve IFN-alpha/beta, IFN-gamma, TNF-alpha, TNF-beta, IL-1, IL-6, and the 40 kDa chain of IL-12. |
| 87 | 7571278 | Infection evokes complex changes which are thought to be caused by production and release of pro-inflammatory cytokines such as tumour necrosis factor (TNF-alpha), interferons (INFs), and interleukins (ILs). |
| 88 | 7571278 | To improve our understanding of the pathophysiology of pro-inflammatory cytokines in ruminants, studies have been performed with TNF-alpha, IL1-alpha/beta, and IFN-alpha/ gamma as well as with cytokine-inducers in dwarf goats. |
| 89 | 7571278 | Although studies of the actions of corticosteroids, nonsteroidal anti-inflammatory and antipyretic agents, antibodies to endotoxin, TNF-alpha, or IL-1, synthetic E. coli lipid A precursors, hydrazine, isoniazid, chloroquine, polymyxin B, bicyclic imidazoles, hydroxamates, and tyrosine kinase inhibitors in endotoxaemic animals have shed further light on inflammatory processes, clinical studies in this field are urgently required to evaluate their beneficial effect. |
| 90 | 7580831 | Twelve asymptomatic patients on antiretroviral therapy for at least 1 year and with CD4 cell counts between 100-300/mm3 were randomized to receive adjuvanted formol-inactivated interferon alpha-2a (IFN alpha) and continue the current antiretroviral treatment, whatever it was, or to receive the adjuvant alone and the current antiretroviral treatment. |
| 91 | 7580835 | All sera from HIV-infected patients were found by ELISA to contain antibodies specifically directed to IFN alpha. |
| 92 | 7684167 | In the past, cytokines such as interferons, IL-2, and TNF have been tested on a large scale in the treatment of advanced renal cell carcinoma. |
| 93 | 7684167 | The combination of IFN-alpha and IL-2 by subcutaneous administration appears to provide results similar to those of other treatment modalities with lower morbidity. |
| 94 | 7881637 | Therapeutic effect of a vaccinia colon oncolysate prepared with interleukin-2 (IL-2) gene-encoded vaccinia virus (IL-2VCO) in combination with recombinant interferon-alpha (IFN-alpha) was studied in a syngeneic murine CC-36 colon hepatic metastasis model. |
| 95 | 7881637 | The only treatment that produced a survival rate similar to the survival rate of IL-2VCO+IFN-alpha was VCO+IL-2 + IFN-alpha (survival rate was 67%). |
| 96 | 7881637 | The mechanism of the induction of antitumor response by the VCO+IL-2+IFN-alpha treatment was analyzed by measuring the direct cytotoxic activity of IFN-alpha on CC-36 tumor cells and by measuring the induction of cytolytic T-cell activity against CC-36 tumor cells. |
| 97 | 7881637 | It was found that the survival rate was affected in mice depleted with CD8-positive T cells and treated with IL-2VCO+IFN-alpha when compared to control mice which had no T-cell depletion and were treated with IL-2VCO+IFN-alpha. |
| 98 | 7881637 | This study suggests that the addition of IFN-alpha along with IL-2VCO increased the survival rate of mice having CC-36 hepatic metastases through the induction of CD8-positive T cells. |
| 99 | 7881637 | Therapeutic effect of a vaccinia colon oncolysate prepared with interleukin-2 (IL-2) gene-encoded vaccinia virus (IL-2VCO) in combination with recombinant interferon-alpha (IFN-alpha) was studied in a syngeneic murine CC-36 colon hepatic metastasis model. |
| 100 | 7881637 | The only treatment that produced a survival rate similar to the survival rate of IL-2VCO+IFN-alpha was VCO+IL-2 + IFN-alpha (survival rate was 67%). |
| 101 | 7881637 | The mechanism of the induction of antitumor response by the VCO+IL-2+IFN-alpha treatment was analyzed by measuring the direct cytotoxic activity of IFN-alpha on CC-36 tumor cells and by measuring the induction of cytolytic T-cell activity against CC-36 tumor cells. |
| 102 | 7881637 | It was found that the survival rate was affected in mice depleted with CD8-positive T cells and treated with IL-2VCO+IFN-alpha when compared to control mice which had no T-cell depletion and were treated with IL-2VCO+IFN-alpha. |
| 103 | 7881637 | This study suggests that the addition of IFN-alpha along with IL-2VCO increased the survival rate of mice having CC-36 hepatic metastases through the induction of CD8-positive T cells. |
| 104 | 7881637 | Therapeutic effect of a vaccinia colon oncolysate prepared with interleukin-2 (IL-2) gene-encoded vaccinia virus (IL-2VCO) in combination with recombinant interferon-alpha (IFN-alpha) was studied in a syngeneic murine CC-36 colon hepatic metastasis model. |
| 105 | 7881637 | The only treatment that produced a survival rate similar to the survival rate of IL-2VCO+IFN-alpha was VCO+IL-2 + IFN-alpha (survival rate was 67%). |
| 106 | 7881637 | The mechanism of the induction of antitumor response by the VCO+IL-2+IFN-alpha treatment was analyzed by measuring the direct cytotoxic activity of IFN-alpha on CC-36 tumor cells and by measuring the induction of cytolytic T-cell activity against CC-36 tumor cells. |
| 107 | 7881637 | It was found that the survival rate was affected in mice depleted with CD8-positive T cells and treated with IL-2VCO+IFN-alpha when compared to control mice which had no T-cell depletion and were treated with IL-2VCO+IFN-alpha. |
| 108 | 7881637 | This study suggests that the addition of IFN-alpha along with IL-2VCO increased the survival rate of mice having CC-36 hepatic metastases through the induction of CD8-positive T cells. |
| 109 | 7881637 | Therapeutic effect of a vaccinia colon oncolysate prepared with interleukin-2 (IL-2) gene-encoded vaccinia virus (IL-2VCO) in combination with recombinant interferon-alpha (IFN-alpha) was studied in a syngeneic murine CC-36 colon hepatic metastasis model. |
| 110 | 7881637 | The only treatment that produced a survival rate similar to the survival rate of IL-2VCO+IFN-alpha was VCO+IL-2 + IFN-alpha (survival rate was 67%). |
| 111 | 7881637 | The mechanism of the induction of antitumor response by the VCO+IL-2+IFN-alpha treatment was analyzed by measuring the direct cytotoxic activity of IFN-alpha on CC-36 tumor cells and by measuring the induction of cytolytic T-cell activity against CC-36 tumor cells. |
| 112 | 7881637 | It was found that the survival rate was affected in mice depleted with CD8-positive T cells and treated with IL-2VCO+IFN-alpha when compared to control mice which had no T-cell depletion and were treated with IL-2VCO+IFN-alpha. |
| 113 | 7881637 | This study suggests that the addition of IFN-alpha along with IL-2VCO increased the survival rate of mice having CC-36 hepatic metastases through the induction of CD8-positive T cells. |
| 114 | 7881637 | Therapeutic effect of a vaccinia colon oncolysate prepared with interleukin-2 (IL-2) gene-encoded vaccinia virus (IL-2VCO) in combination with recombinant interferon-alpha (IFN-alpha) was studied in a syngeneic murine CC-36 colon hepatic metastasis model. |
| 115 | 7881637 | The only treatment that produced a survival rate similar to the survival rate of IL-2VCO+IFN-alpha was VCO+IL-2 + IFN-alpha (survival rate was 67%). |
| 116 | 7881637 | The mechanism of the induction of antitumor response by the VCO+IL-2+IFN-alpha treatment was analyzed by measuring the direct cytotoxic activity of IFN-alpha on CC-36 tumor cells and by measuring the induction of cytolytic T-cell activity against CC-36 tumor cells. |
| 117 | 7881637 | It was found that the survival rate was affected in mice depleted with CD8-positive T cells and treated with IL-2VCO+IFN-alpha when compared to control mice which had no T-cell depletion and were treated with IL-2VCO+IFN-alpha. |
| 118 | 7881637 | This study suggests that the addition of IFN-alpha along with IL-2VCO increased the survival rate of mice having CC-36 hepatic metastases through the induction of CD8-positive T cells. |
| 119 | 7914235 | This second period of the trial, now open and ongoing, should allow us to evaluate further the innocuity of the i-IFN alpha preparation and whether anti-IFN alpha vaccine could provide a long-lasting CD4 cell count as well as CMI stabilization. |
| 120 | 7963533 | IFN-alpha 1 gene expression into a metastatic murine adenocarcinoma (TS/A) results in CD8+ T cell-mediated tumor rejection and development of antitumor immunity. |
| 121 | 7963533 | When the metastatic ability of IFN-alpha-secreting clones was compared with that of previously characterized IFN-gamma-secreting TS/A clones, it was found that the expression of IFN-alpha into TS/A tumor cells resulted in a potent inhibition of metastases formation, whereas IFN-gamma expression either did not affect or even enhanced the metastatic behavior of TS/A cells. |
| 122 | 7963533 | IFN-alpha 1 gene expression into a metastatic murine adenocarcinoma (TS/A) results in CD8+ T cell-mediated tumor rejection and development of antitumor immunity. |
| 123 | 7963533 | When the metastatic ability of IFN-alpha-secreting clones was compared with that of previously characterized IFN-gamma-secreting TS/A clones, it was found that the expression of IFN-alpha into TS/A tumor cells resulted in a potent inhibition of metastases formation, whereas IFN-gamma expression either did not affect or even enhanced the metastatic behavior of TS/A cells. |
| 124 | 8027551 | IL-10, TGF-beta 1, and IFN-alpha (cytokines known to regulate effector functions of activated macrophages) also did not block anti-F. tularensis activity of IFN-gamma-stimulated AM. |
| 125 | 8027551 | Reactive oxygen metabolites, depletion of tryptophan, and sequestration of iron did not contribute to anti-F. tularensis activity because addition of superoxide dismutase or catalase, excess iron, or tryptophan to IFN-gamma-treated AM did not reverse the anti-F. tularensis activity observed in these cells. |
| 126 | 8368734 | In addition to "classical" CD8+ Tc, CD4+ Tc were cloned from the blood of immunized patients. |
| 127 | 8368734 | CD4+ Tc were restricted by HLA Class I antigens, as judged by their killing of HLA Class II-negative melanomas and blocking by anti-class I antibodies. |
| 128 | 8368734 | Other CD4+ clones were blocked by both anti-HLA Class I or anti-Class II MHC monoclonal antibodies, and only two were blocked only by anti-HLA Class II. |
| 129 | 8368734 | Immunohistory revealed CD4+ and CD8+ T cells in lesions under rejection, but the predominant cells were macrophages, suggesting delayed-type hypersensitivity as a possible mechanism. |
| 130 | 8368734 | IFN-alpha 2 b salvaged 8 of 18 patients who failed with the theraccine, regardless of MHC phenotype, perhaps through upregulation of MHC and tumor epitopes on the autochthonous tumor. |
| 131 | 8536277 | Direct inhibitory effects of bacillus Calmette-Guérin (BCG) and interferon alpha 2b (IFN alpha 2b) on six human bladder carcinoma cell lines, UCRU-BL-13, UCRU-BL-17, UCRU-BL-28, 5637, T24 and J82, were studied using an in vitro proliferation assay. |
| 132 | 8797687 | Neither clinical deterioration nor a CD4+ cell count decrease from pretreatment values was observed in IFN-alpha-immunized patients in the follow-up period, whereas clinical and immunological disease progressions were observed among open-comparison patients. |
| 133 | 8845573 | Options currently under investigation include the development of more effective conditioning regimens, as applied in double auto-transplant or with targeted therapy using antibody-radionuclide conjugates, as well as post-transplant immunomodulation with either IFN-alpha, interleukin-2 or idiotype vaccines. |
| 134 | 8914208 | A number of regimens combining IL-2, IFN-alpha, and chemotherapeutic agents have yielded striking response rates in small trials and await confirmation in larger studies. |
| 135 | 9256274 | They furthermore initiate the production of IFN-gamma, IFN-alpha, IFN-beta, and interleukins 12 and 18, all of which foster Th1 responses and enhance cell-mediated immunity. |
| 136 | 9285547 | To investigate if this might be caused by a preferential Th1 cytokine response, interferon (IFN)-gamma and interleukin (IL)-10 production of peripheral blood mononuclear cells (PBMC) was analyzed after measles antigen (M-ag) stimulation in vitro. |
| 137 | 9285547 | The non-specific immune response was measured by IFN-alpha, and IL-12 analyses. |
| 138 | 9285547 | Only a non-significant tendency was seen in IL-10 production (48.6 vs 26.7 pg/ml; NS), whereas no difference was found in IFN-alpha or IL-12 production. |
| 139 | 9285547 | A positive correlation between IFN-gamma and IL-10 production was found (r(s) = 0.49; P < 0.001). |
| 140 | 9285547 | After vaccination of 14 ABMT children, there was an increase in PBMC IFN-gamma production in vitro (2.5 vs <0.1 IU/ml; P < 0.05), whereas no changes were seen in the IL-10, IFN-alpha, or antibody levels. |
| 141 | 9285547 | To investigate if this might be caused by a preferential Th1 cytokine response, interferon (IFN)-gamma and interleukin (IL)-10 production of peripheral blood mononuclear cells (PBMC) was analyzed after measles antigen (M-ag) stimulation in vitro. |
| 142 | 9285547 | The non-specific immune response was measured by IFN-alpha, and IL-12 analyses. |
| 143 | 9285547 | Only a non-significant tendency was seen in IL-10 production (48.6 vs 26.7 pg/ml; NS), whereas no difference was found in IFN-alpha or IL-12 production. |
| 144 | 9285547 | A positive correlation between IFN-gamma and IL-10 production was found (r(s) = 0.49; P < 0.001). |
| 145 | 9285547 | After vaccination of 14 ABMT children, there was an increase in PBMC IFN-gamma production in vitro (2.5 vs <0.1 IU/ml; P < 0.05), whereas no changes were seen in the IL-10, IFN-alpha, or antibody levels. |
| 146 | 9285547 | To investigate if this might be caused by a preferential Th1 cytokine response, interferon (IFN)-gamma and interleukin (IL)-10 production of peripheral blood mononuclear cells (PBMC) was analyzed after measles antigen (M-ag) stimulation in vitro. |
| 147 | 9285547 | The non-specific immune response was measured by IFN-alpha, and IL-12 analyses. |
| 148 | 9285547 | Only a non-significant tendency was seen in IL-10 production (48.6 vs 26.7 pg/ml; NS), whereas no difference was found in IFN-alpha or IL-12 production. |
| 149 | 9285547 | A positive correlation between IFN-gamma and IL-10 production was found (r(s) = 0.49; P < 0.001). |
| 150 | 9285547 | After vaccination of 14 ABMT children, there was an increase in PBMC IFN-gamma production in vitro (2.5 vs <0.1 IU/ml; P < 0.05), whereas no changes were seen in the IL-10, IFN-alpha, or antibody levels. |
| 151 | 9514093 | The potency of IFN-alpha transfectants was similar to that of IFN-gamma transfectants previously obtained from TSA. |
| 152 | 9514093 | Admixture of IFN-alpha and IFN-gamma transfectant cells in the same vaccine did not increase the curative effect over that of single vaccines. |
| 153 | 9514093 | In nude mice vaccination with IFN-alpha or IFN-gamma transfectants did not lead to a reduction in the number of lung colonies, indicating that an intact T cell response was required for the therapeutic effect observed in immunocompetent mice. |
| 154 | 9514093 | The potency of IFN-alpha transfectants was similar to that of IFN-gamma transfectants previously obtained from TSA. |
| 155 | 9514093 | Admixture of IFN-alpha and IFN-gamma transfectant cells in the same vaccine did not increase the curative effect over that of single vaccines. |
| 156 | 9514093 | In nude mice vaccination with IFN-alpha or IFN-gamma transfectants did not lead to a reduction in the number of lung colonies, indicating that an intact T cell response was required for the therapeutic effect observed in immunocompetent mice. |
| 157 | 9514093 | The potency of IFN-alpha transfectants was similar to that of IFN-gamma transfectants previously obtained from TSA. |
| 158 | 9514093 | Admixture of IFN-alpha and IFN-gamma transfectant cells in the same vaccine did not increase the curative effect over that of single vaccines. |
| 159 | 9514093 | In nude mice vaccination with IFN-alpha or IFN-gamma transfectants did not lead to a reduction in the number of lung colonies, indicating that an intact T cell response was required for the therapeutic effect observed in immunocompetent mice. |
| 160 | 9570527 | Autologous human monocyte-derived dendritic cells genetically modified to express melanoma antigens elicit primary cytotoxic T cell responses in vitro: enhancement by cotransfection of genes encoding the Th1-biasing cytokines IL-12 and IFN-alpha. |
| 161 | 9570527 | Cultured, monocyte-derived dendritic cells (DC) were transiently transfected with plasmid DNA encoding human MART-1/Melan-A, pMel-17/gp100, tyrosinase, MAGE-1, or MAGE-3 by particle bombardment and used to stimulate autologous PBMC responder T cells. |
| 162 | 9570527 | Coinsertion of genes encoding the Th1-biasing cytokines IL-12 or IFN-alpha consistently enhanced the magnitude of the resulting Ag-specific CTL reactivity. |
| 163 | 9570527 | Autologous human monocyte-derived dendritic cells genetically modified to express melanoma antigens elicit primary cytotoxic T cell responses in vitro: enhancement by cotransfection of genes encoding the Th1-biasing cytokines IL-12 and IFN-alpha. |
| 164 | 9570527 | Cultured, monocyte-derived dendritic cells (DC) were transiently transfected with plasmid DNA encoding human MART-1/Melan-A, pMel-17/gp100, tyrosinase, MAGE-1, or MAGE-3 by particle bombardment and used to stimulate autologous PBMC responder T cells. |
| 165 | 9570527 | Coinsertion of genes encoding the Th1-biasing cytokines IL-12 or IFN-alpha consistently enhanced the magnitude of the resulting Ag-specific CTL reactivity. |
| 166 | 9603331 | Here we present a further characterization of MVA and demonstrate that: (i) MVA can replicate, albeit poorly, in transformed human cell lines, but not in primary human fibroblasts although there is limited cell-to-cell spread; (ii) MVA is a potent inducer of type I interferon (IFN) from primary human cells, which may restrict virus spread in vivo; and (iii) unlike other VV strains, MVA does not express soluble receptors for IFN-gamma, IFN-alpha/beta, tumour necrosis factor and CC chemokines, but does express a soluble interleukin-1beta receptor. |
| 167 | 9617594 | Immunotherapy involving IFNs and interleukin-2 (IL-2) alone or in combination has yielded similar results to those achieved with chemotherapy alone. |
| 168 | 9699714 | The nature of the immune response depends on the route, method, and timing of DNA delivery and can also be influenced by co-delivery of plasmids encoding immunomodulating cytokines like IFN-alpha, IL-2, or IL-12 and costimulatory molecules like B7-1. |
| 169 | 9759581 | After decades of research, the adjuvant therapy of patients with melanoma has recently shown significant survival and relapse-free interval benefit for the intravenous and subcutaneous administration of maximally tolerable dosages of recombinant IFN alpha 2b in a trial conducted by the ECOG (E1684). |
| 170 | 9759581 | A recently emerging area of research is the patient with stage IIA melanoma and the potential role of an abbreviated high-dose regimen of IFN alpha in this patient subset. |
| 171 | 9759581 | After decades of research, the adjuvant therapy of patients with melanoma has recently shown significant survival and relapse-free interval benefit for the intravenous and subcutaneous administration of maximally tolerable dosages of recombinant IFN alpha 2b in a trial conducted by the ECOG (E1684). |
| 172 | 9759581 | A recently emerging area of research is the patient with stage IIA melanoma and the potential role of an abbreviated high-dose regimen of IFN alpha in this patient subset. |
| 173 | 9811777 | Infection of mice lacking a functional IFN system with the IFN-sensitive TC-83 virus resulted in disease equivalent to that produced by the virulent, IFN-resistant TRD virus, further demonstrating that IFN resistance contributes to VEE virus virulence and is a biological marker of epizootic potential. |
| 174 | 9858908 | Using immunohistochemical analysis we demonstrated that after treating with lethally irradiated MBT-2 tumor cells (IRMBT-2) + IL-2 cells of CD4+, CD8+, CD44+ and CD11b+ phenotypes prominently infiltrate the subcutaneous local injection sites. |
| 175 | 9858908 | In contrast, only scanty immune responding cells could be seen locally if treated with IRMBT-2 + IFN-alpha 2b, albeit in the presence of interleukin-2 (IL-2). |
| 176 | 9858908 | However, the spleens of D17TBM treated with IRMBT-2 + IFN-alpha 2b contained the highest percentage of CD44+ memory T cells and cells of the CD11b+ phenotype; moreover, their natural killer (NK), lymphokine activated killer (LAK) and cytotoxic T lymphocytes (CTL) activities were significantly augmented. |
| 177 | 9858908 | Using immunohistochemical analysis we demonstrated that after treating with lethally irradiated MBT-2 tumor cells (IRMBT-2) + IL-2 cells of CD4+, CD8+, CD44+ and CD11b+ phenotypes prominently infiltrate the subcutaneous local injection sites. |
| 178 | 9858908 | In contrast, only scanty immune responding cells could be seen locally if treated with IRMBT-2 + IFN-alpha 2b, albeit in the presence of interleukin-2 (IL-2). |
| 179 | 9858908 | However, the spleens of D17TBM treated with IRMBT-2 + IFN-alpha 2b contained the highest percentage of CD44+ memory T cells and cells of the CD11b+ phenotype; moreover, their natural killer (NK), lymphokine activated killer (LAK) and cytotoxic T lymphocytes (CTL) activities were significantly augmented. |
| 180 | 9862872 | After in vitro stimulation with HBsAg, peripheral blood mononuclear cells (PBMC) of only 1 of 5 acute and 1 of 6 chronic HBV patients, but of all 6 vaccine recipients, secreted varying amounts of interferon gamma (IFN-gamma), but no interleukin-4 (IL-4) or IL-5. |
| 181 | 9862872 | Furthermore, the addition of IFN-gamma, but not of IL-2, -4, -12, or IFN-alpha, resulted in strong increases of anti-HBs-secreting B cells in vaccine recipients and chronic carriers. |
| 182 | 9865682 | Most important for its use as an adjuvant in human cancer vaccine are its ability to introduce T-cell costimulatory activity, to prevent anergy induction, and to induce locally chemokines (eg, RANTES, IP-10) and cytokines (eg, interferon alpha, beta [IFN-alpha, beta] and tumor necrosis factor-alpha [TNFalpha]) that affect T-cell recruitment and activation. |
| 183 | 9865738 | The induction of in vivo proliferation of long-lived CD44hi CD8+ T cells after the injection of tumor cells expressing IFN-alpha1 into syngeneic mice. |
| 184 | 9865738 | The injection of viable cells producing IFN-alpha or IL-12 caused a marked proliferation of CD8+ T lymphocytes in both the spleen and lymph nodes. |
| 185 | 9865738 | In contrast, proliferation of CD8+ T cells did not occur in mice injected with control cells or with cells expressing IL-4, granulocyte colony-stimulating factor, or IFN-gamma. |
| 186 | 9865738 | Pulse-chase studies in mice injected with IFN-alpha-producing cells showed that a proportion of proliferating CD8+ T cells survived for at least 70 days, suggesting that long-lived memory cells are induced using such an approach. |
| 187 | 9865738 | The induction of in vivo proliferation of long-lived CD44hi CD8+ T cells after the injection of tumor cells expressing IFN-alpha1 into syngeneic mice. |
| 188 | 9865738 | The injection of viable cells producing IFN-alpha or IL-12 caused a marked proliferation of CD8+ T lymphocytes in both the spleen and lymph nodes. |
| 189 | 9865738 | In contrast, proliferation of CD8+ T cells did not occur in mice injected with control cells or with cells expressing IL-4, granulocyte colony-stimulating factor, or IFN-gamma. |
| 190 | 9865738 | Pulse-chase studies in mice injected with IFN-alpha-producing cells showed that a proportion of proliferating CD8+ T cells survived for at least 70 days, suggesting that long-lived memory cells are induced using such an approach. |
| 191 | 9865738 | The induction of in vivo proliferation of long-lived CD44hi CD8+ T cells after the injection of tumor cells expressing IFN-alpha1 into syngeneic mice. |
| 192 | 9865738 | The injection of viable cells producing IFN-alpha or IL-12 caused a marked proliferation of CD8+ T lymphocytes in both the spleen and lymph nodes. |
| 193 | 9865738 | In contrast, proliferation of CD8+ T cells did not occur in mice injected with control cells or with cells expressing IL-4, granulocyte colony-stimulating factor, or IFN-gamma. |
| 194 | 9865738 | Pulse-chase studies in mice injected with IFN-alpha-producing cells showed that a proportion of proliferating CD8+ T cells survived for at least 70 days, suggesting that long-lived memory cells are induced using such an approach. |
| 195 | 9973521 | Using PBMCs from bladder cancer patients, IFN-alpha was found to substantially enhance the efficacy of BCG to induce IFN-gamma production. |
| 196 | 9973521 | In addition, IFN-alpha up-regulated BCG-induced IL-12 and TNF-alpha and down-regulated BCG-induced IL-10. |
| 197 | 9973521 | Neutralizing endogenous IL-10 or adding exogenous IL-12 provided further synergy for IFN-gamma production. |
| 198 | 9973521 | In clinical practice, intravesical IFN-alpha 2B (50 million units (MU)/dose) was observed to accelerate urinary IFN-gamma production to low-dose BCG (one-tenth or one-third of a full dose) in patients treated with combination therapy compared with BCG alone. |
| 199 | 9973521 | Using PBMCs from bladder cancer patients, IFN-alpha was found to substantially enhance the efficacy of BCG to induce IFN-gamma production. |
| 200 | 9973521 | In addition, IFN-alpha up-regulated BCG-induced IL-12 and TNF-alpha and down-regulated BCG-induced IL-10. |
| 201 | 9973521 | Neutralizing endogenous IL-10 or adding exogenous IL-12 provided further synergy for IFN-gamma production. |
| 202 | 9973521 | In clinical practice, intravesical IFN-alpha 2B (50 million units (MU)/dose) was observed to accelerate urinary IFN-gamma production to low-dose BCG (one-tenth or one-third of a full dose) in patients treated with combination therapy compared with BCG alone. |
| 203 | 9973521 | Using PBMCs from bladder cancer patients, IFN-alpha was found to substantially enhance the efficacy of BCG to induce IFN-gamma production. |
| 204 | 9973521 | In addition, IFN-alpha up-regulated BCG-induced IL-12 and TNF-alpha and down-regulated BCG-induced IL-10. |
| 205 | 9973521 | Neutralizing endogenous IL-10 or adding exogenous IL-12 provided further synergy for IFN-gamma production. |
| 206 | 9973521 | In clinical practice, intravesical IFN-alpha 2B (50 million units (MU)/dose) was observed to accelerate urinary IFN-gamma production to low-dose BCG (one-tenth or one-third of a full dose) in patients treated with combination therapy compared with BCG alone. |
| 207 | 10052194 | Modifications of IFN-alpha, TNF-alpha and IFN-gamma serum levels in children vaccinated against measles. |
| 208 | 10072560 | The addition of Th1-biasing cytokines IL-12 or IFN-alpha, during priming with Nef-expressing DC, enhanced the Nef-specific CTL responses generated using either Ag-loading approach. |
| 209 | 10080835 | Bladder wash-derived lymphocytes from superficial bladder cancer patients involved in high dose BCG, low dose BCG, and low dose BCG with IFN-alpha treatments were examined. |
| 210 | 10080835 | We found an increasing trend in the percentage of CD3 T cells with each weekly intravesical instillation and the proportion of CD3 T cells expressing the gammadelta T cell receptor was significantly higher in patients receiving standard dose BCG than those receiving low dose BCG or low dose BCG plus IFN-alpha. |
| 211 | 10080835 | Most patients had a predominance of CD4 T cells, while some had more CD8 T cells. |
| 212 | 10080835 | The CD4/CD8 ratio did not vary much during the instillations. |
| 213 | 10080835 | Bladder wash-derived lymphocytes from superficial bladder cancer patients involved in high dose BCG, low dose BCG, and low dose BCG with IFN-alpha treatments were examined. |
| 214 | 10080835 | We found an increasing trend in the percentage of CD3 T cells with each weekly intravesical instillation and the proportion of CD3 T cells expressing the gammadelta T cell receptor was significantly higher in patients receiving standard dose BCG than those receiving low dose BCG or low dose BCG plus IFN-alpha. |
| 215 | 10080835 | Most patients had a predominance of CD4 T cells, while some had more CD8 T cells. |
| 216 | 10080835 | The CD4/CD8 ratio did not vary much during the instillations. |
| 217 | 10096580 | In all, 242 patients, recruited between December 1995 and July 1996 in eight centers in Europe and Israel, with CD4+ counts from 100 to 634 cells/mm3 who were receiving or not receiving antiretroviral therapy (including protease inhibitors) were randomized to receive either anti-IFN-alpha vaccine or placebo. |
| 218 | 10096580 | Despite the unexpectedly low immunogenicity and fewer than expected endpoints, anti-IFN-alpha vaccine recipients, in comparison with placebo recipients, showed a lower rate of disease progression, nonelective treatment changes, and/or CD4+ count decrease to <200 cells/mm3, but the difference was not statistically significant. |
| 219 | 10096580 | In all, 242 patients, recruited between December 1995 and July 1996 in eight centers in Europe and Israel, with CD4+ counts from 100 to 634 cells/mm3 who were receiving or not receiving antiretroviral therapy (including protease inhibitors) were randomized to receive either anti-IFN-alpha vaccine or placebo. |
| 220 | 10096580 | Despite the unexpectedly low immunogenicity and fewer than expected endpoints, anti-IFN-alpha vaccine recipients, in comparison with placebo recipients, showed a lower rate of disease progression, nonelective treatment changes, and/or CD4+ count decrease to <200 cells/mm3, but the difference was not statistically significant. |
| 221 | 10230872 | LI is characterized by CD4+ and CD8+ tumor infiltrating lymphocytes reflecting latent cell-mediated immunity (CMI). |
| 222 | 10230872 | CMI and humoral immune reactivity have been demonstrated to autologous tumor and a variety of tumor-associated antigens (TAA) have been implicated including CEA, HER-2/neu, MAGE-1, p53, T/Tn and MUC-1. |
| 223 | 10230872 | Animal models have employed drug therapy, cytokine transfection, vaccines with autologous tumor, cytokines like interferon alpha (IFN-alpha) and interleukin-2 (IL-2), TAA tumor vaccines, and immunotoxins with evidence of tumor regression by immunologic means. |
| 224 | 10230872 | Positive results have been obtained with natural IFN and interleukins, particularly in combination strategies (but not with high dose recombinant IFN or IL-2), with autologous tumor vaccine (but not yet with transfected autologous tumor); with a mucin carbohydrate vaccine (Theratope) in a combination strategy (but not with mucin core antigen) and with several immunotoxins. |
| 225 | 10230872 | LI is characterized by CD4+ and CD8+ tumor infiltrating lymphocytes reflecting latent cell-mediated immunity (CMI). |
| 226 | 10230872 | CMI and humoral immune reactivity have been demonstrated to autologous tumor and a variety of tumor-associated antigens (TAA) have been implicated including CEA, HER-2/neu, MAGE-1, p53, T/Tn and MUC-1. |
| 227 | 10230872 | Animal models have employed drug therapy, cytokine transfection, vaccines with autologous tumor, cytokines like interferon alpha (IFN-alpha) and interleukin-2 (IL-2), TAA tumor vaccines, and immunotoxins with evidence of tumor regression by immunologic means. |
| 228 | 10230872 | Positive results have been obtained with natural IFN and interleukins, particularly in combination strategies (but not with high dose recombinant IFN or IL-2), with autologous tumor vaccine (but not yet with transfected autologous tumor); with a mucin carbohydrate vaccine (Theratope) in a combination strategy (but not with mucin core antigen) and with several immunotoxins. |
| 229 | 10427987 | In this study, we demonstrate that porcine relaxin, at concentrations ranging from 10(-10) to 10(-6) M, favors the in vitro development of human antigen-specific T cells into Th1-like effectors and enhances both IFN-gamma mRNA expression and IFN-gamma production by established human T cell clones. |
| 230 | 10427987 | The promoting effect of relaxin on the development of IFN-gamma-producing cells was not due to a relaxin-induced release of IL-12 and/or IFN-alpha by antigen-presenting cells. |
| 231 | 10476222 | Using the well characterized beta-galactosidase (beta gal) model Ag system we find that both in vivo gene transfer systems elicit potent and long-lasting anti-beta gal-specific CD8+ and CD4+ T cell responses. |
| 232 | 10476222 | Since viral infections are generally associated with the production of large amounts of IFN-alpha and IL-12, we investigated whether administration of expression plasmids encoding these Th1-associated cytokines along with antigen-encoding cDNA can influence the nature of the immune response resulting from gene gun immunization. |
| 233 | 10476222 | We observed that co-delivery of IFN-alpha or IL-12 resulted in increased production of anti-beta gal gamma 2a antibodies. |
| 234 | 10476222 | Using the well characterized beta-galactosidase (beta gal) model Ag system we find that both in vivo gene transfer systems elicit potent and long-lasting anti-beta gal-specific CD8+ and CD4+ T cell responses. |
| 235 | 10476222 | Since viral infections are generally associated with the production of large amounts of IFN-alpha and IL-12, we investigated whether administration of expression plasmids encoding these Th1-associated cytokines along with antigen-encoding cDNA can influence the nature of the immune response resulting from gene gun immunization. |
| 236 | 10476222 | We observed that co-delivery of IFN-alpha or IL-12 resulted in increased production of anti-beta gal gamma 2a antibodies. |
| 237 | 10482360 | Antibodies against human IFN-alpha and -beta recognized the immunosuppressive domain of HIV-1 gp41 and inhibit gp41-binding to the putative cellular receptor protein p45. |
| 238 | 10482360 | To clarify the relationship between human type I interferon and HIV-1 gp41 and the protective mechanism of an IFN-alpha-vaccine, we prepared antisera against human IFN-alpha, -beta and HIV-1 gp41, and examined crossreaction of these antisera and their inhibition of gp41 binding to its binding protein p45. |
| 239 | 10482360 | Besides, mouse antisera to IFN-alpha and beta, like mouse anti-rsgp41 antiserum, could inhibit gp41-binding to its putative cellular receptor protein p45, while normal mouse serum did not. |
| 240 | 10482360 | Antibodies against human IFN-alpha and -beta recognized the immunosuppressive domain of HIV-1 gp41 and inhibit gp41-binding to the putative cellular receptor protein p45. |
| 241 | 10482360 | To clarify the relationship between human type I interferon and HIV-1 gp41 and the protective mechanism of an IFN-alpha-vaccine, we prepared antisera against human IFN-alpha, -beta and HIV-1 gp41, and examined crossreaction of these antisera and their inhibition of gp41 binding to its binding protein p45. |
| 242 | 10482360 | Besides, mouse antisera to IFN-alpha and beta, like mouse anti-rsgp41 antiserum, could inhibit gp41-binding to its putative cellular receptor protein p45, while normal mouse serum did not. |
| 243 | 10482360 | Antibodies against human IFN-alpha and -beta recognized the immunosuppressive domain of HIV-1 gp41 and inhibit gp41-binding to the putative cellular receptor protein p45. |
| 244 | 10482360 | To clarify the relationship between human type I interferon and HIV-1 gp41 and the protective mechanism of an IFN-alpha-vaccine, we prepared antisera against human IFN-alpha, -beta and HIV-1 gp41, and examined crossreaction of these antisera and their inhibition of gp41 binding to its binding protein p45. |
| 245 | 10482360 | Besides, mouse antisera to IFN-alpha and beta, like mouse anti-rsgp41 antiserum, could inhibit gp41-binding to its putative cellular receptor protein p45, while normal mouse serum did not. |
| 246 | 10533458 | This study investigated whether the antitumour response elicited by BCG could be improved by the addition of recombinant interferon alpha (IFN alpha) in the subcutaneous murine MB49 bladder tumour model. |
| 247 | 10533458 | The combination of BCG and IFN alpha had superior and earlier antitumour activity than BCG alone for MB49 cells in culture. |
| 248 | 10533458 | Whilst BCG therapy alone increased CD4+ and CD8+ populations in spleens, the combination of BCG and IFN alpha also increased alpha beta+ T cells significantly. |
| 249 | 10533458 | Our results suggest that the combination of BCG and IFN alpha may represent a more efficacious therapeutic than BCG alone for superficial bladder cancer. |
| 250 | 10533458 | This study investigated whether the antitumour response elicited by BCG could be improved by the addition of recombinant interferon alpha (IFN alpha) in the subcutaneous murine MB49 bladder tumour model. |
| 251 | 10533458 | The combination of BCG and IFN alpha had superior and earlier antitumour activity than BCG alone for MB49 cells in culture. |
| 252 | 10533458 | Whilst BCG therapy alone increased CD4+ and CD8+ populations in spleens, the combination of BCG and IFN alpha also increased alpha beta+ T cells significantly. |
| 253 | 10533458 | Our results suggest that the combination of BCG and IFN alpha may represent a more efficacious therapeutic than BCG alone for superficial bladder cancer. |
| 254 | 10533458 | This study investigated whether the antitumour response elicited by BCG could be improved by the addition of recombinant interferon alpha (IFN alpha) in the subcutaneous murine MB49 bladder tumour model. |
| 255 | 10533458 | The combination of BCG and IFN alpha had superior and earlier antitumour activity than BCG alone for MB49 cells in culture. |
| 256 | 10533458 | Whilst BCG therapy alone increased CD4+ and CD8+ populations in spleens, the combination of BCG and IFN alpha also increased alpha beta+ T cells significantly. |
| 257 | 10533458 | Our results suggest that the combination of BCG and IFN alpha may represent a more efficacious therapeutic than BCG alone for superficial bladder cancer. |
| 258 | 10533458 | This study investigated whether the antitumour response elicited by BCG could be improved by the addition of recombinant interferon alpha (IFN alpha) in the subcutaneous murine MB49 bladder tumour model. |
| 259 | 10533458 | The combination of BCG and IFN alpha had superior and earlier antitumour activity than BCG alone for MB49 cells in culture. |
| 260 | 10533458 | Whilst BCG therapy alone increased CD4+ and CD8+ populations in spleens, the combination of BCG and IFN alpha also increased alpha beta+ T cells significantly. |
| 261 | 10533458 | Our results suggest that the combination of BCG and IFN alpha may represent a more efficacious therapeutic than BCG alone for superficial bladder cancer. |
| 262 | 10551332 | Pretreatment of PBMCs as a source of antigen-presenting cells (APCs) with interferon (IFN)-gamma, or to some extent with IFN-alpha, but not with any of the other cytokines tested, augmented the peptide-induced CTL activity in HLA-A24 heterozygotes, but not in HLA-A24 homozygotes. |
| 263 | 10551332 | This IFN-gamma-mediated augmentation was inhibited by either interleukin (IL)-4 or IL-10. |
| 264 | 10551332 | This IL-2-mediated activation of CTLs was inhibited by the addition of IFN-gamma, IL-4, or IL-10 to the IL-2 culture. |
| 265 | 10551332 | For further expansion of the CTLs, dendritic cells (DCs) induced from PBMCs with IL-4 and granulocyte macrophage colony-stimulating factor (GM-CSF) were required as APCs. |
| 266 | 10551332 | These results indicate that IFN-gamma and IL-2 are important in the activation of APCs and CTLs, respectively, while GM-CSF and IL-4 are needed for the induction of DCs, which in turn are required for further expansion of mature CTLs. |
| 267 | 10555997 | Previously, we demonstrated that a novel low-molecular-weight synthetic immune response modifier, R-848, induces IL-12 and IFN-alpha secretion from monocytes and macrophages. |
| 268 | 10555997 | Characteristic of dendritic cell maturation, R-848 treatment induces cell surface expression of CD83 and increases cell surface expression of CD80, CD86, CD40, and HLA-DR. |
| 269 | 10555997 | Additionally, R-848 induces cytokine (IL-6, IL-12, TNF-alpha, IFN-alpha) and chemokine (IL-8, MIP-1alpha, MCP-1) secretion from dendritic cells. |
| 270 | 10555997 | Previously, we demonstrated that a novel low-molecular-weight synthetic immune response modifier, R-848, induces IL-12 and IFN-alpha secretion from monocytes and macrophages. |
| 271 | 10555997 | Characteristic of dendritic cell maturation, R-848 treatment induces cell surface expression of CD83 and increases cell surface expression of CD80, CD86, CD40, and HLA-DR. |
| 272 | 10555997 | Additionally, R-848 induces cytokine (IL-6, IL-12, TNF-alpha, IFN-alpha) and chemokine (IL-8, MIP-1alpha, MCP-1) secretion from dendritic cells. |
| 273 | 10614729 | Beta-gal in alum induced IgG1 and IgE antibodies and the CD4+ T cells from these mice secreted interleukin 4 (IL-4) and IL-5 but no interferon-gamma (IFN-gamma) after in vitro antigen stimulation. |
| 274 | 10614729 | In contrast, mice immunized with pCMV-LacZ formed predominantly IgG2a antibodies and their CD4+ T cells secreted IFN-gamma but no IL-4 and IL-5. |
| 275 | 10614729 | Boosting of mice primed with beta-gal in alum with pCMV-LacZ resulted in a 75% decrease in the IgE antibody titer within 6 weeks and IgG2a antibody formation and CD4+ T cells that secreted IFN-gamma in amounts similar to T cells from pDNA primed mice. |
| 276 | 10614729 | As shown by adoptive cell transfer, both CD4+ and CD8+ T cells from pDNA immunized mice inhibited an IgE response to beta-gal in alum in the recipient mice. pDNA immunization also inhibited the eosinophilic infiltration of the lung of ovalbumin (OVA) immunized mice after OVA inhalation challenge in an animal model of the late phase reaction. |
| 277 | 10614729 | IFN-alpha, IL-12). |
| 278 | 10637450 | Interferon-alpha (IFN-alpha) or CD80 transduction of tumor cells individually reduces tumorigenicity and enhances antitumor responses. |
| 279 | 10637450 | Here, we report that the combination of IFN-alpha and CD80 cancer gene therapy in poorly immunogenic murine tumor models, the colorectal adenocarcinoma cell line MC38, and the methylcholanthrene-induced fibrosarcoma cell line MCA205 reduces tumor growth more efficiently without affecting in vitro growth. |
| 280 | 10637450 | Synergistic effects were observed when IFN-alpha- and CD80-transduced tumor cells were mixed and inoculated. |
| 281 | 10637450 | These admixed cells were rejected by 14 of 15 (MC38) or seven of 15 mice (MCA205), whereas, a mixture of IFN-alpha and Neo cells or CD80 and Neo cells led to tumors associated with progressive growth. |
| 282 | 10637450 | The therapeutic efficacy with established WT MC38 tumors was shown when mice were treated with a vaccine consisting of repetitive injections of IFN-alpha- and CD80-transduced MC38 cells into the contralateral flank (P < 0.01). |
| 283 | 10637450 | This treatment was associated with accumulation of CD4+, CD8+ cells and dendritic cells within the established tumor, demonstrating induction of antitumor immune responses. |
| 284 | 10637450 | Combination gene therapy using IFN-alpha and CD80 is an effective immune therapy of cancer and could be considered for clinical trials. |
| 285 | 10637450 | Interferon-alpha (IFN-alpha) or CD80 transduction of tumor cells individually reduces tumorigenicity and enhances antitumor responses. |
| 286 | 10637450 | Here, we report that the combination of IFN-alpha and CD80 cancer gene therapy in poorly immunogenic murine tumor models, the colorectal adenocarcinoma cell line MC38, and the methylcholanthrene-induced fibrosarcoma cell line MCA205 reduces tumor growth more efficiently without affecting in vitro growth. |
| 287 | 10637450 | Synergistic effects were observed when IFN-alpha- and CD80-transduced tumor cells were mixed and inoculated. |
| 288 | 10637450 | These admixed cells were rejected by 14 of 15 (MC38) or seven of 15 mice (MCA205), whereas, a mixture of IFN-alpha and Neo cells or CD80 and Neo cells led to tumors associated with progressive growth. |
| 289 | 10637450 | The therapeutic efficacy with established WT MC38 tumors was shown when mice were treated with a vaccine consisting of repetitive injections of IFN-alpha- and CD80-transduced MC38 cells into the contralateral flank (P < 0.01). |
| 290 | 10637450 | This treatment was associated with accumulation of CD4+, CD8+ cells and dendritic cells within the established tumor, demonstrating induction of antitumor immune responses. |
| 291 | 10637450 | Combination gene therapy using IFN-alpha and CD80 is an effective immune therapy of cancer and could be considered for clinical trials. |
| 292 | 10637450 | Interferon-alpha (IFN-alpha) or CD80 transduction of tumor cells individually reduces tumorigenicity and enhances antitumor responses. |
| 293 | 10637450 | Here, we report that the combination of IFN-alpha and CD80 cancer gene therapy in poorly immunogenic murine tumor models, the colorectal adenocarcinoma cell line MC38, and the methylcholanthrene-induced fibrosarcoma cell line MCA205 reduces tumor growth more efficiently without affecting in vitro growth. |
| 294 | 10637450 | Synergistic effects were observed when IFN-alpha- and CD80-transduced tumor cells were mixed and inoculated. |
| 295 | 10637450 | These admixed cells were rejected by 14 of 15 (MC38) or seven of 15 mice (MCA205), whereas, a mixture of IFN-alpha and Neo cells or CD80 and Neo cells led to tumors associated with progressive growth. |
| 296 | 10637450 | The therapeutic efficacy with established WT MC38 tumors was shown when mice were treated with a vaccine consisting of repetitive injections of IFN-alpha- and CD80-transduced MC38 cells into the contralateral flank (P < 0.01). |
| 297 | 10637450 | This treatment was associated with accumulation of CD4+, CD8+ cells and dendritic cells within the established tumor, demonstrating induction of antitumor immune responses. |
| 298 | 10637450 | Combination gene therapy using IFN-alpha and CD80 is an effective immune therapy of cancer and could be considered for clinical trials. |
| 299 | 10637450 | Interferon-alpha (IFN-alpha) or CD80 transduction of tumor cells individually reduces tumorigenicity and enhances antitumor responses. |
| 300 | 10637450 | Here, we report that the combination of IFN-alpha and CD80 cancer gene therapy in poorly immunogenic murine tumor models, the colorectal adenocarcinoma cell line MC38, and the methylcholanthrene-induced fibrosarcoma cell line MCA205 reduces tumor growth more efficiently without affecting in vitro growth. |
| 301 | 10637450 | Synergistic effects were observed when IFN-alpha- and CD80-transduced tumor cells were mixed and inoculated. |
| 302 | 10637450 | These admixed cells were rejected by 14 of 15 (MC38) or seven of 15 mice (MCA205), whereas, a mixture of IFN-alpha and Neo cells or CD80 and Neo cells led to tumors associated with progressive growth. |
| 303 | 10637450 | The therapeutic efficacy with established WT MC38 tumors was shown when mice were treated with a vaccine consisting of repetitive injections of IFN-alpha- and CD80-transduced MC38 cells into the contralateral flank (P < 0.01). |
| 304 | 10637450 | This treatment was associated with accumulation of CD4+, CD8+ cells and dendritic cells within the established tumor, demonstrating induction of antitumor immune responses. |
| 305 | 10637450 | Combination gene therapy using IFN-alpha and CD80 is an effective immune therapy of cancer and could be considered for clinical trials. |
| 306 | 10637450 | Interferon-alpha (IFN-alpha) or CD80 transduction of tumor cells individually reduces tumorigenicity and enhances antitumor responses. |
| 307 | 10637450 | Here, we report that the combination of IFN-alpha and CD80 cancer gene therapy in poorly immunogenic murine tumor models, the colorectal adenocarcinoma cell line MC38, and the methylcholanthrene-induced fibrosarcoma cell line MCA205 reduces tumor growth more efficiently without affecting in vitro growth. |
| 308 | 10637450 | Synergistic effects were observed when IFN-alpha- and CD80-transduced tumor cells were mixed and inoculated. |
| 309 | 10637450 | These admixed cells were rejected by 14 of 15 (MC38) or seven of 15 mice (MCA205), whereas, a mixture of IFN-alpha and Neo cells or CD80 and Neo cells led to tumors associated with progressive growth. |
| 310 | 10637450 | The therapeutic efficacy with established WT MC38 tumors was shown when mice were treated with a vaccine consisting of repetitive injections of IFN-alpha- and CD80-transduced MC38 cells into the contralateral flank (P < 0.01). |
| 311 | 10637450 | This treatment was associated with accumulation of CD4+, CD8+ cells and dendritic cells within the established tumor, demonstrating induction of antitumor immune responses. |
| 312 | 10637450 | Combination gene therapy using IFN-alpha and CD80 is an effective immune therapy of cancer and could be considered for clinical trials. |
| 313 | 10637450 | Interferon-alpha (IFN-alpha) or CD80 transduction of tumor cells individually reduces tumorigenicity and enhances antitumor responses. |
| 314 | 10637450 | Here, we report that the combination of IFN-alpha and CD80 cancer gene therapy in poorly immunogenic murine tumor models, the colorectal adenocarcinoma cell line MC38, and the methylcholanthrene-induced fibrosarcoma cell line MCA205 reduces tumor growth more efficiently without affecting in vitro growth. |
| 315 | 10637450 | Synergistic effects were observed when IFN-alpha- and CD80-transduced tumor cells were mixed and inoculated. |
| 316 | 10637450 | These admixed cells were rejected by 14 of 15 (MC38) or seven of 15 mice (MCA205), whereas, a mixture of IFN-alpha and Neo cells or CD80 and Neo cells led to tumors associated with progressive growth. |
| 317 | 10637450 | The therapeutic efficacy with established WT MC38 tumors was shown when mice were treated with a vaccine consisting of repetitive injections of IFN-alpha- and CD80-transduced MC38 cells into the contralateral flank (P < 0.01). |
| 318 | 10637450 | This treatment was associated with accumulation of CD4+, CD8+ cells and dendritic cells within the established tumor, demonstrating induction of antitumor immune responses. |
| 319 | 10637450 | Combination gene therapy using IFN-alpha and CD80 is an effective immune therapy of cancer and could be considered for clinical trials. |
| 320 | 10715530 | Immunoadjuvant activities of E. coli- and plasmid-expressed recombinant chicken IFN-alpha/beta, IFN-gamma and IL-1beta in 1-day- and 3-week-old chickens. |
| 321 | 10715530 | In the present study we assessed the capacity of recombinant E. coli- or plasmid-expressed chicken interferons (IFN) and chicken IL-1beta, to exert immunostimulatory activities for humoral immune responses, in day-old and adult chickens. |
| 322 | 10715530 | We observed that both recombinant E. coli-expressed chicken IFN-alpha/beta and IFN-gamma facilitated the induction of a primary and also a secondary antibody response, using tetanus toxoid (TT) as a bacterial model antigen, in immunologically mature 3-week-old chickens. |
| 323 | 10715530 | Combined administration of IFN-alpha/beta plus IFN-gamma or IL-beta increased responses to TT in an additive, but not synergistic fashion. |
| 324 | 10715530 | Remarkably, no augmentation of antibody responses specific for TT, nor IBDV, was noted in day-old birds, receiving IFN-alpha/beta or IFN-gamma as adjuvant. |
| 325 | 10715530 | Immunoadjuvant activities of E. coli- and plasmid-expressed recombinant chicken IFN-alpha/beta, IFN-gamma and IL-1beta in 1-day- and 3-week-old chickens. |
| 326 | 10715530 | In the present study we assessed the capacity of recombinant E. coli- or plasmid-expressed chicken interferons (IFN) and chicken IL-1beta, to exert immunostimulatory activities for humoral immune responses, in day-old and adult chickens. |
| 327 | 10715530 | We observed that both recombinant E. coli-expressed chicken IFN-alpha/beta and IFN-gamma facilitated the induction of a primary and also a secondary antibody response, using tetanus toxoid (TT) as a bacterial model antigen, in immunologically mature 3-week-old chickens. |
| 328 | 10715530 | Combined administration of IFN-alpha/beta plus IFN-gamma or IL-beta increased responses to TT in an additive, but not synergistic fashion. |
| 329 | 10715530 | Remarkably, no augmentation of antibody responses specific for TT, nor IBDV, was noted in day-old birds, receiving IFN-alpha/beta or IFN-gamma as adjuvant. |
| 330 | 10715530 | Immunoadjuvant activities of E. coli- and plasmid-expressed recombinant chicken IFN-alpha/beta, IFN-gamma and IL-1beta in 1-day- and 3-week-old chickens. |
| 331 | 10715530 | In the present study we assessed the capacity of recombinant E. coli- or plasmid-expressed chicken interferons (IFN) and chicken IL-1beta, to exert immunostimulatory activities for humoral immune responses, in day-old and adult chickens. |
| 332 | 10715530 | We observed that both recombinant E. coli-expressed chicken IFN-alpha/beta and IFN-gamma facilitated the induction of a primary and also a secondary antibody response, using tetanus toxoid (TT) as a bacterial model antigen, in immunologically mature 3-week-old chickens. |
| 333 | 10715530 | Combined administration of IFN-alpha/beta plus IFN-gamma or IL-beta increased responses to TT in an additive, but not synergistic fashion. |
| 334 | 10715530 | Remarkably, no augmentation of antibody responses specific for TT, nor IBDV, was noted in day-old birds, receiving IFN-alpha/beta or IFN-gamma as adjuvant. |
| 335 | 10715530 | Immunoadjuvant activities of E. coli- and plasmid-expressed recombinant chicken IFN-alpha/beta, IFN-gamma and IL-1beta in 1-day- and 3-week-old chickens. |
| 336 | 10715530 | In the present study we assessed the capacity of recombinant E. coli- or plasmid-expressed chicken interferons (IFN) and chicken IL-1beta, to exert immunostimulatory activities for humoral immune responses, in day-old and adult chickens. |
| 337 | 10715530 | We observed that both recombinant E. coli-expressed chicken IFN-alpha/beta and IFN-gamma facilitated the induction of a primary and also a secondary antibody response, using tetanus toxoid (TT) as a bacterial model antigen, in immunologically mature 3-week-old chickens. |
| 338 | 10715530 | Combined administration of IFN-alpha/beta plus IFN-gamma or IL-beta increased responses to TT in an additive, but not synergistic fashion. |
| 339 | 10715530 | Remarkably, no augmentation of antibody responses specific for TT, nor IBDV, was noted in day-old birds, receiving IFN-alpha/beta or IFN-gamma as adjuvant. |
| 340 | 10717256 | Changes of the quasispecies population are more pronounced after initiation of treatment with IFN-a or interleukin-12 than during the natural course of disease. |
| 341 | 10775586 | This study demonstrates that (i) supernatants from peripheral blood mononuclear cells (PBMC) stimulated with influenza A virus inhibit replication of CCR5- and CXCR4-tropic HIV-1 isolates prior to reverse transcription; (ii) the HIV-suppressive supernatants can be generated by CD4- or CD8-depleted PBMC; (iii) this anti-HIV activity is partially due to alpha interferon (IFN-alpha), but not to IFN-gamma, IFN-beta, the beta-chemokines MIP-1alpha, MIP-1beta, and RANTES, or interleukin-16; (iv) the anti-HIV activity is generated equally well by PBMC cultured with either infectious or UV-inactivated influenza A virus; and (v) the antiviral activity can be generated by influenza A-stimulated PBMC from HIV-infected individuals. |
| 342 | 10775586 | These findings represent a novel mechanism for inhibition of HIV-1 replication that differs from the previously described CD8 anti-HIV factors (MIP-1alpha, MIP-1beta, RANTES, and CD8 antiviral factor). |
| 343 | 10813851 | The present study was conducted to examine whether or not the sperm cell has the expression of receptors for interferon (IFN) -alpha and -gamma. |
| 344 | 10813851 | Antibody to IFN-alpha receptor reacted with the acrosomal and tail regions of the murine sperm cell in the indirect immunofluorescence technique (IFT) and immunoscanning electron microscopic procedure (ISEP). |
| 345 | 10813851 | In the immunoprecipitation and Western blot procedures, this antibody specifically recognized a protein band of approximately 100 kD, which corresponds to the molecular weight of IFN-alpha receptor present in other cell types. |
| 346 | 10813851 | Antibody to IFN-gamma receptor specifically reacted with the posterior head, midpiece, and tail regions of sperm cell in IFT and ISEP, and recognized a band of approximately 85 kD in the immunoprecipitation and Western blot procedures, corresponding to the IFN-alpha receptor. |
| 347 | 10813851 | These findings indicate that the mammalian sperm cell has expression of IFN-alpha and IFN-gamma receptors, which seem to develop during spermatogenesis in the testes. |
| 348 | 10813851 | The present study was conducted to examine whether or not the sperm cell has the expression of receptors for interferon (IFN) -alpha and -gamma. |
| 349 | 10813851 | Antibody to IFN-alpha receptor reacted with the acrosomal and tail regions of the murine sperm cell in the indirect immunofluorescence technique (IFT) and immunoscanning electron microscopic procedure (ISEP). |
| 350 | 10813851 | In the immunoprecipitation and Western blot procedures, this antibody specifically recognized a protein band of approximately 100 kD, which corresponds to the molecular weight of IFN-alpha receptor present in other cell types. |
| 351 | 10813851 | Antibody to IFN-gamma receptor specifically reacted with the posterior head, midpiece, and tail regions of sperm cell in IFT and ISEP, and recognized a band of approximately 85 kD in the immunoprecipitation and Western blot procedures, corresponding to the IFN-alpha receptor. |
| 352 | 10813851 | These findings indicate that the mammalian sperm cell has expression of IFN-alpha and IFN-gamma receptors, which seem to develop during spermatogenesis in the testes. |
| 353 | 10813851 | The present study was conducted to examine whether or not the sperm cell has the expression of receptors for interferon (IFN) -alpha and -gamma. |
| 354 | 10813851 | Antibody to IFN-alpha receptor reacted with the acrosomal and tail regions of the murine sperm cell in the indirect immunofluorescence technique (IFT) and immunoscanning electron microscopic procedure (ISEP). |
| 355 | 10813851 | In the immunoprecipitation and Western blot procedures, this antibody specifically recognized a protein band of approximately 100 kD, which corresponds to the molecular weight of IFN-alpha receptor present in other cell types. |
| 356 | 10813851 | Antibody to IFN-gamma receptor specifically reacted with the posterior head, midpiece, and tail regions of sperm cell in IFT and ISEP, and recognized a band of approximately 85 kD in the immunoprecipitation and Western blot procedures, corresponding to the IFN-alpha receptor. |
| 357 | 10813851 | These findings indicate that the mammalian sperm cell has expression of IFN-alpha and IFN-gamma receptors, which seem to develop during spermatogenesis in the testes. |
| 358 | 10813851 | The present study was conducted to examine whether or not the sperm cell has the expression of receptors for interferon (IFN) -alpha and -gamma. |
| 359 | 10813851 | Antibody to IFN-alpha receptor reacted with the acrosomal and tail regions of the murine sperm cell in the indirect immunofluorescence technique (IFT) and immunoscanning electron microscopic procedure (ISEP). |
| 360 | 10813851 | In the immunoprecipitation and Western blot procedures, this antibody specifically recognized a protein band of approximately 100 kD, which corresponds to the molecular weight of IFN-alpha receptor present in other cell types. |
| 361 | 10813851 | Antibody to IFN-gamma receptor specifically reacted with the posterior head, midpiece, and tail regions of sperm cell in IFT and ISEP, and recognized a band of approximately 85 kD in the immunoprecipitation and Western blot procedures, corresponding to the IFN-alpha receptor. |
| 362 | 10813851 | These findings indicate that the mammalian sperm cell has expression of IFN-alpha and IFN-gamma receptors, which seem to develop during spermatogenesis in the testes. |
| 363 | 10813851 | The present study was conducted to examine whether or not the sperm cell has the expression of receptors for interferon (IFN) -alpha and -gamma. |
| 364 | 10813851 | Antibody to IFN-alpha receptor reacted with the acrosomal and tail regions of the murine sperm cell in the indirect immunofluorescence technique (IFT) and immunoscanning electron microscopic procedure (ISEP). |
| 365 | 10813851 | In the immunoprecipitation and Western blot procedures, this antibody specifically recognized a protein band of approximately 100 kD, which corresponds to the molecular weight of IFN-alpha receptor present in other cell types. |
| 366 | 10813851 | Antibody to IFN-gamma receptor specifically reacted with the posterior head, midpiece, and tail regions of sperm cell in IFT and ISEP, and recognized a band of approximately 85 kD in the immunoprecipitation and Western blot procedures, corresponding to the IFN-alpha receptor. |
| 367 | 10813851 | These findings indicate that the mammalian sperm cell has expression of IFN-alpha and IFN-gamma receptors, which seem to develop during spermatogenesis in the testes. |
| 368 | 10816614 | Il-1, EGF, and HGF suppress the antiviral activity of interferon in primary monkey hepatic parenchymal cells. |
| 369 | 10816614 | Interleukin-1 alpha, EGF, and HGF showed suppressive effects on the antiviral activity of IFN-alpha, -beta in primary monkey hepatic cells when examined by the yield reduction method using vesicular stomatitis virus (VSV). |
| 370 | 10816614 | In contrast, 50 ng/ml of TNF and IL-6 had no suppressive effect on the IFN-induced antiviral state in the hepatic cells. |
| 371 | 10838666 | Generation of monocyte-derived dendritic cells from patients with renal cell cancer: modulation of their functional properties after therapy with biological response modifiers (IFN-alpha plus IL-2 and IL-12). |
| 372 | 10838666 | The combination of interferon-alpha (IFN-alpha) plus interleukin (IL-2) has been accepted in the treatment of metastatic renal cell carcinoma (MRCC), whereas vaccines based on IL-12 or dendritic cells (DCs) are still being investigated. |
| 373 | 10838666 | Eight and 13 MRCC patients received IL-2 plus IFN-alpha or IL-12 immunotherapy, respectively. |
| 374 | 10838666 | The adherent fraction of mononuclear cells from patients' blood drawn before, during, and after immunotherapy was incubated in clinically approved culture medium supplemented with 5% autologous serum, rhu granulocyte macrophage colony-stimulating factor, and rhuIL-4 for a week. |
| 375 | 10838666 | Morphologic and phenotypical analyses revealed immature DCs with low levels of CD1a or CD83 expression throughout therapy with BRMs. |
| 376 | 10838666 | IL-12 expression levels under IFN-gamma and CD40L stimulation were significantly lower in MDDC cultures from patients with MRCC compared with healthy volunteers. |
| 377 | 10838666 | Generation of monocyte-derived dendritic cells from patients with renal cell cancer: modulation of their functional properties after therapy with biological response modifiers (IFN-alpha plus IL-2 and IL-12). |
| 378 | 10838666 | The combination of interferon-alpha (IFN-alpha) plus interleukin (IL-2) has been accepted in the treatment of metastatic renal cell carcinoma (MRCC), whereas vaccines based on IL-12 or dendritic cells (DCs) are still being investigated. |
| 379 | 10838666 | Eight and 13 MRCC patients received IL-2 plus IFN-alpha or IL-12 immunotherapy, respectively. |
| 380 | 10838666 | The adherent fraction of mononuclear cells from patients' blood drawn before, during, and after immunotherapy was incubated in clinically approved culture medium supplemented with 5% autologous serum, rhu granulocyte macrophage colony-stimulating factor, and rhuIL-4 for a week. |
| 381 | 10838666 | Morphologic and phenotypical analyses revealed immature DCs with low levels of CD1a or CD83 expression throughout therapy with BRMs. |
| 382 | 10838666 | IL-12 expression levels under IFN-gamma and CD40L stimulation were significantly lower in MDDC cultures from patients with MRCC compared with healthy volunteers. |
| 383 | 10838666 | Generation of monocyte-derived dendritic cells from patients with renal cell cancer: modulation of their functional properties after therapy with biological response modifiers (IFN-alpha plus IL-2 and IL-12). |
| 384 | 10838666 | The combination of interferon-alpha (IFN-alpha) plus interleukin (IL-2) has been accepted in the treatment of metastatic renal cell carcinoma (MRCC), whereas vaccines based on IL-12 or dendritic cells (DCs) are still being investigated. |
| 385 | 10838666 | Eight and 13 MRCC patients received IL-2 plus IFN-alpha or IL-12 immunotherapy, respectively. |
| 386 | 10838666 | The adherent fraction of mononuclear cells from patients' blood drawn before, during, and after immunotherapy was incubated in clinically approved culture medium supplemented with 5% autologous serum, rhu granulocyte macrophage colony-stimulating factor, and rhuIL-4 for a week. |
| 387 | 10838666 | Morphologic and phenotypical analyses revealed immature DCs with low levels of CD1a or CD83 expression throughout therapy with BRMs. |
| 388 | 10838666 | IL-12 expression levels under IFN-gamma and CD40L stimulation were significantly lower in MDDC cultures from patients with MRCC compared with healthy volunteers. |
| 389 | 10851462 | Cytokine detection in patients' sera by ELISA showed significant increases (p < 0.05) for IFN-gamma and TNF-alpha but not for IFN-alpha four h post vaccination. |
| 390 | 10861647 | Until recently, the only treatment for chronic hepatitis B was the immune modulator, interferon (IFN) alpha. |
| 391 | 10861647 | IFN alpha treatment has several disadvantages; it is expensive, it must be administered by injection, there are side effects, and IFN alpha is poorly tolerated. |
| 392 | 10861647 | Until recently, the only treatment for chronic hepatitis B was the immune modulator, interferon (IFN) alpha. |
| 393 | 10861647 | IFN alpha treatment has several disadvantages; it is expensive, it must be administered by injection, there are side effects, and IFN alpha is poorly tolerated. |
| 394 | 10866836 | It has been proposed that the more aggressive liver disease observed in individuals infected with HAV in addition to chronic HBV/HCV is a result of the induction of interferon (IFN)-alpha during acute HAV infection. |
| 395 | 10866836 | Alternatively, HAV may indirectly stimulate the T helper 1 (Th1)-type cytokine responses, such as interleukin (IL)-2, IFN-gamma and tumour necrosis factor (TNF)-alpha, which directly promote the antiviral CTL response. |
| 396 | 10868900 | Interferon (IFN)-alpha has proven benefit in a well-defined group of those with hepatitis B but has made little impact on the global burden of chronic liver disease. |
| 397 | 10906201 | MV is thus able to suppress the synthesis of the earliest mediator of antiviral immunity, IFN-alpha/beta. |
| 398 | 10945227 | HIV-1 gp41-like human type I interferon (IFN) could inhibit lymphocyte proliferation and up-modulate MHC class I and II and ICAM-1 molecule expression. |
| 399 | 10945227 | Sequence comparison indicates that a similar epitope RILAV-YLKD exists between N-domain of gp41 and two regions in IFN-alpha(aa29-35 and 113-129), IFN-beta (aa31-37 and 125-138) and IFN-omega (aa29-35 and 123-136), which was shown to form IFN-alpha/beta-receptor binding site. |
| 400 | 10945227 | Experimental studies indicated that a common immunological epitope exists between gp41 and IFN-alpha and -beta. |
| 401 | 10945227 | Antibodies against human IFN-alpha and -beta recognized the common immunological epitope and inhibited gp41-binding to the potential cellular receptor protein p45. |
| 402 | 10945227 | Moreover, the polyclonal antibody to IFN-beta completely inhibited gp41-binding to human T, B cells and monocytic cells, while IFN-alpha could only inhibit this binding incompletely. |
| 403 | 10945227 | It was observed that the increased levels of antibodies against human IFN-alpha and -beta exist in HIV-1-infected individuals and are associated with the common epitope on gp41. |
| 404 | 10945227 | HIV-1 gp41-like human type I interferon (IFN) could inhibit lymphocyte proliferation and up-modulate MHC class I and II and ICAM-1 molecule expression. |
| 405 | 10945227 | Sequence comparison indicates that a similar epitope RILAV-YLKD exists between N-domain of gp41 and two regions in IFN-alpha(aa29-35 and 113-129), IFN-beta (aa31-37 and 125-138) and IFN-omega (aa29-35 and 123-136), which was shown to form IFN-alpha/beta-receptor binding site. |
| 406 | 10945227 | Experimental studies indicated that a common immunological epitope exists between gp41 and IFN-alpha and -beta. |
| 407 | 10945227 | Antibodies against human IFN-alpha and -beta recognized the common immunological epitope and inhibited gp41-binding to the potential cellular receptor protein p45. |
| 408 | 10945227 | Moreover, the polyclonal antibody to IFN-beta completely inhibited gp41-binding to human T, B cells and monocytic cells, while IFN-alpha could only inhibit this binding incompletely. |
| 409 | 10945227 | It was observed that the increased levels of antibodies against human IFN-alpha and -beta exist in HIV-1-infected individuals and are associated with the common epitope on gp41. |
| 410 | 10945227 | HIV-1 gp41-like human type I interferon (IFN) could inhibit lymphocyte proliferation and up-modulate MHC class I and II and ICAM-1 molecule expression. |
| 411 | 10945227 | Sequence comparison indicates that a similar epitope RILAV-YLKD exists between N-domain of gp41 and two regions in IFN-alpha(aa29-35 and 113-129), IFN-beta (aa31-37 and 125-138) and IFN-omega (aa29-35 and 123-136), which was shown to form IFN-alpha/beta-receptor binding site. |
| 412 | 10945227 | Experimental studies indicated that a common immunological epitope exists between gp41 and IFN-alpha and -beta. |
| 413 | 10945227 | Antibodies against human IFN-alpha and -beta recognized the common immunological epitope and inhibited gp41-binding to the potential cellular receptor protein p45. |
| 414 | 10945227 | Moreover, the polyclonal antibody to IFN-beta completely inhibited gp41-binding to human T, B cells and monocytic cells, while IFN-alpha could only inhibit this binding incompletely. |
| 415 | 10945227 | It was observed that the increased levels of antibodies against human IFN-alpha and -beta exist in HIV-1-infected individuals and are associated with the common epitope on gp41. |
| 416 | 10945227 | HIV-1 gp41-like human type I interferon (IFN) could inhibit lymphocyte proliferation and up-modulate MHC class I and II and ICAM-1 molecule expression. |
| 417 | 10945227 | Sequence comparison indicates that a similar epitope RILAV-YLKD exists between N-domain of gp41 and two regions in IFN-alpha(aa29-35 and 113-129), IFN-beta (aa31-37 and 125-138) and IFN-omega (aa29-35 and 123-136), which was shown to form IFN-alpha/beta-receptor binding site. |
| 418 | 10945227 | Experimental studies indicated that a common immunological epitope exists between gp41 and IFN-alpha and -beta. |
| 419 | 10945227 | Antibodies against human IFN-alpha and -beta recognized the common immunological epitope and inhibited gp41-binding to the potential cellular receptor protein p45. |
| 420 | 10945227 | Moreover, the polyclonal antibody to IFN-beta completely inhibited gp41-binding to human T, B cells and monocytic cells, while IFN-alpha could only inhibit this binding incompletely. |
| 421 | 10945227 | It was observed that the increased levels of antibodies against human IFN-alpha and -beta exist in HIV-1-infected individuals and are associated with the common epitope on gp41. |
| 422 | 10945227 | HIV-1 gp41-like human type I interferon (IFN) could inhibit lymphocyte proliferation and up-modulate MHC class I and II and ICAM-1 molecule expression. |
| 423 | 10945227 | Sequence comparison indicates that a similar epitope RILAV-YLKD exists between N-domain of gp41 and two regions in IFN-alpha(aa29-35 and 113-129), IFN-beta (aa31-37 and 125-138) and IFN-omega (aa29-35 and 123-136), which was shown to form IFN-alpha/beta-receptor binding site. |
| 424 | 10945227 | Experimental studies indicated that a common immunological epitope exists between gp41 and IFN-alpha and -beta. |
| 425 | 10945227 | Antibodies against human IFN-alpha and -beta recognized the common immunological epitope and inhibited gp41-binding to the potential cellular receptor protein p45. |
| 426 | 10945227 | Moreover, the polyclonal antibody to IFN-beta completely inhibited gp41-binding to human T, B cells and monocytic cells, while IFN-alpha could only inhibit this binding incompletely. |
| 427 | 10945227 | It was observed that the increased levels of antibodies against human IFN-alpha and -beta exist in HIV-1-infected individuals and are associated with the common epitope on gp41. |
| 428 | 10954520 | Treatment of cells with recombinant universal IFN-alpha A/D or IFN-beta revealed severe inhibition of single and double deletion mutants, whereas growth of full-length BRSV was not greatly affected. |
| 429 | 10954520 | Surprisingly, all NS deletion mutants were equally repressed, indicating an obligatory cooperation of NS1 and NS2 in antagonizing IFN-mediated antiviral mechanisms. |
| 430 | 10954520 | To verify this finding, we generated recombinant rabies virus (rRV) expressing either NS1 or NS2 and determined their IFN sensitivity. |
| 431 | 10954520 | Treatment of cells with recombinant universal IFN-alpha A/D or IFN-beta revealed severe inhibition of single and double deletion mutants, whereas growth of full-length BRSV was not greatly affected. |
| 432 | 10954520 | Surprisingly, all NS deletion mutants were equally repressed, indicating an obligatory cooperation of NS1 and NS2 in antagonizing IFN-mediated antiviral mechanisms. |
| 433 | 10954520 | To verify this finding, we generated recombinant rabies virus (rRV) expressing either NS1 or NS2 and determined their IFN sensitivity. |
| 434 | 10954520 | Treatment of cells with recombinant universal IFN-alpha A/D or IFN-beta revealed severe inhibition of single and double deletion mutants, whereas growth of full-length BRSV was not greatly affected. |
| 435 | 10954520 | Surprisingly, all NS deletion mutants were equally repressed, indicating an obligatory cooperation of NS1 and NS2 in antagonizing IFN-mediated antiviral mechanisms. |
| 436 | 10954520 | To verify this finding, we generated recombinant rabies virus (rRV) expressing either NS1 or NS2 and determined their IFN sensitivity. |
| 437 | 11006019 | R-848 and imiquimod belong to a class of immune response modifiers that are potent inducers of cytokines, including IFN-alpha, TNF-alpha, IL-12, and IFN-gamma. |
| 438 | 11006019 | The mechanism of R-848's adjuvant activity is linked to cytokine production, where increases in IgG2a levels are associated with IFN-alpha, TNF-alpha, IL-12, and IFN-gamma induction, and decreases in IgE levels are associated with IFN-alpha and TNF-alpha. |
| 439 | 11006019 | R-848 and imiquimod belong to a class of immune response modifiers that are potent inducers of cytokines, including IFN-alpha, TNF-alpha, IL-12, and IFN-gamma. |
| 440 | 11006019 | The mechanism of R-848's adjuvant activity is linked to cytokine production, where increases in IgG2a levels are associated with IFN-alpha, TNF-alpha, IL-12, and IFN-gamma induction, and decreases in IgE levels are associated with IFN-alpha and TNF-alpha. |
| 441 | 11053627 | Influenza vaccine stimulated significantly lower production of interferon-gamma (IFN-gamma) compared with live and heat inactivated viruses, whereas both vaccine and heat-inactivated influenza induced lower levels of IFN-alpha compared with live virus. |
| 442 | 11053627 | A significant increase in monocyte expression of CD80, CD86, CD40, and human leukocyte antigen-DR (HLA-DR) was also induced by live influenza virus. |
| 443 | 11053627 | Our results suggest that immunization with live influenza vaccines might induce immune responses that would not be induced by conventional inactivated vaccines, including CTL generation, antiviral IFN-gamma and IFN-alpha cytokine production, and increased antigen presentation and costimulatory capacity on antigen presenting cells (APC). |
| 444 | 11053627 | Influenza vaccine stimulated significantly lower production of interferon-gamma (IFN-gamma) compared with live and heat inactivated viruses, whereas both vaccine and heat-inactivated influenza induced lower levels of IFN-alpha compared with live virus. |
| 445 | 11053627 | A significant increase in monocyte expression of CD80, CD86, CD40, and human leukocyte antigen-DR (HLA-DR) was also induced by live influenza virus. |
| 446 | 11053627 | Our results suggest that immunization with live influenza vaccines might induce immune responses that would not be induced by conventional inactivated vaccines, including CTL generation, antiviral IFN-gamma and IFN-alpha cytokine production, and increased antigen presentation and costimulatory capacity on antigen presenting cells (APC). |
| 447 | 11054277 | Here, pigs were vaccinated by a single coinjection of three plasmids encoding PRV glycoproteins gB, gC, and gD, with plasmid expressing porcine granulocytemacrophage colony-stimulating factor (GM-CSF) or porcine interferon-alpha (IFN-alpha). |
| 448 | 11054277 | DNA immunization induced a primary T cell-mediated response characterized by low rates of IFN-gamma, interleukin-2 (IL-2), and IL4 mRNA in peripheral blood mononuclear cells (PBMC). |
| 449 | 11054277 | Codelivery of plasmid expressing GM-CSF or IFN-alpha had no effect on cytokine mRNA expression or on B cell response. |
| 450 | 11054277 | Codelivery of GMCSF gene significantly increased both Th immune response (i.e., IFN-gamma and IL-4 mRNA expression) and clinical protection but had no effect on secondary B immune response. |
| 451 | 11054277 | Here, pigs were vaccinated by a single coinjection of three plasmids encoding PRV glycoproteins gB, gC, and gD, with plasmid expressing porcine granulocytemacrophage colony-stimulating factor (GM-CSF) or porcine interferon-alpha (IFN-alpha). |
| 452 | 11054277 | DNA immunization induced a primary T cell-mediated response characterized by low rates of IFN-gamma, interleukin-2 (IL-2), and IL4 mRNA in peripheral blood mononuclear cells (PBMC). |
| 453 | 11054277 | Codelivery of plasmid expressing GM-CSF or IFN-alpha had no effect on cytokine mRNA expression or on B cell response. |
| 454 | 11054277 | Codelivery of GMCSF gene significantly increased both Th immune response (i.e., IFN-gamma and IL-4 mRNA expression) and clinical protection but had no effect on secondary B immune response. |
| 455 | 11092043 | Patients treated with repeated injections of a polyvalent melanoma vaccine (PMV), interferon-alpha-2b (IFN-alpha 2b) or interleukin-2 (IL-2) were followed during treatment duration. |
| 456 | 11092043 | Before treatment, patients treated with PMV or IFN-alpha 2b had comparable low MIA concentrations, whereas most IL-2-treated patients had higher MIA levels. |
| 457 | 11092043 | At the end of treatment, MIA concentrations were higher in patients with progressive disease (PD) than in patients with no clinical evidence of melanoma (NPD) for PMV, IFN-alpha 2b or IL-2 therapy (3.7 +/- 0.2 vs 11.5 +/- 5.4 ng/ml, 3.8 +/- 0.2 vs 8.3 +/- 1.7 ng/ml, and 2.3 +/- 0.7 vs 20.2 +/- 7.4 ng/ml, respectively, p < 0.05). |
| 458 | 11092043 | For PMV- and IFN-alpha 2b-treated patients, a rise in MIA levels occurred significantly earlier than clinical diagnosis of melanoma recurrence. |
| 459 | 11092043 | Patients treated with repeated injections of a polyvalent melanoma vaccine (PMV), interferon-alpha-2b (IFN-alpha 2b) or interleukin-2 (IL-2) were followed during treatment duration. |
| 460 | 11092043 | Before treatment, patients treated with PMV or IFN-alpha 2b had comparable low MIA concentrations, whereas most IL-2-treated patients had higher MIA levels. |
| 461 | 11092043 | At the end of treatment, MIA concentrations were higher in patients with progressive disease (PD) than in patients with no clinical evidence of melanoma (NPD) for PMV, IFN-alpha 2b or IL-2 therapy (3.7 +/- 0.2 vs 11.5 +/- 5.4 ng/ml, 3.8 +/- 0.2 vs 8.3 +/- 1.7 ng/ml, and 2.3 +/- 0.7 vs 20.2 +/- 7.4 ng/ml, respectively, p < 0.05). |
| 462 | 11092043 | For PMV- and IFN-alpha 2b-treated patients, a rise in MIA levels occurred significantly earlier than clinical diagnosis of melanoma recurrence. |
| 463 | 11092043 | Patients treated with repeated injections of a polyvalent melanoma vaccine (PMV), interferon-alpha-2b (IFN-alpha 2b) or interleukin-2 (IL-2) were followed during treatment duration. |
| 464 | 11092043 | Before treatment, patients treated with PMV or IFN-alpha 2b had comparable low MIA concentrations, whereas most IL-2-treated patients had higher MIA levels. |
| 465 | 11092043 | At the end of treatment, MIA concentrations were higher in patients with progressive disease (PD) than in patients with no clinical evidence of melanoma (NPD) for PMV, IFN-alpha 2b or IL-2 therapy (3.7 +/- 0.2 vs 11.5 +/- 5.4 ng/ml, 3.8 +/- 0.2 vs 8.3 +/- 1.7 ng/ml, and 2.3 +/- 0.7 vs 20.2 +/- 7.4 ng/ml, respectively, p < 0.05). |
| 466 | 11092043 | For PMV- and IFN-alpha 2b-treated patients, a rise in MIA levels occurred significantly earlier than clinical diagnosis of melanoma recurrence. |
| 467 | 11092043 | Patients treated with repeated injections of a polyvalent melanoma vaccine (PMV), interferon-alpha-2b (IFN-alpha 2b) or interleukin-2 (IL-2) were followed during treatment duration. |
| 468 | 11092043 | Before treatment, patients treated with PMV or IFN-alpha 2b had comparable low MIA concentrations, whereas most IL-2-treated patients had higher MIA levels. |
| 469 | 11092043 | At the end of treatment, MIA concentrations were higher in patients with progressive disease (PD) than in patients with no clinical evidence of melanoma (NPD) for PMV, IFN-alpha 2b or IL-2 therapy (3.7 +/- 0.2 vs 11.5 +/- 5.4 ng/ml, 3.8 +/- 0.2 vs 8.3 +/- 1.7 ng/ml, and 2.3 +/- 0.7 vs 20.2 +/- 7.4 ng/ml, respectively, p < 0.05). |
| 470 | 11092043 | For PMV- and IFN-alpha 2b-treated patients, a rise in MIA levels occurred significantly earlier than clinical diagnosis of melanoma recurrence. |
| 471 | 11112484 | The transcription of both IFN-alpha and IFN-beta genes was detected by RT-PCR in stimulated cells. |
| 472 | 11112484 | The ability of poliovirus-antibody complexes to induce IFN-alpha was specifically inhibited when PBMCs were preincubated with an excess of the Fc fragment of IgG. |
| 473 | 11112484 | Monoclonal antibodies directed to FcgammaRII (CD32) were also inhibitory, whereas antibodies to the two other classes of Fcgamma receptors, CD16 and CD64, were not. |
| 474 | 11112484 | The transcription of both IFN-alpha and IFN-beta genes was detected by RT-PCR in stimulated cells. |
| 475 | 11112484 | The ability of poliovirus-antibody complexes to induce IFN-alpha was specifically inhibited when PBMCs were preincubated with an excess of the Fc fragment of IgG. |
| 476 | 11112484 | Monoclonal antibodies directed to FcgammaRII (CD32) were also inhibitory, whereas antibodies to the two other classes of Fcgamma receptors, CD16 and CD64, were not. |
| 477 | 11163460 | Influenza A virus-infected respiratory epithelial cells produce limited amounts of chemokines (RANTES, MCP-1, IL-8) and IFN-alpha/beta, whereas monocytes/macrophages readily produce chemokines such as RANTES, MIP-1alpha, MCP-1, MCP-3, IP-10 and cytokines TNF-alpha, IL-1beta, IL-6, IL-18 and IFN-alpha/beta. |
| 478 | 11182147 | Here we describe the interferon-alpha (IFN-alpha) and interleukin-6 (IL-6) inducing properties of a commonly used eukaryotic expression vector, pcDNA3, in porcine leukocytes. |
| 479 | 11182147 | The plasmid, as well as poly(I):poly(C), required lipofectin to induce IFN-alpha production whereas both preparations induced IL-6 irrespective of preincubation with lipofectin. |
| 480 | 11182147 | Here we describe the interferon-alpha (IFN-alpha) and interleukin-6 (IL-6) inducing properties of a commonly used eukaryotic expression vector, pcDNA3, in porcine leukocytes. |
| 481 | 11182147 | The plasmid, as well as poly(I):poly(C), required lipofectin to induce IFN-alpha production whereas both preparations induced IL-6 irrespective of preincubation with lipofectin. |
| 482 | 11207657 | When compared with control BCG, rhIFN-alpha BCG was substantially more active in inducing the production of IFN-gamma and IFN-inducible protein 10 (IP-10) from human peripheral blood mononuclear cells, while IL-10 production was correspondingly decreased. |
| 483 | 11207657 | The observation that the maximum IFN-gamma induction depends on the simultaneous presence of both IFN-alpha and BCG highlights the advantages of rhIFN-alpha BCG. |
| 484 | 11214223 | Until recently, the only treatment for chronic hepatitis B was the immune modulator, interferon (IFN) alpha. |
| 485 | 11214223 | However, IFN alpha treatment has several disadvantages; it is expensive, it must be administered by injection, there are side-effects, and IFN alpha is poorly tolerated. |
| 486 | 11214223 | Until recently, the only treatment for chronic hepatitis B was the immune modulator, interferon (IFN) alpha. |
| 487 | 11214223 | However, IFN alpha treatment has several disadvantages; it is expensive, it must be administered by injection, there are side-effects, and IFN alpha is poorly tolerated. |
| 488 | 11237823 | Vaccination of control subjects and HIV patients induced increases in production of interleukin-2 and interferon (IFN)-gamma, but not of IFN-alpha. |
| 489 | 11264339 | Exposure to live dengue virus led to maturation and activation of both the infected and surrounding, uninfected DCs and stimulated production of tumor necrosis factor alpha (TNF-alpha) and alpha interferon (IFN-alpha). |
| 490 | 11264339 | Activation of the dengue virus-infected DCs was blunted compared to the surrounding, uninfected DCs, and dengue virus infection induced low-level release of interleukin-12 p70 (IL-12 p70), a key cytokine in the development of cell-mediated immunity (CMI). |
| 491 | 11264339 | Upon the addition of IFN-gamma, there was enhanced activation of dengue virus-infected DCs and enhanced dengue virus-induced IL-12 p70 release. |
| 492 | 11264369 | In this study, we established HeLa cell lines stably expressing the C, Y1, and Y2 proteins individually and examined the capacities of these cells to circumvent the antiviral action of alpha/beta IFN (IFN-alpha/beta) and IFN-gamma and to inhibit viral transcription. |
| 493 | 11264369 | The assay protocols included monitoring of IFN-alpha/beta-mediated signaling by interferon-stimulated response element-driven reporter gene expression and of the antiviral state induced by IFN-alpha/beta and IFN-gamma and measurement of reporter gene expression from an SeV minigenome, as well as quantification of SeV primary transcripts. |
| 494 | 11264369 | In this study, we established HeLa cell lines stably expressing the C, Y1, and Y2 proteins individually and examined the capacities of these cells to circumvent the antiviral action of alpha/beta IFN (IFN-alpha/beta) and IFN-gamma and to inhibit viral transcription. |
| 495 | 11264369 | The assay protocols included monitoring of IFN-alpha/beta-mediated signaling by interferon-stimulated response element-driven reporter gene expression and of the antiviral state induced by IFN-alpha/beta and IFN-gamma and measurement of reporter gene expression from an SeV minigenome, as well as quantification of SeV primary transcripts. |
| 496 | 11305184 | Promising treatment options are melanoma vaccines to obtain an efficient immunoresponse, the combination of chemotherapy with Interleukin (IL)-2 and Interferon alfa (IFN-alpha) as a way of improving response rates and survival. |
| 497 | 11325600 | Influenza A virus infection results in the production of chemotactic (RANTES, MIP-1 alpha, MCP-1, MCP-3, and IP-10), pro-inflammatory (IL-1 beta, IL-6, IL-18, and TNF-alpha), and antiviral (IFN-alpha/beta) cytokines. |
| 498 | 11325600 | Cytokine gene expression is associated with the activation of NF-kappa B, AP-1, STAT and IRF signal transducing molecules in influenza A virus-infected cells. |
| 499 | 11325600 | IFN-alpha/beta also prolongs T cell survival, upregulates IL-12 and IL-18 receptor gene expression and together with IL-18 stimulates NK and T cell IFN-gamma production and the development of Th1-type immune response. |
| 500 | 11325600 | Influenza A virus infection results in the production of chemotactic (RANTES, MIP-1 alpha, MCP-1, MCP-3, and IP-10), pro-inflammatory (IL-1 beta, IL-6, IL-18, and TNF-alpha), and antiviral (IFN-alpha/beta) cytokines. |
| 501 | 11325600 | Cytokine gene expression is associated with the activation of NF-kappa B, AP-1, STAT and IRF signal transducing molecules in influenza A virus-infected cells. |
| 502 | 11325600 | IFN-alpha/beta also prolongs T cell survival, upregulates IL-12 and IL-18 receptor gene expression and together with IL-18 stimulates NK and T cell IFN-gamma production and the development of Th1-type immune response. |
| 503 | 11352664 | Monocyte-derived human macrophages and peripheral blood mononuclear cells infected with ebola virus secrete MIP-1alpha and TNF-alpha and inhibit poly-IC-induced IFN-alpha in vitro. |
| 504 | 11352664 | We demonstrate that direct infection of human PBMC results in the induction of MCP-1, MIP-1alpha, RANTES, and TNF-alpha as early as 24 h p.i. in response to live virus. |
| 505 | 11352664 | Monocyte-derived macrophages infected with live Ebola-virus secreted MIP-1alpha and TNF-alpha specifically while RANTES and MCP-1 were secreted by with both live or inactivated virus stimulation and do not require viral replication. |
| 506 | 11352664 | Type I interferons (IFN-alpha and -beta), IL-1beta and IL-10, were not induced by Ebola virus. |
| 507 | 11352664 | Monocyte-derived human macrophages and peripheral blood mononuclear cells infected with ebola virus secrete MIP-1alpha and TNF-alpha and inhibit poly-IC-induced IFN-alpha in vitro. |
| 508 | 11352664 | We demonstrate that direct infection of human PBMC results in the induction of MCP-1, MIP-1alpha, RANTES, and TNF-alpha as early as 24 h p.i. in response to live virus. |
| 509 | 11352664 | Monocyte-derived macrophages infected with live Ebola-virus secreted MIP-1alpha and TNF-alpha specifically while RANTES and MCP-1 were secreted by with both live or inactivated virus stimulation and do not require viral replication. |
| 510 | 11352664 | Type I interferons (IFN-alpha and -beta), IL-1beta and IL-10, were not induced by Ebola virus. |
| 511 | 11567773 | Adjuvant effects of IL-1beta, IL-2, IL-8, IL-15, IFN-alpha, IFN-gamma TGF-beta4 and lymphotactin on DNA vaccination against Eimeria acervulina. |
| 512 | 11567773 | Eight chicken cytokine genes (IL-1beta, IL-2, IL-8, IL-15, IFN-alpha, IFN-gamma, TGF-beta4, lymphotactin) were evaluated for their adjuvant effect on a suboptimal dose of an Eimeria DNA vaccine carrying the 3-1E parasite gene (pcDNA3-1E). |
| 513 | 11567773 | IFN-alpha (1 microg) or 10 microg of lymphotactin expressing plasmids, when given simultaneously with the pcDNA3-1E vaccine, significantly protected against body weight loss induced by E. acervulina. |
| 514 | 11567773 | Parasite replication was significantly reduced in chickens given the pcDNA3-1E vaccine along with 10 microg of the IL-8, lymphotactin, IFN-gamma, IL-15, TGF-beta4, or IL-1beta plasmids compared with chickens given the pcDNA3-1E vaccine alone. |
| 515 | 11567773 | Flow cytometric analysis of duodenum intraepithelial lymphocytes showed chickens that received the pcDNA3-1E vaccine simultaneously with the IL-8 or IL-15 genes had significantly increased CD3+ cells compared with vaccination using pcDNA3-1E alone or in combination with the other cytokine genes tested. |
| 516 | 11567773 | Adjuvant effects of IL-1beta, IL-2, IL-8, IL-15, IFN-alpha, IFN-gamma TGF-beta4 and lymphotactin on DNA vaccination against Eimeria acervulina. |
| 517 | 11567773 | Eight chicken cytokine genes (IL-1beta, IL-2, IL-8, IL-15, IFN-alpha, IFN-gamma, TGF-beta4, lymphotactin) were evaluated for their adjuvant effect on a suboptimal dose of an Eimeria DNA vaccine carrying the 3-1E parasite gene (pcDNA3-1E). |
| 518 | 11567773 | IFN-alpha (1 microg) or 10 microg of lymphotactin expressing plasmids, when given simultaneously with the pcDNA3-1E vaccine, significantly protected against body weight loss induced by E. acervulina. |
| 519 | 11567773 | Parasite replication was significantly reduced in chickens given the pcDNA3-1E vaccine along with 10 microg of the IL-8, lymphotactin, IFN-gamma, IL-15, TGF-beta4, or IL-1beta plasmids compared with chickens given the pcDNA3-1E vaccine alone. |
| 520 | 11567773 | Flow cytometric analysis of duodenum intraepithelial lymphocytes showed chickens that received the pcDNA3-1E vaccine simultaneously with the IL-8 or IL-15 genes had significantly increased CD3+ cells compared with vaccination using pcDNA3-1E alone or in combination with the other cytokine genes tested. |
| 521 | 11567773 | Adjuvant effects of IL-1beta, IL-2, IL-8, IL-15, IFN-alpha, IFN-gamma TGF-beta4 and lymphotactin on DNA vaccination against Eimeria acervulina. |
| 522 | 11567773 | Eight chicken cytokine genes (IL-1beta, IL-2, IL-8, IL-15, IFN-alpha, IFN-gamma, TGF-beta4, lymphotactin) were evaluated for their adjuvant effect on a suboptimal dose of an Eimeria DNA vaccine carrying the 3-1E parasite gene (pcDNA3-1E). |
| 523 | 11567773 | IFN-alpha (1 microg) or 10 microg of lymphotactin expressing plasmids, when given simultaneously with the pcDNA3-1E vaccine, significantly protected against body weight loss induced by E. acervulina. |
| 524 | 11567773 | Parasite replication was significantly reduced in chickens given the pcDNA3-1E vaccine along with 10 microg of the IL-8, lymphotactin, IFN-gamma, IL-15, TGF-beta4, or IL-1beta plasmids compared with chickens given the pcDNA3-1E vaccine alone. |
| 525 | 11567773 | Flow cytometric analysis of duodenum intraepithelial lymphocytes showed chickens that received the pcDNA3-1E vaccine simultaneously with the IL-8 or IL-15 genes had significantly increased CD3+ cells compared with vaccination using pcDNA3-1E alone or in combination with the other cytokine genes tested. |
| 526 | 11642602 | In contrast, exposure to serum-free medium and interferon-gamma (IFN-gamma) rapidly influences CD83+ DCs to secrete high levels of IL-12, IL-6, and MIP-1beta, and promotes Dcl differentiation. |
| 527 | 11642602 | In contrast, CD83+ DCs matured in serum-free medium in the absence of IFN-gamma, or in the presence of calcium signaling agents, prostaglandin-E2, or IFN-alpha, produce no IL-12, scant IL-6, and prodigious IL-8, MDC, and TARC, and promote Dc2 differentiation. |
| 528 | 11722649 | RA + PIC-treated rats had significantly higher levels of interleukin (IL)-10, IL-12, and signal transducer and activator of transcription-1 (STAT-1) mRNA (P < 0.05), and STAT-1 protein (P < 0.02). |
| 529 | 11722649 | Treatments administered in vivo significantly modulated T-cell proliferation to anti-CD3/phorbol myristyl acetate + IFN-alpha ex vivo. |
| 530 | 11726219 | Generation of CD4(+) and CD8(+) T lymphocyte responses by dendritic cells armed with PSA/anti-PSA (antigen/antibody) complexes. |
| 531 | 11726219 | We compared the capacity of DC to generate CD4(+) and CD8(+) T cell responses after exposure to prostate-specific antigen (PSA) alone, PSA targeted to the mannose receptor (mannosylated PSA (PSA-m)), or PSA targeted to Fc receptors by combining PSA with an anti-PSA antibody (AR47.47). |
| 532 | 11726219 | Autologous CD3(+) T cells were added to monocyte-derived immature DC that had been cultured with GM-CSF/IL-4 for 4 days, exposed to antigen, and matured with CD40L or TNFalpha/IFN-alpha. |
| 533 | 11726219 | Both CD4(+) and CD8(+) T cell responses were observed after stimulation with DC exposed to the PSA/anti-PSA complexes, whereas CD4(+) predominated over CD8(+) T cell responses after stimulation with PSA-armed DC or PSA-m. |
| 534 | 11726219 | These CD8(+) T cells responded when rechallenged with DC pulsed with HLA allele-restricted PSA peptides. |
| 535 | 11728234 | Preliminary data have discussed the ex vivo and in vivo generation of cytotoxic effector cells employing IL-2 and/or IFN-alpha/gamma in the auto-PBSCT setting. |
| 536 | 11728234 | Other cytokines such as IL-12, IL-15 and prolactin have likewise been considered. |
| 537 | 11772233 | Features of the pathophysiology of von Hippel Lindau protein are described, with attention to potential novel therapies targeting HIF-1alpha, VEGF, TGF-beta1 and TGF-alpha pathways. |
| 538 | 11772233 | Most basic are cytokine therapies incorporating new IL-2 and IFN-alpha schedules. |
| 539 | 11798457 | We review here recent work that led to the identification of genes for the avian homologs of interferon-alpha/beta (IFN-alpha/beta) and IFN-gamma, various interleukins (IL), and several chemokines. |
| 540 | 11836673 | Systems studied have included lysis by interleukin-2 (IL-2)-activated lymphokine-activated killer (LAK) cells, tumor necrosis factor-alpha (TNF-alpha), a p16-expressing adenovirus vector, suicide gene therapy using the herpes simplex virus-tyrosine kinase (HSV-tk) followed by ganciclovir, and immunomodulatory gene therapy with IL-2, IL-4, interferon-gamma (IFN-gamma), IFN-alpha, TNF-alpha, granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-6, and IL-1beta transfected into tumors. |
| 541 | 11836673 | Since platelet-derived growth factor (PDGF) is thought to be an autocrine growth factor for mesothelioma STI-571 (Gleevec; Novartis, Basel, Switzerland), a highly selective inhibitor of the PDGF receptor tyrosine kinase, is being tested in a phase II trial. |
| 542 | 11867164 | We have examined T cell responses against recombinant analogues of the surface-exposed C. ruminantium major antigen 1 (MAP1) a 28.8 kDa protein and MAP2 (21 kDa) antigen in cattle immunised by infection and treatment. |
| 543 | 11867164 | MAP1-specific responses were predominantly restricted to cluster of differentiation four antigen positive T cells (CD4+ T cells). |
| 544 | 11867164 | Reverse transcription polymerase chain reaction (RT-PCR) analysis of cytokine expression by T cell lines derived from this population revealed strong expression of interferon gamma (IFN-gamma), interferon alpha (IFN-alpha), tumour necrosis factor alpha (TNF-alpha), tumour necrosis factor beta (TNF-beta), interleukin-2 receptor alpha (IL-2Ralpha) transcripts, and weak expression of IL-2 and IL-4. |
| 545 | 11867164 | CD4+ T cell clones specific for MAP1 were generated. |
| 546 | 11867164 | RT-PCR analysis of cytokine expression by T cell lines which were dominated by gammadelta T cells revealed expression of IFN-gamma, TNF-alpha, TNF-beta, IL-2Ralpha transcripts. |
| 547 | 11867164 | Our findings indicate that immunisation of cattle by infection with C. ruminantium results in generation of MAP1- and MAP2-specific T cell responses that may play a role in protection against the pathogen. |
| 548 | 11932394 | Bovine respiratory syncytial virus (BRSV) escapes from cellular responses to alpha/beta interferon (IFN-alpha/beta) by a concerted action of the two viral nonstructural proteins, NS1 and NS2. |
| 549 | 11945142 | In order to further improve the efficacy of treatment in chronic hepatitis C (HCV) many controlled clinical trials evaluating Amantadine, Micophenolate, alpha1 Thymosin, Maxamine (in combination with IFN or pegylated IFN), Protease, Helicase, Polymerase inhibitors, Ribozymes and anti-sense olygonucleotides, and Interleukin 10 are in progress. |
| 550 | 11964292 | Moreover, DCs either derived from bone marrow cells in vitro or isolated from the spleens of normal animals express IFN-alpha and IFN-beta, suggesting that type I IFNs can act in an autocrine manner to activate DCs. |
| 551 | 11964292 | Furthermore, the addition of neutralizing anti-IFN-alpha/beta antibody to purified splenic DCs in vitro partially blocked the "spontaneous" activation of these cells, inhibiting the up-regulation of costimulatory molecules, secretion of IFN-gamma, and T-cell stimulatory activity. |
| 552 | 11964292 | Moreover, DCs either derived from bone marrow cells in vitro or isolated from the spleens of normal animals express IFN-alpha and IFN-beta, suggesting that type I IFNs can act in an autocrine manner to activate DCs. |
| 553 | 11964292 | Furthermore, the addition of neutralizing anti-IFN-alpha/beta antibody to purified splenic DCs in vitro partially blocked the "spontaneous" activation of these cells, inhibiting the up-regulation of costimulatory molecules, secretion of IFN-gamma, and T-cell stimulatory activity. |
| 554 | 11994440 | IFN-alpha beta promote priming of antigen-specific CD8+ and CD4+ T lymphocytes by immunostimulatory DNA-based vaccines. |
| 555 | 11994440 | Immunostimulatory sequence (ISS) DNA containing unmethylated CpG dinucleotides stimulate NK and APC to secrete proinflammatory cytokines, including IFN-alphabeta and -gamma, TNF-alpha, and IL-6 and -12, and to express costimulatory surface molecules such as CD40, B7-1, and B7-2. |
| 556 | 11994440 | This investigation examines the mechanisms by which ISS DNA primes CD8(+) and CD4(+) lymphocyte activities. |
| 557 | 11994440 | Coordinated regulation of B7 costimulation and TAP-dependent cross-presentation results in priming of Ag-specific CD8(+) CTL, whereas CD40, B7, and IL-12 costimulation is required for priming of CD4(+) Th cells by ISS-based vaccines. |
| 558 | 12052340 | The cytokine inducing capacity of the vaccine vector pcDNA3, a methylated form of the plasmid, and pcDNA3 encoding porcine interleukin (IL)-6 or granulocyte/macrophage colony-stimulating factor (GM-CSF) was studied in pigs, using a model with tissue chambers implanted subcutaneously. |
| 559 | 12052340 | The production of interferon (IFN)-alpha, IFN-gamma, IL-6 and GM-CSF was studied at local (tissue chamber fluid (TCF)) and systemic (serum) levels during 3 days post-injection. |
| 560 | 12052340 | All forms of the plasmid, except the methylated, induced a transient local production of IFN-alpha but no plasmid-induced production of IFN-gamma, GM-CSF or IL-6 could be detected after injection of the plasmids. |
| 561 | 12052340 | The cytokine inducing capacity of the vaccine vector pcDNA3, a methylated form of the plasmid, and pcDNA3 encoding porcine interleukin (IL)-6 or granulocyte/macrophage colony-stimulating factor (GM-CSF) was studied in pigs, using a model with tissue chambers implanted subcutaneously. |
| 562 | 12052340 | The production of interferon (IFN)-alpha, IFN-gamma, IL-6 and GM-CSF was studied at local (tissue chamber fluid (TCF)) and systemic (serum) levels during 3 days post-injection. |
| 563 | 12052340 | All forms of the plasmid, except the methylated, induced a transient local production of IFN-alpha but no plasmid-induced production of IFN-gamma, GM-CSF or IL-6 could be detected after injection of the plasmids. |
| 564 | 12079487 | IL-12/IL-2 combination cytokine therapy for solid tumours: translation from bench to bedside. |
| 565 | 12079487 | Several cytokines have demonstrated unique activity in the preclinical setting, including IL-2 and IFN-alpha -inducing cytokines such as IL12 and IL18. |
| 566 | 12079487 | Several lines of evidence suggest that IL-12 and IL-2 provide complementary immunoregulatory signals and have now shown that in combination, these two cytokines mediate synergistic antitumour activity in preclinical tumour models. |
| 567 | 12079487 | This paper will review existing data regarding mechanisms of interaction between IL-2 and IL-12 in vitro and in preclinial models and describe future opportunities for the investigation of these potentially promising cytokines in the treatment of cancer. |
| 568 | 12184917 | This assay detected guinea pig IFN and human IFN-alpha, but not IFN-gamma from human, mouse, rat, pig, or dog. |
| 569 | 12228285 | Infection of mice with Dam(+) Salmonella resulted in the induction of host genes known to be indicators of IFN bioactivity and regulated by either IFN-alpha/beta (Mx1) or IFN-gamma (class II transactivator protein [CIITA] and inducible nitric oxide synthase [iNOS]) or by both IFN-alpha/beta and IFN-gamma (RNA-specific adenosine deaminase [ADAR1] and RNA-dependent protein kinase [PKR]) in a tissue-specific manner compared to uninfected animals. |
| 570 | 12228285 | Since the Mx1 promoter is IFN-alpha/beta specific and the Mx1 gene is not inducible directly by IFN-gamma, these data suggest a role of IFN-alpha/beta in the host response to Salmonella infection. |
| 571 | 12228285 | Finally, although no Dam(-) organisms were recovered from the liver or spleen after oral infection of mice, ADAR, PKR, Mx, and CIITA expression levels were elevated in these tissues relative to those in uninfected mice, suggestive of the distant action of a signaling molecule(s) in the activation of ISG expression. |
| 572 | 12228285 | Infection of mice with Dam(+) Salmonella resulted in the induction of host genes known to be indicators of IFN bioactivity and regulated by either IFN-alpha/beta (Mx1) or IFN-gamma (class II transactivator protein [CIITA] and inducible nitric oxide synthase [iNOS]) or by both IFN-alpha/beta and IFN-gamma (RNA-specific adenosine deaminase [ADAR1] and RNA-dependent protein kinase [PKR]) in a tissue-specific manner compared to uninfected animals. |
| 573 | 12228285 | Since the Mx1 promoter is IFN-alpha/beta specific and the Mx1 gene is not inducible directly by IFN-gamma, these data suggest a role of IFN-alpha/beta in the host response to Salmonella infection. |
| 574 | 12228285 | Finally, although no Dam(-) organisms were recovered from the liver or spleen after oral infection of mice, ADAR, PKR, Mx, and CIITA expression levels were elevated in these tissues relative to those in uninfected mice, suggestive of the distant action of a signaling molecule(s) in the activation of ISG expression. |
| 575 | 12356284 | Recombinant interferon (IFN)-alpha-2a, used as a model peptide drug, was efficiently entrapped within the alginate microcores using a high-speed stirrer and then microencapsulated into PELA copolymer using a water-in-oil-in-water solvent extraction method. |
| 576 | 12407510 | Various interleukin-2 (IL-2) dosing schedules and combinations with interferon alpha (IFN-alpha) have been tested in patients with advanced melanoma during the past decade. |
| 577 | 12407510 | The response rates reported with IL-2 as a single agent or in combination with IFN-alpha varies from 10% to 41%, with a small, but remarkable proportion of durable responses. |
| 578 | 12407510 | Subsequently, biochemotherapy regimens combining IL-2, IFN-alpha, and chemotherapy have been evaluated in phase II trials, which have suggested improved response rates. |
| 579 | 12407510 | Various interleukin-2 (IL-2) dosing schedules and combinations with interferon alpha (IFN-alpha) have been tested in patients with advanced melanoma during the past decade. |
| 580 | 12407510 | The response rates reported with IL-2 as a single agent or in combination with IFN-alpha varies from 10% to 41%, with a small, but remarkable proportion of durable responses. |
| 581 | 12407510 | Subsequently, biochemotherapy regimens combining IL-2, IFN-alpha, and chemotherapy have been evaluated in phase II trials, which have suggested improved response rates. |
| 582 | 12407510 | Various interleukin-2 (IL-2) dosing schedules and combinations with interferon alpha (IFN-alpha) have been tested in patients with advanced melanoma during the past decade. |
| 583 | 12407510 | The response rates reported with IL-2 as a single agent or in combination with IFN-alpha varies from 10% to 41%, with a small, but remarkable proportion of durable responses. |
| 584 | 12407510 | Subsequently, biochemotherapy regimens combining IL-2, IFN-alpha, and chemotherapy have been evaluated in phase II trials, which have suggested improved response rates. |
| 585 | 12464152 | Imiquimod and its homologues act by activating macrophages and other cells via binding to cell surface receptors, such as Toll receptor 7, thereby inducing secretion of pro-inflammatory cytokines, predominantly interferon (IFN)-alpha, tumour necrosis factor (TNF)-alpha and interleukin (IL)-12. |
| 586 | 12502879 | In the present study, we constructed recombinant, replication-defective human adenovirus type 5 vectors containing either porcine IFN-alpha or IFN-beta (Ad5-pIFNalpha or Ad5-pIFNbeta). |
| 587 | 12502879 | Swine inoculated with 10(9) PFU of a control Ad5 virus lacking the IFN gene and challenged 24 h later with FMDV developed typical signs of foot-and-mouth disease (FMD), including fever, vesicular lesions, and viremia. |
| 588 | 12502879 | In the present study, we constructed recombinant, replication-defective human adenovirus type 5 vectors containing either porcine IFN-alpha or IFN-beta (Ad5-pIFNalpha or Ad5-pIFNbeta). |
| 589 | 12502879 | Swine inoculated with 10(9) PFU of a control Ad5 virus lacking the IFN gene and challenged 24 h later with FMDV developed typical signs of foot-and-mouth disease (FMD), including fever, vesicular lesions, and viremia. |
| 590 | 12507600 | However, cancer treatment by recombinant IL-2 or IFN-alpha still represents today the best therapeutic way for the treatment of renal carcinoma, melanoma and in some cases lymphoma. |
| 591 | 12513929 | Interferon-alpha (IFN-alpha), tumor necrosis factor (TNF-alpha), interleukin-1 (IL-1), and -6 (IL-6) were determined by bioassay, and IL-8 by a commercial ELISA. |
| 592 | 12513929 | Mean levels of IFN-alpha, TNF-alpha, and IL-6, but not IL-1 or IL-8, were lower than in both other groups. |
| 593 | 12513929 | Virus titers in the lungs of individual pigs showed highly significant correlations with IFN-alpha and IL-6, and lower correlations with TNF-alpha and IL-8. |
| 594 | 12513929 | Clinical signs were most closely associated with IFN-alpha, IL-6, and TNF-alpha. |
| 595 | 12513929 | The relationship between disease and IL-8 or IL-1 was much weaker. |
| 596 | 12513929 | Our data provide further evidence for a role of IFN-alpha, TNF-alpha, and IL-6 in the pathogenesis of SIV. |
| 597 | 12513929 | Interferon-alpha (IFN-alpha), tumor necrosis factor (TNF-alpha), interleukin-1 (IL-1), and -6 (IL-6) were determined by bioassay, and IL-8 by a commercial ELISA. |
| 598 | 12513929 | Mean levels of IFN-alpha, TNF-alpha, and IL-6, but not IL-1 or IL-8, were lower than in both other groups. |
| 599 | 12513929 | Virus titers in the lungs of individual pigs showed highly significant correlations with IFN-alpha and IL-6, and lower correlations with TNF-alpha and IL-8. |
| 600 | 12513929 | Clinical signs were most closely associated with IFN-alpha, IL-6, and TNF-alpha. |
| 601 | 12513929 | The relationship between disease and IL-8 or IL-1 was much weaker. |
| 602 | 12513929 | Our data provide further evidence for a role of IFN-alpha, TNF-alpha, and IL-6 in the pathogenesis of SIV. |
| 603 | 12513929 | Interferon-alpha (IFN-alpha), tumor necrosis factor (TNF-alpha), interleukin-1 (IL-1), and -6 (IL-6) were determined by bioassay, and IL-8 by a commercial ELISA. |
| 604 | 12513929 | Mean levels of IFN-alpha, TNF-alpha, and IL-6, but not IL-1 or IL-8, were lower than in both other groups. |
| 605 | 12513929 | Virus titers in the lungs of individual pigs showed highly significant correlations with IFN-alpha and IL-6, and lower correlations with TNF-alpha and IL-8. |
| 606 | 12513929 | Clinical signs were most closely associated with IFN-alpha, IL-6, and TNF-alpha. |
| 607 | 12513929 | The relationship between disease and IL-8 or IL-1 was much weaker. |
| 608 | 12513929 | Our data provide further evidence for a role of IFN-alpha, TNF-alpha, and IL-6 in the pathogenesis of SIV. |
| 609 | 12513929 | Interferon-alpha (IFN-alpha), tumor necrosis factor (TNF-alpha), interleukin-1 (IL-1), and -6 (IL-6) were determined by bioassay, and IL-8 by a commercial ELISA. |
| 610 | 12513929 | Mean levels of IFN-alpha, TNF-alpha, and IL-6, but not IL-1 or IL-8, were lower than in both other groups. |
| 611 | 12513929 | Virus titers in the lungs of individual pigs showed highly significant correlations with IFN-alpha and IL-6, and lower correlations with TNF-alpha and IL-8. |
| 612 | 12513929 | Clinical signs were most closely associated with IFN-alpha, IL-6, and TNF-alpha. |
| 613 | 12513929 | The relationship between disease and IL-8 or IL-1 was much weaker. |
| 614 | 12513929 | Our data provide further evidence for a role of IFN-alpha, TNF-alpha, and IL-6 in the pathogenesis of SIV. |
| 615 | 12513929 | Interferon-alpha (IFN-alpha), tumor necrosis factor (TNF-alpha), interleukin-1 (IL-1), and -6 (IL-6) were determined by bioassay, and IL-8 by a commercial ELISA. |
| 616 | 12513929 | Mean levels of IFN-alpha, TNF-alpha, and IL-6, but not IL-1 or IL-8, were lower than in both other groups. |
| 617 | 12513929 | Virus titers in the lungs of individual pigs showed highly significant correlations with IFN-alpha and IL-6, and lower correlations with TNF-alpha and IL-8. |
| 618 | 12513929 | Clinical signs were most closely associated with IFN-alpha, IL-6, and TNF-alpha. |
| 619 | 12513929 | The relationship between disease and IL-8 or IL-1 was much weaker. |
| 620 | 12513929 | Our data provide further evidence for a role of IFN-alpha, TNF-alpha, and IL-6 in the pathogenesis of SIV. |
| 621 | 12519390 | The addition of TNF-alpha, polyriboinosinic polyribocytidylic acid (Poly(I:C)) and LPS to autologous DCs resulted in the emergence of only a small percentage of CD83+ DCs, IFN-alpha having no demonstrable effect. |
| 622 | 12519390 | Only the addition of Poly(I:C) to DCs resulted in modestly increased specific cytotoxicity to B-CLL targets, IFN-alpha and LPS having no effect. |
| 623 | 12519390 | The addition of TNF-alpha, polyriboinosinic polyribocytidylic acid (Poly(I:C)) and LPS to autologous DCs resulted in the emergence of only a small percentage of CD83+ DCs, IFN-alpha having no demonstrable effect. |
| 624 | 12519390 | Only the addition of Poly(I:C) to DCs resulted in modestly increased specific cytotoxicity to B-CLL targets, IFN-alpha and LPS having no effect. |
| 625 | 12594246 | In this study, we show that human plasmacytoid DC, activated by either CpG oligodeoxynucleotides or viral infection, also respond to histamine through H2 receptors, leading to a marked down-regulation of IFN-alpha and TNF-alpha and a moderate switch in their capacity to polarize naive T cells. |
| 626 | 12665415 | Within the immune model of therapy, progress in the application of immune-related drugs including older cytokines (IL-2, IFN-alpha) and of newer cytokine-variant and other cytokines are discussed. |
| 627 | 12668155 | Functional abolishment of any one of these cytokines (IL-2, IL-6, IL-12, IL-18, GMCSF, TNF-alpha, or IFN-alpha, except IL-10) by neutralizing antibodies leads to reduced IFN-gamma production (19-82% inhibition in mouse and 44-77% inhibition in human systems, respectively). |
| 628 | 12668155 | In mice cytokines IL-2, IL-12, IL-18, and GMCSF are observed to synergize with BCG for IFN-gamma production, whereas in human cytokines IL-2, IL-12, TNF-alpha, and IFN-alpha exhibit similar synergistic effects. |
| 629 | 12668155 | Rational combinations of these Th1-stimulating cytokines (IL-12 plus IL-18 in mice and IL-2 plus IL-12 in humans, respectively) dramatically up-regulate IFN-gamma production that is incomparably superior to BCG for induction of this cytokine. |
| 630 | 12668155 | Functional abolishment of any one of these cytokines (IL-2, IL-6, IL-12, IL-18, GMCSF, TNF-alpha, or IFN-alpha, except IL-10) by neutralizing antibodies leads to reduced IFN-gamma production (19-82% inhibition in mouse and 44-77% inhibition in human systems, respectively). |
| 631 | 12668155 | In mice cytokines IL-2, IL-12, IL-18, and GMCSF are observed to synergize with BCG for IFN-gamma production, whereas in human cytokines IL-2, IL-12, TNF-alpha, and IFN-alpha exhibit similar synergistic effects. |
| 632 | 12668155 | Rational combinations of these Th1-stimulating cytokines (IL-12 plus IL-18 in mice and IL-2 plus IL-12 in humans, respectively) dramatically up-regulate IFN-gamma production that is incomparably superior to BCG for induction of this cytokine. |
| 633 | 12687252 | It has been demonstrated that amixin and poludan, the drugs made in our country, cause an increase of the serum IFN level, enhance the ability of leukocytes and lymphocytes to produce IFN-alpha and IFN-gamma, and lead to the activation of NK and peripheral blood phagocytes. |
| 634 | 12687252 | The number of CD3(+), CD4(+), CD8(+), CD19(+) cells, the level of the Ig A, IgG, IgM and several other parameters of the immune system were not affected by these drugs. |
| 635 | 12688838 | The two most widely investigated immunotherapy drugs for melanoma are interferon (IFN)-alpha and interleukin-2 (IL-2). |
| 636 | 12688838 | Vaccines are also being tested in patients with metastatic melanoma to determine their immune effects and to define their activity in combination with other immunotherapeutic agents such as IL-2 or IFNalpha. |
| 637 | 12716489 | To study whether altered and reduced functional capacities of type I and type II IFNs would affect rotavirus-induced diarrhea and viral replication, we obtained signal transducers and activators of transcription 1 (Stat1) knock-out mice (Stat1(-/-)) that lack many IFN-induced responses. |
| 638 | 12716489 | Thus, modulating IFN function through the loss of Stat1 caused a defective innate immune response in adult mice but had no effect on rotavirus-induced diarrhea and replication in suckling mice. |
| 639 | 12716489 | Furthermore, adult Stat1(-/-), IFN-gamma, and IFN-alpha/beta receptor(-/-) (IFNAR-2(-/-)) mice infected with rotavirus or vaccinated with VP6 vaccine and adjuvant were fully protected against rotavirus shedding following a subsequent challenge with rotavirus. |
| 640 | 12857909 | Moreover, we detected high levels of active chicken alpha/beta IFN (IFN-alpha/beta) in supernatants of MVA-DeltaE3L-infected CEF, while moderate IFN quantities were found after MVA or MVA-E3rev infection and no IFN activity was present upon infection with wild-type vaccinia viruses. |
| 641 | 12857909 | Interestingly, pretreatment of CEF with similar amounts of recombinant chicken IFN-alpha inhibited growth of vaccinia viruses, including MVA. |
| 642 | 12857909 | Moreover, we detected high levels of active chicken alpha/beta IFN (IFN-alpha/beta) in supernatants of MVA-DeltaE3L-infected CEF, while moderate IFN quantities were found after MVA or MVA-E3rev infection and no IFN activity was present upon infection with wild-type vaccinia viruses. |
| 643 | 12857909 | Interestingly, pretreatment of CEF with similar amounts of recombinant chicken IFN-alpha inhibited growth of vaccinia viruses, including MVA. |
| 644 | 12860162 | IL-2 is itself a useful component of combination immunotherapy, such as with melanoma peptide vaccines, or with interferon-alfa-2b, (IFN-a), as a dual combination or part of a biochemotherapy regimen. |
| 645 | 12874261 | CD11c+CD8+B220- cells were the most potent producers of interleukin (IL)-12 p70 and interferon (IFN)-gamma, while plasmacytoid DCs were the only subset capable of secreting IFN-alpha. |
| 646 | 12874266 | Immunization of hu-PBL-SCID mice with DCs generated after exposure of monocytes to GM-CSF/IFN-alpha (IFN-DCs) and pulsed with inactivated HIV-1 resulted in a marked induction of human anti-HIV-1 antibodies, which was associated with the detection of anti-HIV neutralizing activity in the serum. |
| 647 | 12874266 | This vaccination schedule also promoted the generation of a human CD8+ T cell response against HIV-1, as measured by IFN-gamma Elispot analysis. |
| 648 | 12885891 | Neutralizing antibodies against human RANTES, MIP-1alpha, MIP-1beta, alpha interferon (IFN-alpha), IFN-beta, IFN-gamma, interleukin-4 (IL-4), IL-10, IL-13, IL-16, MCP-1, MCP-3, tumor necrosis factor alpha (TNF-alpha), or TNF-beta failed to reverse the HIV-1-suppressive activity. |
| 649 | 12910808 | In the following years, the research on evaluation of the efficacy of the recombinant interferons or interferons made with genetics engineering (IFN alpha 2a, IFN alpha 2b and IFN Consensus) has given results comparable with the results obtained with IFN alpha. |
| 650 | 12942200 | IL-2 is itself a useful component of combination immunotherapy, such as with melanoma peptide vaccines, or with interferon alpha-2b, (IFN-alpha), as a dual combination or part of a biochemotherapy regimen. |
| 651 | 12942200 | Combinations of 5-fluorouracil (5-FU) and IFN-alpha or levamisole have had efficacy in colon and head and neck cancers, but here the biological agents have been biochemical modulators, not immunotherapy. |
| 652 | 12942200 | IL-2 is itself a useful component of combination immunotherapy, such as with melanoma peptide vaccines, or with interferon alpha-2b, (IFN-alpha), as a dual combination or part of a biochemotherapy regimen. |
| 653 | 12942200 | Combinations of 5-fluorouracil (5-FU) and IFN-alpha or levamisole have had efficacy in colon and head and neck cancers, but here the biological agents have been biochemical modulators, not immunotherapy. |
| 654 | 12943498 | Biological therapies with IFN-alpha and IL-2 have demonstrated a real but minimal effect. |
| 655 | 12959322 | During the course of HIV-1 infection secretion of T-helper type 1 (Th1) cytokines, such as interleukin (IL)-2, and antiviral interferon (IFN)-gamma, is generally decreased, whereas production of T helper type 2 (Th2) cytokines, IL-4, IL-10, proinflammatory cytokines (IL-1, IL-6, IL-8) and tumour necrosis factor (TNF)-alpha, is increased. |
| 656 | 12959322 | HIV-inductive cytokines include: TNF-alpha, TNF-beta, IL-1 and IL-6, which stimulate HIV-1 replication in T cells and monocyte-derived macrophages (MDM), IL-2, IL-7 and IL-15, which upregulate HIV-1 in T cells, and macrophage-colony stimulating factor, which stimulates HIV-1 in MDM. |
| 657 | 12959322 | HIV-suppressive cytokines include: IFN-alpha, IFN-beta and IL-16, which inhibit HIV-1 replication in T cells and MDM, and IL-10 and IL-13, which inhibit HIV-1 in MDM. |
| 658 | 12959322 | Bifunctional cytokines such as IFN-gamma, IL-4 and granulocyte-macrophage colony-stimulating factor have been shown to have both inhibitory and stimulatory effects on HIV-1. |
| 659 | 12959322 | The beta-chemokines, macrophage-inflammatory protein (MIP)-1alpha, MIP-1beta and RANTES are important inhibitors of macrophage-tropic strains of HIV-1, whereas the alpha-chemokine stromal-derived factor-1 suppresses infection of T-tropic strains of HIV-1. |
| 660 | 14502286 | Activation of cross-priming by IFN-alpha/beta was independent of CD4+ T cell help or interaction of CD40 and CD40 ligand, and involved direct stimulation of dendritic cells. |
| 661 | 14511462 | We have demonstrated previously that swine inoculated with replication-defective human adenovirus type 5 (Ad5) vector expressing porcine IFN-alpha (Ad5-PoIFN-alpha) were completely protected from FMD virus (FMDV) challenge. |
| 662 | 14511462 | To extend this approach to bovines, we constructed Ad5 vectors that express bovine IFN-alpha or IFN-beta (Ad5-BoIFN-alpha and Ad5-BoIFN-beta). |
| 663 | 14511462 | We have demonstrated previously that swine inoculated with replication-defective human adenovirus type 5 (Ad5) vector expressing porcine IFN-alpha (Ad5-PoIFN-alpha) were completely protected from FMD virus (FMDV) challenge. |
| 664 | 14511462 | To extend this approach to bovines, we constructed Ad5 vectors that express bovine IFN-alpha or IFN-beta (Ad5-BoIFN-alpha and Ad5-BoIFN-beta). |
| 665 | 14530357 | PDCs, which express TLR7 and TLR9, responded to imidazoquinolines (imiquimod and R-848) and to CpG oligodeoxynucleotides stimulation, resulting in enhancement in expression of costimulatory molecules and induction of IFN-alpha and IL-12p70. |
| 666 | 14530357 | In contrast, MDCs, which express TLR3, TLR4, and TLR7, responded to poly(I:C), LPS, and imidazoquinolines with phenotypic maturation and high production of IL-12 p70 without producing detectable IFN-alpha. |
| 667 | 14530357 | Optimally TLR ligand-stimulated PDCs or MDCs exposed to CMV or HIV-1 Ags enhanced autologous CMV- and HIV-1-specific memory T cell responses as measured by effector cytokine production compared with TLR ligand-activated monocytes and B cells or unstimulated PDCs and MDCs. |
| 668 | 14530357 | PDCs, which express TLR7 and TLR9, responded to imidazoquinolines (imiquimod and R-848) and to CpG oligodeoxynucleotides stimulation, resulting in enhancement in expression of costimulatory molecules and induction of IFN-alpha and IL-12p70. |
| 669 | 14530357 | In contrast, MDCs, which express TLR3, TLR4, and TLR7, responded to poly(I:C), LPS, and imidazoquinolines with phenotypic maturation and high production of IL-12 p70 without producing detectable IFN-alpha. |
| 670 | 14530357 | Optimally TLR ligand-stimulated PDCs or MDCs exposed to CMV or HIV-1 Ags enhanced autologous CMV- and HIV-1-specific memory T cell responses as measured by effector cytokine production compared with TLR ligand-activated monocytes and B cells or unstimulated PDCs and MDCs. |
| 671 | 14575692 | Although dsRNA is a virus-specific signature and a ligand for human Toll-like receptor 3 (TLR3), largely uncharacterized multiple pathways associate virus-mediated IFN-beta induction. |
| 672 | 14575692 | The kinetics experiments with the laboratory MV strain revealed that TLR3 was induced late compared to IFN-beta and required new protein synthesis. |
| 673 | 14575692 | Furthermore, neutralizing antibodies against IFN-beta or IFNAR (Interferon-alpha/beta receptor) suppressed MV-induced TLR3 induction, indicating that type I IFN, IFN-alpha/beta, is critical for MV-mediated TLR3 induction. |
| 674 | 14575692 | Yet, a recently identified virus-inducible IFN, the IFN-lambda, did not contribute to TLR3 expression. |
| 675 | 14575692 | The ISRE, a recently reported site for IFN-beta induction, but not STAT binding site, located around -30bp of TLR3 promoter responded to MV to induce TLR3 expression. |
| 676 | 14575692 | This further indicates the importance of type I IFN for TLR3 up-regulation in the case of viral infection. |
| 677 | 14575692 | In HeLa and MRC5 cells, augmented production of IFN-beta was observed in response to dsRNA when TLR3 had been induced beforehand. |
| 678 | 14575692 | Thus, the MV-induced expression of TLR3 may reflect amplified IFN production that plays a part in host defense to viral infection. |
| 679 | 14575692 | Although dsRNA is a virus-specific signature and a ligand for human Toll-like receptor 3 (TLR3), largely uncharacterized multiple pathways associate virus-mediated IFN-beta induction. |
| 680 | 14575692 | The kinetics experiments with the laboratory MV strain revealed that TLR3 was induced late compared to IFN-beta and required new protein synthesis. |
| 681 | 14575692 | Furthermore, neutralizing antibodies against IFN-beta or IFNAR (Interferon-alpha/beta receptor) suppressed MV-induced TLR3 induction, indicating that type I IFN, IFN-alpha/beta, is critical for MV-mediated TLR3 induction. |
| 682 | 14575692 | Yet, a recently identified virus-inducible IFN, the IFN-lambda, did not contribute to TLR3 expression. |
| 683 | 14575692 | The ISRE, a recently reported site for IFN-beta induction, but not STAT binding site, located around -30bp of TLR3 promoter responded to MV to induce TLR3 expression. |
| 684 | 14575692 | This further indicates the importance of type I IFN for TLR3 up-regulation in the case of viral infection. |
| 685 | 14575692 | In HeLa and MRC5 cells, augmented production of IFN-beta was observed in response to dsRNA when TLR3 had been induced beforehand. |
| 686 | 14575692 | Thus, the MV-induced expression of TLR3 may reflect amplified IFN production that plays a part in host defense to viral infection. |
| 687 | 14575692 | Although dsRNA is a virus-specific signature and a ligand for human Toll-like receptor 3 (TLR3), largely uncharacterized multiple pathways associate virus-mediated IFN-beta induction. |
| 688 | 14575692 | The kinetics experiments with the laboratory MV strain revealed that TLR3 was induced late compared to IFN-beta and required new protein synthesis. |
| 689 | 14575692 | Furthermore, neutralizing antibodies against IFN-beta or IFNAR (Interferon-alpha/beta receptor) suppressed MV-induced TLR3 induction, indicating that type I IFN, IFN-alpha/beta, is critical for MV-mediated TLR3 induction. |
| 690 | 14575692 | Yet, a recently identified virus-inducible IFN, the IFN-lambda, did not contribute to TLR3 expression. |
| 691 | 14575692 | The ISRE, a recently reported site for IFN-beta induction, but not STAT binding site, located around -30bp of TLR3 promoter responded to MV to induce TLR3 expression. |
| 692 | 14575692 | This further indicates the importance of type I IFN for TLR3 up-regulation in the case of viral infection. |
| 693 | 14575692 | In HeLa and MRC5 cells, augmented production of IFN-beta was observed in response to dsRNA when TLR3 had been induced beforehand. |
| 694 | 14575692 | Thus, the MV-induced expression of TLR3 may reflect amplified IFN production that plays a part in host defense to viral infection. |
| 695 | 14575692 | Although dsRNA is a virus-specific signature and a ligand for human Toll-like receptor 3 (TLR3), largely uncharacterized multiple pathways associate virus-mediated IFN-beta induction. |
| 696 | 14575692 | The kinetics experiments with the laboratory MV strain revealed that TLR3 was induced late compared to IFN-beta and required new protein synthesis. |
| 697 | 14575692 | Furthermore, neutralizing antibodies against IFN-beta or IFNAR (Interferon-alpha/beta receptor) suppressed MV-induced TLR3 induction, indicating that type I IFN, IFN-alpha/beta, is critical for MV-mediated TLR3 induction. |
| 698 | 14575692 | Yet, a recently identified virus-inducible IFN, the IFN-lambda, did not contribute to TLR3 expression. |
| 699 | 14575692 | The ISRE, a recently reported site for IFN-beta induction, but not STAT binding site, located around -30bp of TLR3 promoter responded to MV to induce TLR3 expression. |
| 700 | 14575692 | This further indicates the importance of type I IFN for TLR3 up-regulation in the case of viral infection. |
| 701 | 14575692 | In HeLa and MRC5 cells, augmented production of IFN-beta was observed in response to dsRNA when TLR3 had been induced beforehand. |
| 702 | 14575692 | Thus, the MV-induced expression of TLR3 may reflect amplified IFN production that plays a part in host defense to viral infection. |
| 703 | 14632664 | RNA samples from stimulated and unstimulated chicken thymocytes were assayed for messenger RNA encoding the cytokines interleukin-1beta (IL-1beta), IL-2, interferon-alpha (IFN-alpha), IFN-beta, IFN-gamma and transforming growth factor-beta4 (TGF-beta4), and also components of the major histocompatibility complex (MHC), beta2-microglobulin (beta2M) and the MHC class I alpha-chain (MHC IA). |
| 704 | 14632664 | Mitogen stimulation of embryonic day 18 and day 1 post-hatch thymocytes induced up-regulation of IFN-gamma, IL-1beta and TGF-beta transcripts, and down-regulation of IFN-alpha, IFN-beta and IL-2 transcripts, with a higher induction of IFN-gamma, IL-1beta and TGF-beta transcripts in more immature T-cell-receptor-negative (TCR-) than TCR+ (TCR1+, TCR2+, or TCR3+) subsets. |
| 705 | 14632664 | Thymocytes from embryonic day 14 chicks responded to mitogen with a short burst of unsustained proliferation, and transcriptional down-regulation of the cytokines IL-2, IL-1beta, IFN-alpha, IFN-beta and IFN-gamma. |
| 706 | 14632664 | Transcripts encoding TGF-beta and type I interferons (IFN-alpha and IFN-beta) were constitutively expressed at high levels in very early thymocytes at embryonic day 14. |
| 707 | 14632664 | RNA samples from stimulated and unstimulated chicken thymocytes were assayed for messenger RNA encoding the cytokines interleukin-1beta (IL-1beta), IL-2, interferon-alpha (IFN-alpha), IFN-beta, IFN-gamma and transforming growth factor-beta4 (TGF-beta4), and also components of the major histocompatibility complex (MHC), beta2-microglobulin (beta2M) and the MHC class I alpha-chain (MHC IA). |
| 708 | 14632664 | Mitogen stimulation of embryonic day 18 and day 1 post-hatch thymocytes induced up-regulation of IFN-gamma, IL-1beta and TGF-beta transcripts, and down-regulation of IFN-alpha, IFN-beta and IL-2 transcripts, with a higher induction of IFN-gamma, IL-1beta and TGF-beta transcripts in more immature T-cell-receptor-negative (TCR-) than TCR+ (TCR1+, TCR2+, or TCR3+) subsets. |
| 709 | 14632664 | Thymocytes from embryonic day 14 chicks responded to mitogen with a short burst of unsustained proliferation, and transcriptional down-regulation of the cytokines IL-2, IL-1beta, IFN-alpha, IFN-beta and IFN-gamma. |
| 710 | 14632664 | Transcripts encoding TGF-beta and type I interferons (IFN-alpha and IFN-beta) were constitutively expressed at high levels in very early thymocytes at embryonic day 14. |
| 711 | 14632664 | RNA samples from stimulated and unstimulated chicken thymocytes were assayed for messenger RNA encoding the cytokines interleukin-1beta (IL-1beta), IL-2, interferon-alpha (IFN-alpha), IFN-beta, IFN-gamma and transforming growth factor-beta4 (TGF-beta4), and also components of the major histocompatibility complex (MHC), beta2-microglobulin (beta2M) and the MHC class I alpha-chain (MHC IA). |
| 712 | 14632664 | Mitogen stimulation of embryonic day 18 and day 1 post-hatch thymocytes induced up-regulation of IFN-gamma, IL-1beta and TGF-beta transcripts, and down-regulation of IFN-alpha, IFN-beta and IL-2 transcripts, with a higher induction of IFN-gamma, IL-1beta and TGF-beta transcripts in more immature T-cell-receptor-negative (TCR-) than TCR+ (TCR1+, TCR2+, or TCR3+) subsets. |
| 713 | 14632664 | Thymocytes from embryonic day 14 chicks responded to mitogen with a short burst of unsustained proliferation, and transcriptional down-regulation of the cytokines IL-2, IL-1beta, IFN-alpha, IFN-beta and IFN-gamma. |
| 714 | 14632664 | Transcripts encoding TGF-beta and type I interferons (IFN-alpha and IFN-beta) were constitutively expressed at high levels in very early thymocytes at embryonic day 14. |
| 715 | 14632664 | RNA samples from stimulated and unstimulated chicken thymocytes were assayed for messenger RNA encoding the cytokines interleukin-1beta (IL-1beta), IL-2, interferon-alpha (IFN-alpha), IFN-beta, IFN-gamma and transforming growth factor-beta4 (TGF-beta4), and also components of the major histocompatibility complex (MHC), beta2-microglobulin (beta2M) and the MHC class I alpha-chain (MHC IA). |
| 716 | 14632664 | Mitogen stimulation of embryonic day 18 and day 1 post-hatch thymocytes induced up-regulation of IFN-gamma, IL-1beta and TGF-beta transcripts, and down-regulation of IFN-alpha, IFN-beta and IL-2 transcripts, with a higher induction of IFN-gamma, IL-1beta and TGF-beta transcripts in more immature T-cell-receptor-negative (TCR-) than TCR+ (TCR1+, TCR2+, or TCR3+) subsets. |
| 717 | 14632664 | Thymocytes from embryonic day 14 chicks responded to mitogen with a short burst of unsustained proliferation, and transcriptional down-regulation of the cytokines IL-2, IL-1beta, IFN-alpha, IFN-beta and IFN-gamma. |
| 718 | 14632664 | Transcripts encoding TGF-beta and type I interferons (IFN-alpha and IFN-beta) were constitutively expressed at high levels in very early thymocytes at embryonic day 14. |
| 719 | 14732882 | Various interleukin 2 (IL-2) dosing schedules and combinations with interferon alpha (IFN-alpha) have been tested in patients with advanced melanoma in phase I and II studies. |
| 720 | 14732882 | The response rate reported with cytokines alone (IL-2 as a single agent or in combination with IFN-alpha) varies from 10-41%. |
| 721 | 14732882 | Subsequently, biochemotherapy regimens combining IL-2, IFN-alpha and chemotherapy have been evaluated in phase II trials suggesting improved response rates. |
| 722 | 14732882 | Various interleukin 2 (IL-2) dosing schedules and combinations with interferon alpha (IFN-alpha) have been tested in patients with advanced melanoma in phase I and II studies. |
| 723 | 14732882 | The response rate reported with cytokines alone (IL-2 as a single agent or in combination with IFN-alpha) varies from 10-41%. |
| 724 | 14732882 | Subsequently, biochemotherapy regimens combining IL-2, IFN-alpha and chemotherapy have been evaluated in phase II trials suggesting improved response rates. |
| 725 | 14732882 | Various interleukin 2 (IL-2) dosing schedules and combinations with interferon alpha (IFN-alpha) have been tested in patients with advanced melanoma in phase I and II studies. |
| 726 | 14732882 | The response rate reported with cytokines alone (IL-2 as a single agent or in combination with IFN-alpha) varies from 10-41%. |
| 727 | 14732882 | Subsequently, biochemotherapy regimens combining IL-2, IFN-alpha and chemotherapy have been evaluated in phase II trials suggesting improved response rates. |
| 728 | 15000839 | The secretion of interferon (IFN)-alpha and IFN-gamma and non-major histocompatability complex (MHC)-restricted cytotoxic activity were assayed with CpG-ODN-stimulated peripheral blood mononuclear cells (PBMC). |
| 729 | 15000839 | As expected, ODN 2216 was a potent inducer of IFN-alpha secretion by both bovine and ovine PBMC, but ODN 2007 also induced dose-dependent, CpG-specific IFN-alpha secretion by ovine PBMC. |
| 730 | 15000839 | The secretion of interferon (IFN)-alpha and IFN-gamma and non-major histocompatability complex (MHC)-restricted cytotoxic activity were assayed with CpG-ODN-stimulated peripheral blood mononuclear cells (PBMC). |
| 731 | 15000839 | As expected, ODN 2216 was a potent inducer of IFN-alpha secretion by both bovine and ovine PBMC, but ODN 2007 also induced dose-dependent, CpG-specific IFN-alpha secretion by ovine PBMC. |
| 732 | 15039522 | Host-dependent type 1 cytokine responses driven by inactivated viruses may fail to default in the absence of IL-12 or IFN-alpha/beta. |
| 733 | 15039522 | Strikingly, immunizations in gene-disrupted mice showed that a functional IFN-alpha/beta, IFN-gamma or interleukin (IL)-12 pathway was not required for the generation of a polarized Th1 type immune response initiated by inactivated virus particles. |
| 734 | 15039522 | Host-dependent type 1 cytokine responses driven by inactivated viruses may fail to default in the absence of IL-12 or IFN-alpha/beta. |
| 735 | 15039522 | Strikingly, immunizations in gene-disrupted mice showed that a functional IFN-alpha/beta, IFN-gamma or interleukin (IL)-12 pathway was not required for the generation of a polarized Th1 type immune response initiated by inactivated virus particles. |
| 736 | 15051512 | Elevated serum 2'5'-A synthetase activity suggested that CpG ODN acted through the induction of either interferon (IFN)-alpha or IFN-gamma. |
| 737 | 15051512 | ODN 2007 did not induce detectable levels of IFN-alpha or IFN-gamma when incubated with peripheral blood mononuclear cells, but both IFN-alpha and IFN-gamma were detected following stimulation of lymph node cells with ODN 2007. |
| 738 | 15051512 | CpG ODN induction of 2'5'-A synthetase in vitro correlated with the secretion of both IFN-alpha and IFN-gamma. |
| 739 | 15051512 | Many of the cells recruited to the site of ODN 2007 injection expressed IFN-alpha and some IFN-gamma. |
| 740 | 15051512 | Elevated serum 2'5'-A synthetase activity suggested that CpG ODN acted through the induction of either interferon (IFN)-alpha or IFN-gamma. |
| 741 | 15051512 | ODN 2007 did not induce detectable levels of IFN-alpha or IFN-gamma when incubated with peripheral blood mononuclear cells, but both IFN-alpha and IFN-gamma were detected following stimulation of lymph node cells with ODN 2007. |
| 742 | 15051512 | CpG ODN induction of 2'5'-A synthetase in vitro correlated with the secretion of both IFN-alpha and IFN-gamma. |
| 743 | 15051512 | Many of the cells recruited to the site of ODN 2007 injection expressed IFN-alpha and some IFN-gamma. |
| 744 | 15051512 | Elevated serum 2'5'-A synthetase activity suggested that CpG ODN acted through the induction of either interferon (IFN)-alpha or IFN-gamma. |
| 745 | 15051512 | ODN 2007 did not induce detectable levels of IFN-alpha or IFN-gamma when incubated with peripheral blood mononuclear cells, but both IFN-alpha and IFN-gamma were detected following stimulation of lymph node cells with ODN 2007. |
| 746 | 15051512 | CpG ODN induction of 2'5'-A synthetase in vitro correlated with the secretion of both IFN-alpha and IFN-gamma. |
| 747 | 15051512 | Many of the cells recruited to the site of ODN 2007 injection expressed IFN-alpha and some IFN-gamma. |
| 748 | 15051512 | Elevated serum 2'5'-A synthetase activity suggested that CpG ODN acted through the induction of either interferon (IFN)-alpha or IFN-gamma. |
| 749 | 15051512 | ODN 2007 did not induce detectable levels of IFN-alpha or IFN-gamma when incubated with peripheral blood mononuclear cells, but both IFN-alpha and IFN-gamma were detected following stimulation of lymph node cells with ODN 2007. |
| 750 | 15051512 | CpG ODN induction of 2'5'-A synthetase in vitro correlated with the secretion of both IFN-alpha and IFN-gamma. |
| 751 | 15051512 | Many of the cells recruited to the site of ODN 2007 injection expressed IFN-alpha and some IFN-gamma. |
| 752 | 15096181 | The present work demonstrated that the CpG oligonucleotides (CpG-ODN) 2216, D32 and D19 induce high amounts of interferon-alpha (IFN-alpha), tumour-necrosis factor-alpha (TNF-alpha) and interleukin (IL)-12 in porcine peripheral blood mononuclear cells (PBMCs). |
| 753 | 15096181 | These cells did not express CD6, CD8 or CD45RA. |
| 754 | 15096181 | Importantly, monocyte-derived DC did not respond to CpG-ODN by secretion of IFN-alpha or TNF-alpha or by the up-regulation of costimulatory molecule expression. |
| 755 | 15096181 | The present work demonstrated that the CpG oligonucleotides (CpG-ODN) 2216, D32 and D19 induce high amounts of interferon-alpha (IFN-alpha), tumour-necrosis factor-alpha (TNF-alpha) and interleukin (IL)-12 in porcine peripheral blood mononuclear cells (PBMCs). |
| 756 | 15096181 | These cells did not express CD6, CD8 or CD45RA. |
| 757 | 15096181 | Importantly, monocyte-derived DC did not respond to CpG-ODN by secretion of IFN-alpha or TNF-alpha or by the up-regulation of costimulatory molecule expression. |
| 758 | 15115649 | Psoralen and ultraviolet A radiation may also be combined with low doses of interferon (IFN)-alpha to treat stage I/II disease. |
| 759 | 15115649 | Once the disease becomes refractory to topical therapy, IFN-alpha single-agent or combination chemotherapy may be administered, but the duration of response is often less than 1 year and ultimately all patients will relapse and become refractory. |
| 760 | 15115649 | Response rates after combined modality therapy with total skin electron beam irradiation and chemotherapy/IFN-alpha appear similar to response rates of chemotherapy alone. |
| 761 | 15115649 | Psoralen and ultraviolet A radiation may also be combined with low doses of interferon (IFN)-alpha to treat stage I/II disease. |
| 762 | 15115649 | Once the disease becomes refractory to topical therapy, IFN-alpha single-agent or combination chemotherapy may be administered, but the duration of response is often less than 1 year and ultimately all patients will relapse and become refractory. |
| 763 | 15115649 | Response rates after combined modality therapy with total skin electron beam irradiation and chemotherapy/IFN-alpha appear similar to response rates of chemotherapy alone. |
| 764 | 15115649 | Psoralen and ultraviolet A radiation may also be combined with low doses of interferon (IFN)-alpha to treat stage I/II disease. |
| 765 | 15115649 | Once the disease becomes refractory to topical therapy, IFN-alpha single-agent or combination chemotherapy may be administered, but the duration of response is often less than 1 year and ultimately all patients will relapse and become refractory. |
| 766 | 15115649 | Response rates after combined modality therapy with total skin electron beam irradiation and chemotherapy/IFN-alpha appear similar to response rates of chemotherapy alone. |
| 767 | 15148341 | Furthermore, the addition of IFN-alpha to PPD-stimulated CD4+ T cells directly inhibited telomerase activity in vitro. |
| 768 | 15148341 | Therefore, these results suggest that the rate of telomere erosion in proliferating, antigen-specific CD4+ T cells may be accelerated by type I IFN during a secondary response in vivo. |
| 769 | 15179984 | Combined treatment with IFN-a, IL-2 and 5-FU has demonstrated a survival benefit in a single randomized controlled trial. |
| 770 | 15249217 | In addition, when compared with IFNs alpha and beta, ATA was approximately 10 times more potent than IFN alpha and 100 times more than interferon beta at their highest concentrations reported in the literature previously. |
| 771 | 15265893 | There are two principle subsets of dendritic cells (DCs); CD11c(+)CD123(-) myeloid DCs (MDCs) and CD11c(-)CD123(+) plasmacytoid DCs (PDCs). |
| 772 | 15265893 | Using lineage (Lin) markers to exclude non-DCs, Lin(-)HLA-DR(+)CD11c(+)CD123(-) MDCs and Lin(-)HLA-DR(+)CD11c(-)CD123(+) PDCs were identified in the blood of uninfected macaques and healthy macaques infected with SIV or simian-human immunodeficiency virus. |
| 773 | 15265893 | Overnight culture of DC-enriched Lin-depleted cells increased CD80 and CD86 expression. |
| 774 | 15265893 | IL-12 production and CD80/CD86 expression by MDC/PDC mixtures was further enhanced by CD40L and ISS-ODN treatment. |
| 775 | 15265893 | A CpG-B ISS-ODN increased CD80/CD86 expression by PDCs, but resulted in little IFN-alpha secretion unless IL-3 was added. |
| 776 | 15265893 | In contrast, a CpG-C ISS-ODN and aldrithiol-2-inactivated (AT-2) SIV induced considerable PDC activation and IFN-alpha release without needing exogenous IL-3. |
| 777 | 15265893 | The CpG-C ISS-ODN also stimulated IL-12 release (unlike AT-2 SIV) and augmented DC immunostimulatory activity, increasing SIV-specific T cell IFN-gamma production induced by AT-2 SIV-presenting MDC/PDC-enriched mixtures. |
| 778 | 15265893 | These data highlight the functional capacities of MDCs and PDCs in naive as well as healthy, infected macaques, revealing a promising CpG-C ISS-ODN-driven DC activation strategy that boosts immune function to augment preventative and therapeutic vaccine efficacy. |
| 779 | 15265893 | There are two principle subsets of dendritic cells (DCs); CD11c(+)CD123(-) myeloid DCs (MDCs) and CD11c(-)CD123(+) plasmacytoid DCs (PDCs). |
| 780 | 15265893 | Using lineage (Lin) markers to exclude non-DCs, Lin(-)HLA-DR(+)CD11c(+)CD123(-) MDCs and Lin(-)HLA-DR(+)CD11c(-)CD123(+) PDCs were identified in the blood of uninfected macaques and healthy macaques infected with SIV or simian-human immunodeficiency virus. |
| 781 | 15265893 | Overnight culture of DC-enriched Lin-depleted cells increased CD80 and CD86 expression. |
| 782 | 15265893 | IL-12 production and CD80/CD86 expression by MDC/PDC mixtures was further enhanced by CD40L and ISS-ODN treatment. |
| 783 | 15265893 | A CpG-B ISS-ODN increased CD80/CD86 expression by PDCs, but resulted in little IFN-alpha secretion unless IL-3 was added. |
| 784 | 15265893 | In contrast, a CpG-C ISS-ODN and aldrithiol-2-inactivated (AT-2) SIV induced considerable PDC activation and IFN-alpha release without needing exogenous IL-3. |
| 785 | 15265893 | The CpG-C ISS-ODN also stimulated IL-12 release (unlike AT-2 SIV) and augmented DC immunostimulatory activity, increasing SIV-specific T cell IFN-gamma production induced by AT-2 SIV-presenting MDC/PDC-enriched mixtures. |
| 786 | 15265893 | These data highlight the functional capacities of MDCs and PDCs in naive as well as healthy, infected macaques, revealing a promising CpG-C ISS-ODN-driven DC activation strategy that boosts immune function to augment preventative and therapeutic vaccine efficacy. |
| 787 | 15331713 | IFN synthesis is regulated by specific transcription factors, including interferon regulatory factor (IRF-3), NF-kappaB, and AP-1. |
| 788 | 15331713 | Likewise, NF-kappaB and AP-1 were activated normally, as shown in electrophoretic mobility shift assays. |
| 789 | 15342370 | We show that IFN-alpha and polyinosinic:polycytidylic acid (p-I:C) synergize with the "classical" type-1-polarizing cytokine cocktail [tumor necrosis factor alpha (TNFalpha)/IL-1beta/IFNgamma], allowing for serum-free generation of fully mature type-1-polarized DCs (DC1). |
| 790 | 15342370 | Such "alpha-type-1-polarized DC(s)" (alphaDC1) show high migratory responses to the CCR7 ligand, 6C-kine but produce much higher levels of IL-12p70 as compared to TNFalpha/IL-1beta/IL-6/prostaglandin E2 (PGE2)-matured DCs (sDC), the current "gold standard" in DC-based cancer vaccination. |
| 791 | 15342370 | A single round of in vitro sensitization with alphaDC1 (versus sDCs) induces up to 40-fold higher numbers of long-lived CTLs against melanoma-associated antigens: MART-1, gp100, and tyrosinase. |
| 792 | 15507313 | To improve the immune response, an adjuvant consisting of plasmid encoding either porcine interleukin (IL)-12 or IFN-alpha was co-administered during vaccination. |
| 793 | 15507313 | While this enhancement was only transient (1 week) when the IL-12 expressing plasmid was used, the effect was not only still apparent at 6 weeks after vaccination in the presence of the IFN-alpha expressing plasmid but even after challenge with a virulent genetically divergent PRRSV. |
| 794 | 15507313 | Despite the apparent augmentation of a T helper (Th) 1 type response by the inclusion of IFN-alpha or IL-12 during vaccination, this modulation did not necessarily correlate with a reduction in viremia. |
| 795 | 15507313 | To improve the immune response, an adjuvant consisting of plasmid encoding either porcine interleukin (IL)-12 or IFN-alpha was co-administered during vaccination. |
| 796 | 15507313 | While this enhancement was only transient (1 week) when the IL-12 expressing plasmid was used, the effect was not only still apparent at 6 weeks after vaccination in the presence of the IFN-alpha expressing plasmid but even after challenge with a virulent genetically divergent PRRSV. |
| 797 | 15507313 | Despite the apparent augmentation of a T helper (Th) 1 type response by the inclusion of IFN-alpha or IL-12 during vaccination, this modulation did not necessarily correlate with a reduction in viremia. |
| 798 | 15507313 | To improve the immune response, an adjuvant consisting of plasmid encoding either porcine interleukin (IL)-12 or IFN-alpha was co-administered during vaccination. |
| 799 | 15507313 | While this enhancement was only transient (1 week) when the IL-12 expressing plasmid was used, the effect was not only still apparent at 6 weeks after vaccination in the presence of the IFN-alpha expressing plasmid but even after challenge with a virulent genetically divergent PRRSV. |
| 800 | 15507313 | Despite the apparent augmentation of a T helper (Th) 1 type response by the inclusion of IFN-alpha or IL-12 during vaccination, this modulation did not necessarily correlate with a reduction in viremia. |
| 801 | 15515120 | Double-stranded secondary structures on mRNA induce type I interferon (IFN alpha/beta) production and maturation of mRNA-transfected monocyte-derived dendritic cells. |
| 802 | 15528139 | However, their activation program for cytokine production was different, being IL-12 mainly produced by myeloid DCs and IL-12, IL-10 and IFN-alpha mainly produced by plasmacytoid DCs. |
| 803 | 15542655 | Replication-deficient NS1 mutant viruses induced a rapid local release of proinflammatory cytokines such as interleukin-1beta (IL-1beta) and IL-6. |
| 804 | 15542655 | The most rapid onset of the recall CD8(+)-T-cell response upon the wild-type virus challenge was detected in mice primed with NS1 mutant viruses eliciting high levels of cytokines. |
| 805 | 15542655 | It is noteworthy that there was one NS1 mutant virus encoding NS1 protein with a deletion of 40 amino acids predominantly in the RNA-binding domain that induced the highest levels of IFN-alpha/beta, IL-6 and IL-1beta after infection. |
| 806 | 15543094 | The elevated levels of immunoglobulins, about 20% more muscle in the pulmonary arteries, increased airway smooth muscle cells, and increased fetal hemoglobin and erythropoietin are evidence of chronic hypoxia before death. |
| 807 | 15543094 | These proinflammatory cytokines down-regulate gene expression of major cytochrome P-450 and/or other enzymes with the specific effects on mRNA levels, protein expression, and enzyme activity, thus affecting metabolism of several endogenous lipophilic substances, such as steroids, lipid-soluble vitamins, prostaglandins, leukotrienes, thromboxanes, and exogenous substances. |
| 808 | 15543094 | PEPCK deficit found in SIDS infants (caused also by vitamin A deficiency) and eventually enhanced by PACAP lipolysis of adipocyte triglycerides resulted in an increased FA level in blood because of their impaired reesterification to triacylglycerol in adipocytes. |
| 809 | 15543094 | Pulmonary edema and petechial hemorrhages often present in SIDS victims may be the result of the vascular leak syndrome caused by IL-2 and IFN-alpha. |
| 810 | 15543094 | Chronic hypoxia with the release of proinflammatory mediators IL-1alpha, IL-1beta and IL-6, and overloading of the cardiovascular and respiratory systems due to the narrowing airways and small pulmonary arteries of these children could also contribute to the development of these abnormalities. |
| 811 | 15543094 | Moreover, chronic hypoxia of SIDS infants induced also production of hypoxia-inducible factor 1alpha (HIF-1alpha), which stimulated synthesis and release of different growth factors by vascular endothelial cells and intensified subclinical inflammatory reactions in the central nervous system, perhaps potentiated also by PACAP and VIP gene mutations. |
| 812 | 15550117 | Zymosan, poly(I:C) and CpG DNA, which signal through TLR2/6, 3 and 9, respectively, were found to strongly induce the production of IgG2a antibodies, whereas R-848 (TLR7) and LPS (TLR4) did so much more weakly. |
| 813 | 15550117 | In contrast, LPS, poly(I:C) and CpG DNA, but not zymosan, induced functional CD8+ T-cell responses against OVA; peptidoglycan (TLR2/?) |
| 814 | 15550117 | In addition, our results demonstrate that the ability of TLR stimuli to initiate CD8+ T-cell responses against soluble protein antigens is largely dependent on the IFN-alpha/beta signalling pathway. |
| 815 | 15602727 | The aim of this study was to assess the capacity of IFN-alpha to augment the cellular immune response to DNA vaccination against HCV core protein. |
| 816 | 15602727 | Three types of IFN-alpha were investigated: the non-species-specific hybrid IFN A/D, human pegylated IFN-alpha, and a plasmid that expressed murine IFN-alpha. |
| 817 | 15602727 | These findings demonstrate that the immunomodulatory properties of IFN-alpha can be exploited to augment DNA based immunization, but it is important to consider the effects of dose on both cellular and humoral immune response for optimal augmentation. |
| 818 | 15602727 | The aim of this study was to assess the capacity of IFN-alpha to augment the cellular immune response to DNA vaccination against HCV core protein. |
| 819 | 15602727 | Three types of IFN-alpha were investigated: the non-species-specific hybrid IFN A/D, human pegylated IFN-alpha, and a plasmid that expressed murine IFN-alpha. |
| 820 | 15602727 | These findings demonstrate that the immunomodulatory properties of IFN-alpha can be exploited to augment DNA based immunization, but it is important to consider the effects of dose on both cellular and humoral immune response for optimal augmentation. |
| 821 | 15602727 | The aim of this study was to assess the capacity of IFN-alpha to augment the cellular immune response to DNA vaccination against HCV core protein. |
| 822 | 15602727 | Three types of IFN-alpha were investigated: the non-species-specific hybrid IFN A/D, human pegylated IFN-alpha, and a plasmid that expressed murine IFN-alpha. |
| 823 | 15602727 | These findings demonstrate that the immunomodulatory properties of IFN-alpha can be exploited to augment DNA based immunization, but it is important to consider the effects of dose on both cellular and humoral immune response for optimal augmentation. |
| 824 | 15606336 | In the adjuvant setting, cytokine monotherapy (interferon [IFN]-alpha or interleukin [IL]-2) is not effective in improving progression-free or overall survival. |
| 825 | 15606336 | In metastatic kidney cancer patients with the tumor-bearing kidney in situ, a combination of radical nephrectomy plus IFN-alpha is more effective than IFN-alpha alone. |
| 826 | 15606336 | In metastatic kidney cancer without the option of operative removal of the primary tumor and/or metastases, cytokines such as IFN-alpha, IL-2 and IL-12 and their combinations result in response rates of 10-30%, but the 5-year overall survival is less than 10%. |
| 827 | 15606336 | In the adjuvant setting, cytokine monotherapy (interferon [IFN]-alpha or interleukin [IL]-2) is not effective in improving progression-free or overall survival. |
| 828 | 15606336 | In metastatic kidney cancer patients with the tumor-bearing kidney in situ, a combination of radical nephrectomy plus IFN-alpha is more effective than IFN-alpha alone. |
| 829 | 15606336 | In metastatic kidney cancer without the option of operative removal of the primary tumor and/or metastases, cytokines such as IFN-alpha, IL-2 and IL-12 and their combinations result in response rates of 10-30%, but the 5-year overall survival is less than 10%. |
| 830 | 15606336 | In the adjuvant setting, cytokine monotherapy (interferon [IFN]-alpha or interleukin [IL]-2) is not effective in improving progression-free or overall survival. |
| 831 | 15606336 | In metastatic kidney cancer patients with the tumor-bearing kidney in situ, a combination of radical nephrectomy plus IFN-alpha is more effective than IFN-alpha alone. |
| 832 | 15606336 | In metastatic kidney cancer without the option of operative removal of the primary tumor and/or metastases, cytokines such as IFN-alpha, IL-2 and IL-12 and their combinations result in response rates of 10-30%, but the 5-year overall survival is less than 10%. |
| 833 | 15611232 | Type I IFN negatively regulates CD8+ T cell responses through IL-10-producing CD4+ T regulatory 1 cells. |
| 834 | 15611232 | We used vaccine-induced, antiviral CD8(+) T cell responses in IFN-beta (IFN-beta(-/-))- or type I IFN receptor (IFNAR(-/-))-deficient mice to study immunomodulating effects of type I IFN that are not complicated by the interference of a concomitant virus infection. |
| 835 | 15611232 | Compared with normal B6 mice, IFNAR(-/-) or IFN-beta(-/-) mice have normal numbers of CD4(+) and CD8(+) T cells, and CD25(+)FoxP3(+) T regulatory (T(R)) cells in liver and spleen. |
| 836 | 15611232 | IFN-gamma and TNF-alpha production and clonal expansion of specific CD8(+) T cells from normal and knockout mice are similar. |
| 837 | 15611232 | CD25(+)FoxP3(+) T(R) cells down-modulate vaccine-primed CD8(+) T cell responses in normal, IFNAR(-/-), or IFN-beta(-/-) mice to a comparable extent. |
| 838 | 15611232 | Low IFN-alpha or IFN-beta doses (500-10(3) U/mouse) down-modulate CD8(+) T cells priming in vivo. |
| 839 | 15611232 | IFNAR- and IFN-beta-deficient mice generate 2- to 3-fold lower numbers of IL-10-producing CD4(+) T cells after polyclonal or specific stimulation in vitro or in vivo. |
| 840 | 15611232 | CD8(+) T cell responses are thus subjected to negative control by both CD25(+)FoxP3(+) T(R) cells and CD4(+)IL-10(+) T(R1) cells, but only development of the latter T(R) cells depends on type I IFN. |
| 841 | 15634897 | Dendritic cells and NK cells stimulate bystander T cell activation in response to TLR agonists through secretion of IFN-alpha beta and IFN-gamma. |
| 842 | 15634897 | In vitro, IFN-alphabeta, IL-18, and IL-12 all contributed to DC stimulation of NK cell IFN-gamma, whereas IFN-alphabeta was shown to be important for induction of T cell bystander activation and NK cell IFN-gamma production in vivo. |
| 843 | 15661382 | When exposed to inactivated pseudorabiesvirus (iPRV), plasmacytoid but not myeloid DCs released IFN-alpha and IL-12. |
| 844 | 15722233 | Interferon regulatory factor-1 (IRF-1) mediates an antiviral state in cells by regulating the expression of the interferon (IFN-alpha/beta) system. |
| 845 | 15744581 | Such interaction was reported to induce the hematopoietic cells to release large amounts of Th2 cytokines IL-4, IL-5, IL-10 and IL-13. |
| 846 | 15744581 | Type I IFNs reactivate the patients' inhibited Th1 cells to synthesize IL-2 and IL-12 cytokines that activate the maturation of CTL precursors. |
| 847 | 15744581 | The CpG ODNs A and B bind to Toll like receptors that are present in pDCs and B cells, respectively, CpG ODN - A is the ligand for TLR9+ pDCs and induce the release of large amounts of IFN-alpha, beta. |
| 848 | 15744581 | Based on these studies, a hypothesis is presented that treatment of HIV-1 infected and AIDS patients with CpG ODN-A and B or CpG ODN-C have the potential to inhibit IL-4 synthesis and release from FcrepsilonRI+ hematopoietic cells by inducing TLR9+ pDCs to release large amounts of type I IFNs. |
| 849 | 15744581 | Type I IFNs reactivate the patients' Th1 cells to synthesize IL-2 and IL-12 cytokines, activators of the precursor cytotoxic T cells (CTLs), leading to the reactivation of the inhibited adaptive immune response. |
| 850 | 15781661 | Administration of IFN-alpha enhances the efficacy of a granulocyte macrophage colony stimulating factor-secreting tumor cell vaccine. |
| 851 | 15781661 | The studies reported herein show that 50% of mice reject established B16 tumors following treatment with the combination of a granulocyte macrophage colony-stimulating factor-secreting tumor cell vaccine (B16.GM) and subclinical doses of recombinant murine IFN-alpha delivered at the vaccine site. |
| 852 | 15781661 | Furthermore, a 30-fold increase in the frequency of melanoma-associated antigen (Trp-2 and gp100) specific T cells was observed in mice treated with the combination when compared with unvaccinated controls. |
| 853 | 15781661 | These data show that IFN-alpha combined with a granulocyte macrophage colony-stimulating factor-secreting tumor cell vaccine significantly enhances vaccine potency and may represent a potential new approach for tumor immunotherapy. |
| 854 | 15781661 | Administration of IFN-alpha enhances the efficacy of a granulocyte macrophage colony stimulating factor-secreting tumor cell vaccine. |
| 855 | 15781661 | The studies reported herein show that 50% of mice reject established B16 tumors following treatment with the combination of a granulocyte macrophage colony-stimulating factor-secreting tumor cell vaccine (B16.GM) and subclinical doses of recombinant murine IFN-alpha delivered at the vaccine site. |
| 856 | 15781661 | Furthermore, a 30-fold increase in the frequency of melanoma-associated antigen (Trp-2 and gp100) specific T cells was observed in mice treated with the combination when compared with unvaccinated controls. |
| 857 | 15781661 | These data show that IFN-alpha combined with a granulocyte macrophage colony-stimulating factor-secreting tumor cell vaccine significantly enhances vaccine potency and may represent a potential new approach for tumor immunotherapy. |
| 858 | 15781661 | Administration of IFN-alpha enhances the efficacy of a granulocyte macrophage colony stimulating factor-secreting tumor cell vaccine. |
| 859 | 15781661 | The studies reported herein show that 50% of mice reject established B16 tumors following treatment with the combination of a granulocyte macrophage colony-stimulating factor-secreting tumor cell vaccine (B16.GM) and subclinical doses of recombinant murine IFN-alpha delivered at the vaccine site. |
| 860 | 15781661 | Furthermore, a 30-fold increase in the frequency of melanoma-associated antigen (Trp-2 and gp100) specific T cells was observed in mice treated with the combination when compared with unvaccinated controls. |
| 861 | 15781661 | These data show that IFN-alpha combined with a granulocyte macrophage colony-stimulating factor-secreting tumor cell vaccine significantly enhances vaccine potency and may represent a potential new approach for tumor immunotherapy. |
| 862 | 15827150 | Effects of nonstructural proteins NS1 and NS2 of human respiratory syncytial virus on interferon regulatory factor 3, NF-kappaB, and proinflammatory cytokines. |
| 863 | 15827150 | It has been shown previously that HRSV nonstructural proteins 1 and 2 (NS1 and NS2) inhibit the induction of alpha/beta interferon (IFN-alpha/beta) in A549 cells and human macrophages. |
| 864 | 15827150 | Two principal transcription factors for the early IFN-beta and -alpha1 response are interferon regulatory factor 3 (IRF-3) and nuclear factor kappaB (NF-kappaB). |
| 865 | 15827150 | At early times postinfection, wild-type HRSV and the NS1/NS2 deletion mutants were very similar in the ability to activate IRF-3. |
| 866 | 15827150 | However, once NS1 and NS2 were expressed significantly, they acted cooperatively to suppress activation and nuclear translocation of IRF-3. |
| 867 | 15827150 | Since these viruses differed greatly in the induction of IFN-alpha/beta, NF-kappaB activation was evaluated in Vero cells, which lack the structural genes for IFN-alpha/beta and would preclude confounding effects of IFN-alpha/beta. |
| 868 | 15827150 | Since recombinant HRSVs from which the NS1 or NS2 genes have been deleted are being developed as vaccine candidates, we investigated whether the changes in activation of host transcription factors and increased IFN-alpha/beta production had an effect on the epithelial production of proinflammatory factors. |
| 869 | 15827150 | Viruses lacking NS1 and/or NS2 stimulated modestly lower production of RANTES (Regulated on Activation Normal T-cell Expressed and Secreted), interleukin 8, and tumor necrosis factor alpha compared to wild-type recombinant RSV, supporting their use as attenuated vaccine candidates. |
| 870 | 15827150 | Effects of nonstructural proteins NS1 and NS2 of human respiratory syncytial virus on interferon regulatory factor 3, NF-kappaB, and proinflammatory cytokines. |
| 871 | 15827150 | It has been shown previously that HRSV nonstructural proteins 1 and 2 (NS1 and NS2) inhibit the induction of alpha/beta interferon (IFN-alpha/beta) in A549 cells and human macrophages. |
| 872 | 15827150 | Two principal transcription factors for the early IFN-beta and -alpha1 response are interferon regulatory factor 3 (IRF-3) and nuclear factor kappaB (NF-kappaB). |
| 873 | 15827150 | At early times postinfection, wild-type HRSV and the NS1/NS2 deletion mutants were very similar in the ability to activate IRF-3. |
| 874 | 15827150 | However, once NS1 and NS2 were expressed significantly, they acted cooperatively to suppress activation and nuclear translocation of IRF-3. |
| 875 | 15827150 | Since these viruses differed greatly in the induction of IFN-alpha/beta, NF-kappaB activation was evaluated in Vero cells, which lack the structural genes for IFN-alpha/beta and would preclude confounding effects of IFN-alpha/beta. |
| 876 | 15827150 | Since recombinant HRSVs from which the NS1 or NS2 genes have been deleted are being developed as vaccine candidates, we investigated whether the changes in activation of host transcription factors and increased IFN-alpha/beta production had an effect on the epithelial production of proinflammatory factors. |
| 877 | 15827150 | Viruses lacking NS1 and/or NS2 stimulated modestly lower production of RANTES (Regulated on Activation Normal T-cell Expressed and Secreted), interleukin 8, and tumor necrosis factor alpha compared to wild-type recombinant RSV, supporting their use as attenuated vaccine candidates. |
| 878 | 15827150 | Effects of nonstructural proteins NS1 and NS2 of human respiratory syncytial virus on interferon regulatory factor 3, NF-kappaB, and proinflammatory cytokines. |
| 879 | 15827150 | It has been shown previously that HRSV nonstructural proteins 1 and 2 (NS1 and NS2) inhibit the induction of alpha/beta interferon (IFN-alpha/beta) in A549 cells and human macrophages. |
| 880 | 15827150 | Two principal transcription factors for the early IFN-beta and -alpha1 response are interferon regulatory factor 3 (IRF-3) and nuclear factor kappaB (NF-kappaB). |
| 881 | 15827150 | At early times postinfection, wild-type HRSV and the NS1/NS2 deletion mutants were very similar in the ability to activate IRF-3. |
| 882 | 15827150 | However, once NS1 and NS2 were expressed significantly, they acted cooperatively to suppress activation and nuclear translocation of IRF-3. |
| 883 | 15827150 | Since these viruses differed greatly in the induction of IFN-alpha/beta, NF-kappaB activation was evaluated in Vero cells, which lack the structural genes for IFN-alpha/beta and would preclude confounding effects of IFN-alpha/beta. |
| 884 | 15827150 | Since recombinant HRSVs from which the NS1 or NS2 genes have been deleted are being developed as vaccine candidates, we investigated whether the changes in activation of host transcription factors and increased IFN-alpha/beta production had an effect on the epithelial production of proinflammatory factors. |
| 885 | 15827150 | Viruses lacking NS1 and/or NS2 stimulated modestly lower production of RANTES (Regulated on Activation Normal T-cell Expressed and Secreted), interleukin 8, and tumor necrosis factor alpha compared to wild-type recombinant RSV, supporting their use as attenuated vaccine candidates. |
| 886 | 15832293 | They strongly activate DC and monocytes, leading to TNF-alpha and IFN-alpha secretion. |
| 887 | 15832293 | The detailed analysis of the activated cell types, the study of the cytokines released from PBMC cultured with protamine-RNA complexes and recently published results suggest that TLR-7 and TLR-8 may be involved in the recognition of protamine-stabilized RNA. |
| 888 | 15832296 | However, HPV16 VLP induced pDC to secrete of IFN-alpha and IL-6, both cytokines that play a role in the generation of antibody responses, as well as TNFalpha and IL-8. |
| 889 | 15832296 | Finally, CpG-activated pDC, but not pDC exposed to HPV16 VLP, activated lymphocytes to secrete IL-10 and low levels of IFN-gamma. |
| 890 | 15845642 | Mycobacterium bovis Bacillus Calmette-Guerin infects DC-SIGN- dendritic cell and causes the inhibition of IL-12 and the enhancement of IL-10 production. |
| 891 | 15845642 | Recent studies have shown that BCG and Mtb target the DC-specific C-type lectin intercellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN) to infect DC and inhibit their immunostimulatory function. |
| 892 | 15845642 | This would occur through the interaction of the mycobacterial mannosylated lipoarabinomannan to DC-SIGN, which would prevent DC maturation and induce the immunosuppressive cytokine interleukin (IL)-10 synthesis. |
| 893 | 15845642 | Here, we confirm that DC-SIGN is expressed in DC derived from monocytes cultured in granulocyte macrophage-colony stimulating factor (GM-CSF) and IL-4 and show that it is not expressed in DC derived from monocytes cultured in GM-CSF and interferon-alpha (IFN-alpha). |
| 894 | 15845642 | We also demonstrate that DC-SIGN(-) DC cultured in GM-CSF and IFN-alpha are able to phagocytose BCG and to undergo a maturation program as well as DC-SIGN(+) DC cultured in IL-4 and GM-CSF. |
| 895 | 15845642 | We also show that BCG causes the impairment of IL-12 and the induction of IL-10 secretion by DC, irrespective of DC-SIGN expression. |
| 896 | 15845642 | Mycobacterium bovis Bacillus Calmette-Guerin infects DC-SIGN- dendritic cell and causes the inhibition of IL-12 and the enhancement of IL-10 production. |
| 897 | 15845642 | Recent studies have shown that BCG and Mtb target the DC-specific C-type lectin intercellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN) to infect DC and inhibit their immunostimulatory function. |
| 898 | 15845642 | This would occur through the interaction of the mycobacterial mannosylated lipoarabinomannan to DC-SIGN, which would prevent DC maturation and induce the immunosuppressive cytokine interleukin (IL)-10 synthesis. |
| 899 | 15845642 | Here, we confirm that DC-SIGN is expressed in DC derived from monocytes cultured in granulocyte macrophage-colony stimulating factor (GM-CSF) and IL-4 and show that it is not expressed in DC derived from monocytes cultured in GM-CSF and interferon-alpha (IFN-alpha). |
| 900 | 15845642 | We also demonstrate that DC-SIGN(-) DC cultured in GM-CSF and IFN-alpha are able to phagocytose BCG and to undergo a maturation program as well as DC-SIGN(+) DC cultured in IL-4 and GM-CSF. |
| 901 | 15845642 | We also show that BCG causes the impairment of IL-12 and the induction of IL-10 secretion by DC, irrespective of DC-SIGN expression. |
| 902 | 15877606 | Monocyte-derived dendritic cells (mDC), the most frequently applied DC subset in clinical studies, which can be obtained easily from peripheral blood monocytes after incubation with GM-CSF and IL-4, have not been clearly demonstrated to be activated by CpG oligodeoxynucleotides (ODN). |
| 903 | 15877606 | However, we did not observe increased expression of maturation-associated and functionally relevant surface antigens (CD14, HLA-DR, CD40, CD83, CD80 and CD86), significant secretion of IL-12 and IFN-alpha in culture supernatant, or enhanced antitumour activation of cytokine-induced killer cells. |
| 904 | 15905497 | In addition to CD45RA(high) plasmacytoid DC, two distinct CD24(high) and CD11b(high) cDC subsets were present, and these subsets showed equivalent properties to splenic CD8(+) and CD8(-) cDC, respectively, in the following: 1) surface expression of CD11b, CD24, and signal regulatory protein-alpha; 2) developmental dependence on, and mRNA expression of, IFN regulatory factor-8; 3) mRNA expression of TLRs and chemokine receptors; 4) production of IL-12 p40/70, IFN-alpha, MIP-1alpha, and RANTES in response to TLR ligands; 5) expression of cystatin C; and 6) cross-presentation of exogenous Ag to CD8 T cells. |
| 905 | 15905497 | Furthermore, despite lacking surface CD8 expression, the CD24(high) subset contained CD8 mRNA and up-regulated surface expression when transferred into mice. |
| 906 | 15919908 | It has been shown previously that the nonstructural protein NS1 of influenza virus is an alpha/beta interferon (IFN-alpha/beta) antagonist, both in vitro and in experimental animal model systems. |
| 907 | 15919908 | Here we investigated the role of the NS1 protein in the virulence of a swine influenza virus (SIV) isolate in pigs by using reverse genetics. |
| 908 | 15919908 | Growth properties of TX/98 viruses with mutated NS1, induction of IFN in tissue culture, and virulence-attenuation in pigs were analyzed and compared to those of the recombinant wild-type TX/98 virus. |
| 909 | 15919908 | Our results indicate that deletions in the NS1 protein decrease the ability of the TX/98 virus to prevent IFN-alpha/beta synthesis in pig cells. |
| 910 | 15919908 | Moreover, all NS1 mutant viruses were attenuated in pigs, and this correlated with the amount of IFN-alpha/beta induced in vitro. |
| 911 | 15919908 | These data suggest that the NS1 protein of SIV is a virulence factor. |
| 912 | 15919908 | Due to their attenuation, NS1-mutated swine influenza viruses might have a great potential as live attenuated vaccine candidates against SIV infections of pigs. |
| 913 | 15919908 | It has been shown previously that the nonstructural protein NS1 of influenza virus is an alpha/beta interferon (IFN-alpha/beta) antagonist, both in vitro and in experimental animal model systems. |
| 914 | 15919908 | Here we investigated the role of the NS1 protein in the virulence of a swine influenza virus (SIV) isolate in pigs by using reverse genetics. |
| 915 | 15919908 | Growth properties of TX/98 viruses with mutated NS1, induction of IFN in tissue culture, and virulence-attenuation in pigs were analyzed and compared to those of the recombinant wild-type TX/98 virus. |
| 916 | 15919908 | Our results indicate that deletions in the NS1 protein decrease the ability of the TX/98 virus to prevent IFN-alpha/beta synthesis in pig cells. |
| 917 | 15919908 | Moreover, all NS1 mutant viruses were attenuated in pigs, and this correlated with the amount of IFN-alpha/beta induced in vitro. |
| 918 | 15919908 | These data suggest that the NS1 protein of SIV is a virulence factor. |
| 919 | 15919908 | Due to their attenuation, NS1-mutated swine influenza viruses might have a great potential as live attenuated vaccine candidates against SIV infections of pigs. |
| 920 | 15919908 | It has been shown previously that the nonstructural protein NS1 of influenza virus is an alpha/beta interferon (IFN-alpha/beta) antagonist, both in vitro and in experimental animal model systems. |
| 921 | 15919908 | Here we investigated the role of the NS1 protein in the virulence of a swine influenza virus (SIV) isolate in pigs by using reverse genetics. |
| 922 | 15919908 | Growth properties of TX/98 viruses with mutated NS1, induction of IFN in tissue culture, and virulence-attenuation in pigs were analyzed and compared to those of the recombinant wild-type TX/98 virus. |
| 923 | 15919908 | Our results indicate that deletions in the NS1 protein decrease the ability of the TX/98 virus to prevent IFN-alpha/beta synthesis in pig cells. |
| 924 | 15919908 | Moreover, all NS1 mutant viruses were attenuated in pigs, and this correlated with the amount of IFN-alpha/beta induced in vitro. |
| 925 | 15919908 | These data suggest that the NS1 protein of SIV is a virulence factor. |
| 926 | 15919908 | Due to their attenuation, NS1-mutated swine influenza viruses might have a great potential as live attenuated vaccine candidates against SIV infections of pigs. |
| 927 | 15919908 | It has been shown previously that the nonstructural protein NS1 of influenza virus is an alpha/beta interferon (IFN-alpha/beta) antagonist, both in vitro and in experimental animal model systems. |
| 928 | 15919908 | Here we investigated the role of the NS1 protein in the virulence of a swine influenza virus (SIV) isolate in pigs by using reverse genetics. |
| 929 | 15919908 | Growth properties of TX/98 viruses with mutated NS1, induction of IFN in tissue culture, and virulence-attenuation in pigs were analyzed and compared to those of the recombinant wild-type TX/98 virus. |
| 930 | 15919908 | Our results indicate that deletions in the NS1 protein decrease the ability of the TX/98 virus to prevent IFN-alpha/beta synthesis in pig cells. |
| 931 | 15919908 | Moreover, all NS1 mutant viruses were attenuated in pigs, and this correlated with the amount of IFN-alpha/beta induced in vitro. |
| 932 | 15919908 | These data suggest that the NS1 protein of SIV is a virulence factor. |
| 933 | 15919908 | Due to their attenuation, NS1-mutated swine influenza viruses might have a great potential as live attenuated vaccine candidates against SIV infections of pigs. |
| 934 | 15944268 | Immunization with HIV-1 Gag protein conjugated to a TLR7/8 agonist results in the generation of HIV-1 Gag-specific Th1 and CD8+ T cell responses. |
| 935 | 15944268 | Injection of R-848 and CpG oligodeoxynucleotides alone enhanced the innate immune responses in vivo as demonstrated by high serum levels of inflammatory cytokines, including IL-12p70 and IFN-alpha, and increased expression of CD80, CD86, and CD40 on CD11c(+) dendritic cells. |
| 936 | 15944268 | By contrast, R-848 was a relatively poor adjuvant for inducing primary Th1 or CD8(+) T cell responses when administered with HIV-1 Gag protein. |
| 937 | 15944268 | However, when a TLR7/8 agonist structurally and functionally similar to R-848 was conjugated to HIV-1 Gag protein both Th1 and CD8(+) T cells responses were elicited as determined by intracellular cytokine and tetramer staining. |
| 938 | 15944297 | HPV16 L1 VLP also activate production of proinflammatory factors IFN-alpha, IL-6, MIP-1alpha, RANTES, and KC, up-regulate the expression of costimulatory molecules by naive B cells, and increase the B1 B cell subpopulation. |
| 939 | 15944297 | Thus HPV16 L1 VLP directly activate B cells to induce CD4(+) T cell independent humoral immune responses via TLR4- and MyD88-dependent signaling. |
| 940 | 15961575 | It is interesting that the K-type CpG motif-modified plasmid stimulated significant levels of interferon (IFN)-gamma and IFN-alpha from human PBMC. |
| 941 | 16037410 | Dendritic cells differentiated in the presence of IFN-{beta} and IL-3 are potent inducers of an antigen-specific CD8+ T cell response. |
| 942 | 16037410 | Classically, mature monocyte-derived DC are generated in vitro in the presence of interleukin (IL)-4, granulocyte macrophage-colony stimulating factor, and inflammatory cytokines (G4-DC). |
| 943 | 16037410 | Recently, it has been described that DC can also be generated in the presence of IL-3 and interferon (IFN)-beta and that these DC are efficiently matured using polyriboinosinic polyribocytidylic acid (I3-DC). |
| 944 | 16037410 | Phenotypic characterization of the DC revealed differences in the expression of the monocyte marker CD14 and the maturation marker CD83. |
| 945 | 16037410 | Low expression of CD14 and high expression of CD83 characterized G4-DC, whereas I3-DC displayed intermediate expression of CD14 and CD83. |
| 946 | 16037410 | Upon CD40 ligation, G4-DC produced lower amounts of IFN-alpha and pulmonary and activation-regulated chemokine, similar amounts of IL-6, macrophage-inflammatory protein (MIP)-1alpha, and MIP-1beta, and higher amounts of IL-12 p70, tumor necrosis factor alpha, and MIP-3beta than I3-DC. |
| 947 | 16037410 | Finally, in vitro stimulations showed that fresh and frozen peptide-loaded I3-DC are more potent inducers of Melan-A-specific CD8(+) T cell responses than G4-DC. |
| 948 | 16081851 | Mice bearing intracranial GL261 glioma or MCA205 sarcoma received peripheral immunizations with corresponding irradiated tumor cells engineered to express IL-4 or GM-CSFs, respectively, as well as intratumoral delivery of DC-IFN-alpha. |
| 949 | 16081851 | This regimen prolonged survival of the animals and induced tumor-specific CTLs that expressed TRAIL, which in concert with perforin and Fas ligand (FasL) was involved in the tumor-specific CTL activity of these cells. |
| 950 | 16081851 | The in vivo antitumor activity associated with this approach was abrogated by administration of neutralizing mAbs against TRAIL or FasL and was not observed in perforin-/-, IFN-gamma-/-, or FasL-/- mice. |
| 951 | 16081851 | Transduction of the tumor cells with antiapoptotic protein cellular FLIP rendered the gene-modified cells resistant to TRAIL- or FasL-mediated apoptosis and to CTL killing activity in vitro. |
| 952 | 16113607 | Twenty-two HLA A*0201 patients with stage IV melanoma were enrolled in a phase 1 safety and feasibility trial using a composite dendritic cell (DC) vaccine generated by culturing CD34 hematopoietic progenitors and activated with IFN-alpha. |
| 953 | 16113607 | The DC vaccine was loaded with peptides derived from four melanoma tissue differentiation antigens (MART-1, tyrosinase, MAGE-3, and gp100) and influenza matrix peptide (Flu-MP). |
| 954 | 16113607 | Melanoma-peptide-specific recall memory CD8 T cells able to secrete IFN-gamma and to proliferate could be detected in six of the seven analyzed patients. |
| 955 | 16116238 | Viral vectors may address both of these issues, as they can be used to deliver intact tumor Ags to DCs, and have been shown to inhibit the suppression mediated by CD4+CD25+ regulatory T cells. |
| 956 | 16116238 | VRP infection of immature DCs was superior to TNF-alpha treatment at inducing phenotypic maturation of DCs, and was comparable to LPS stimulation. |
| 957 | 16116238 | Additionally, VRP-infected DC cultures secreted substantial amounts of the proinflammatory cytokines IL-6, TNF-alpha, and IFN-alpha. |
| 958 | 16116238 | Finally, DCs transduced with a VRP encoding the influenza matrix protein (FMP) stimulated 50% greater expansion of FMP-specific CD8+ CTL when compared with TNF-alpha-matured DCs pulsed with an HLA-A*0201-restricted FMP peptide. |
| 959 | 16148144 | In addition to IL-12p40, HKBA induces other Th1-like cytokines, namely, IFN-alpha and IFN-gamma, in a TLR9-dependent manner. |
| 960 | 16165219 | Five groups received MLV vaccine with either bacterial endotoxin-derived adjuvant (ET), mixed open reading frame 5 (ORF5) peptides derived from various PRRSV isolates, porcine interferon alpha (IFNalpha), polyinosinic-polycytidylic acid stabilized with polylysine and carboxymethylcellulose (poly-ICLC), or porcine interleukin-12 (IL-12). |
| 961 | 16165219 | Four-color flow cytometry was utilized to simultaneously identify three major porcine T-cell surface markers (CD4, CD8, and gammadelta TCR) and detect activation marker CD25 (alpha chain of IL-2 receptor) or intracellular IFNgamma. |
| 962 | 16165219 | The MLV PRRSV vaccine alone successfully primed CD4(-)CD8(+)gammadelta- T-cells as demonstrated by a significant increase in %IFNgamma+ cells when live PRRSV was used as a recall antigen. |
| 963 | 16165219 | Booster immunizations of mixed ORF5 peptides and co-administration of IL-12 with MLV PRRSV vaccine significantly enhanced IFNgamma expression by some T-cell subsets (CD4(-)CD8(+)gammadelta+ and CD4(-)CD8(-)gammadelta+ for mixed ORF5 peptides and CD4(+)CD8(+)gammadelta- and CD4(-)CD8(+)gammadelta+ for IL-12). |
| 964 | 16165219 | Expression of IFNgamma by several T-cell subsets correlated with reduced lung lesions and viremia, whereas expression of CD25 did not. |
| 965 | 16165219 | Expression of surface CD25 did not correlate with IFNgamma production. |
| 966 | 16186238 | Interleukin 1 alpha (IL1alpha), alpha interferon (IFN-alpha), IL6, tumour necrosis factor alpha (TNF-alpha), GROalpha and MIP-1beta mRNA were elevated soon after infection, and expression coincided with virus replication. |
| 967 | 16186238 | A biphasic response was observed for RANTES, IFN-gamma, IL4, IL10 and IL12-p40, with increased mRNA levels early during virus replication followed by a later increase that coincided with pulmonary inflammation. |
| 968 | 16215718 | A phase II trial of vaccination with autologous, tumor-derived heat-shock protein peptide complexes Gp96, in combination with GM-CSF and interferon-alpha in metastatic melanoma patients. |
| 969 | 16215718 | The aim of this study was to determine the immunogenicity and antitumor activity of autologous, tumor-derived heat shock protein gp96-peptide complex vaccine (HSPPC-96; Oncophage given with GM-CSF and IFN-alpha in pre-treated metastatic (AJCC stage IV) melanoma patients. |
| 970 | 16215718 | GM-CSF was given s.c. at the same site at days -1, 0 and +1, while IFN-alpha (3 MU) was administered s.c. at a different site at days +4 and +6. |
| 971 | 16215718 | Vaccination with autologous HSPPC-96 together with GM-CSF and IFN-alpha is feasible and accompanied by mild local and systemic toxicity. |
| 972 | 16215718 | A phase II trial of vaccination with autologous, tumor-derived heat-shock protein peptide complexes Gp96, in combination with GM-CSF and interferon-alpha in metastatic melanoma patients. |
| 973 | 16215718 | The aim of this study was to determine the immunogenicity and antitumor activity of autologous, tumor-derived heat shock protein gp96-peptide complex vaccine (HSPPC-96; Oncophage given with GM-CSF and IFN-alpha in pre-treated metastatic (AJCC stage IV) melanoma patients. |
| 974 | 16215718 | GM-CSF was given s.c. at the same site at days -1, 0 and +1, while IFN-alpha (3 MU) was administered s.c. at a different site at days +4 and +6. |
| 975 | 16215718 | Vaccination with autologous HSPPC-96 together with GM-CSF and IFN-alpha is feasible and accompanied by mild local and systemic toxicity. |
| 976 | 16215718 | A phase II trial of vaccination with autologous, tumor-derived heat-shock protein peptide complexes Gp96, in combination with GM-CSF and interferon-alpha in metastatic melanoma patients. |
| 977 | 16215718 | The aim of this study was to determine the immunogenicity and antitumor activity of autologous, tumor-derived heat shock protein gp96-peptide complex vaccine (HSPPC-96; Oncophage given with GM-CSF and IFN-alpha in pre-treated metastatic (AJCC stage IV) melanoma patients. |
| 978 | 16215718 | GM-CSF was given s.c. at the same site at days -1, 0 and +1, while IFN-alpha (3 MU) was administered s.c. at a different site at days +4 and +6. |
| 979 | 16215718 | Vaccination with autologous HSPPC-96 together with GM-CSF and IFN-alpha is feasible and accompanied by mild local and systemic toxicity. |
| 980 | 16278038 | In comparison to microparticles containing only OVA, bulk cultures of bone marrow-derived plasmacytoid and myeloid dendritic cells produced more (P<0.05) IL-12 and interferon (IFN)-alpha when stimulated with microparticles containing OVA and poly-U. |
| 981 | 16415100 | In vivo antibody blocking experiments revealed that CD8(+) T cells, but not CD4(+) T, NK or NKT cells, were the major effector cells mediating tumor eradication. |
| 982 | 16415100 | Neither IFN-gamma(-/-) nor IL-12(-/-) mice showed impaired induction of tetramer(+) CTLs. |
| 983 | 16415100 | Thus, these findings revealed that CpG-ODN-induced IFN-alpha/beta, but not IL-12 or IFN-gamma, is critical for the generation of tumor-specific CTLs in response to vaccination. |
| 984 | 16499575 | These cells can be generated from peripheral blood monocytes cultured with granulocyte macrophage-colony stimulating factor (GM-CSF) and interleukin-4 (IL-4). |
| 985 | 16499575 | We found that 24-h IFN-alpha co-culture of day 7 monocyte-derived DC generated with GM-CSF and IL-4 induces increased numbers of DC positive for CD54 and CD40 together with the co-stimulatory molecule CD80 but not the activation marker CD83. |
| 986 | 16499575 | Also, IFN-alpha maturation leads to an increase in IP-10 and MCP-1 chemokine secretion, but only a minor increase in IL-12p40 secretion. |
| 987 | 16499575 | These cells can be generated from peripheral blood monocytes cultured with granulocyte macrophage-colony stimulating factor (GM-CSF) and interleukin-4 (IL-4). |
| 988 | 16499575 | We found that 24-h IFN-alpha co-culture of day 7 monocyte-derived DC generated with GM-CSF and IL-4 induces increased numbers of DC positive for CD54 and CD40 together with the co-stimulatory molecule CD80 but not the activation marker CD83. |
| 989 | 16499575 | Also, IFN-alpha maturation leads to an increase in IP-10 and MCP-1 chemokine secretion, but only a minor increase in IL-12p40 secretion. |
| 990 | 16585561 | We have investigated how IFN-alphabeta induces cross-priming, comparing CD8+ T cell responses generated against soluble protein Ags in the presence or absence of IFN-alphabeta. |
| 991 | 16585561 | Injection of IFN-alpha was found to prolong the proliferation and expansion of Ag-specific CD8+ T cells, which was associated with marked up-regulation of IL-2 and IL-15 receptors on Ag-specific cells and expression of IL-15 in the draining lymph node. |
| 992 | 16585561 | Surprisingly, neither IL-2 nor IL-15 was required for IFN-alpha-induced cross-priming. |
| 993 | 16585561 | We have investigated how IFN-alphabeta induces cross-priming, comparing CD8+ T cell responses generated against soluble protein Ags in the presence or absence of IFN-alphabeta. |
| 994 | 16585561 | Injection of IFN-alpha was found to prolong the proliferation and expansion of Ag-specific CD8+ T cells, which was associated with marked up-regulation of IL-2 and IL-15 receptors on Ag-specific cells and expression of IL-15 in the draining lymph node. |
| 995 | 16585561 | Surprisingly, neither IL-2 nor IL-15 was required for IFN-alpha-induced cross-priming. |
| 996 | 16630025 | Interferon-alpha (IFN-alpha) alone was a poor inducer of MoDC maturation, but in association with tumour necrosis factor-alpha (TNF-alpha), or TLR ligands such as lipopolysaccharide and polyinosinic-polycytidylic acid I:C, an up-regulation of major histocompatibility complex II and CD80/86 expression was noted, along with reduced endocytic activity. |
| 997 | 16630025 | Indeed, MoDC did not respond to transmissible gastroenteritis virus (TGEV), whereas NIPC produced high levels of IFN-alpha and TNF-alpha after TGEV stimulation. |
| 998 | 16630025 | Interferon-alpha (IFN-alpha) alone was a poor inducer of MoDC maturation, but in association with tumour necrosis factor-alpha (TNF-alpha), or TLR ligands such as lipopolysaccharide and polyinosinic-polycytidylic acid I:C, an up-regulation of major histocompatibility complex II and CD80/86 expression was noted, along with reduced endocytic activity. |
| 999 | 16630025 | Indeed, MoDC did not respond to transmissible gastroenteritis virus (TGEV), whereas NIPC produced high levels of IFN-alpha and TNF-alpha after TGEV stimulation. |
| 1000 | 16641294 | Neutralization of IFN-alpha with monoclonal antibody (MAb) against one of its receptor chains, IFNAR2, or of IFN-lambda with MAb against either of its receptor chains, IFN-lambdaR1 (interleukin 28R [IL-28R]) or IL-10R2, had a modest effect. |
| 1001 | 16651452 | Immunization of stage IV melanoma patients with Melan-A/MART-1 and gp100 peptides plus IFN-alpha results in the activation of specific CD8(+) T cells and monocyte/dendritic cell precursors. |
| 1002 | 16651452 | We have carried out a pilot phase I-II trial to determine the effects of IFN-alpha, administered as an adjuvant of Melan-A/MART-1:26-35(27L) and gp100:209-217(210M) peptides, on immune responses in stage IV melanoma patients. |
| 1003 | 16651452 | In five of the seven evaluable patients, a consistent enhancement of CD8(+) T cells recognizing modified and native MART-1 and gp100 peptides and MART-1(+)gp100(+) melanoma cells was observed. |
| 1004 | 16651452 | In all patients, treatment augmented significantly the percentage of CD14(+) monocytes and particularly of the CD14(+)CD16(+) cell fraction. |
| 1005 | 16651452 | An increased expression of CD40 and CD86 costimulatory molecules in monocytes was also observed. |
| 1006 | 16651452 | Notably, postvaccination monocytes from two of the three patients showing stable disease or long disease-free survival showed an enhanced antigen-presenting cell function and capability to secrete IP10/CXCL10 when tested in mixed leukocyte reaction assays, associated to a boost of antigen and melanoma-specific CD8(+) T cells. |
| 1007 | 16651452 | Immunization of stage IV melanoma patients with Melan-A/MART-1 and gp100 peptides plus IFN-alpha results in the activation of specific CD8(+) T cells and monocyte/dendritic cell precursors. |
| 1008 | 16651452 | We have carried out a pilot phase I-II trial to determine the effects of IFN-alpha, administered as an adjuvant of Melan-A/MART-1:26-35(27L) and gp100:209-217(210M) peptides, on immune responses in stage IV melanoma patients. |
| 1009 | 16651452 | In five of the seven evaluable patients, a consistent enhancement of CD8(+) T cells recognizing modified and native MART-1 and gp100 peptides and MART-1(+)gp100(+) melanoma cells was observed. |
| 1010 | 16651452 | In all patients, treatment augmented significantly the percentage of CD14(+) monocytes and particularly of the CD14(+)CD16(+) cell fraction. |
| 1011 | 16651452 | An increased expression of CD40 and CD86 costimulatory molecules in monocytes was also observed. |
| 1012 | 16651452 | Notably, postvaccination monocytes from two of the three patients showing stable disease or long disease-free survival showed an enhanced antigen-presenting cell function and capability to secrete IP10/CXCL10 when tested in mixed leukocyte reaction assays, associated to a boost of antigen and melanoma-specific CD8(+) T cells. |
| 1013 | 16672547 | Using the SIV-macaque system to advance oral vaccine research, we examined macaque PDC and MDC biology, identifying ways to activate DCs and boost antiviral immunity. |
| 1014 | 16672547 | Immunostimulatory oligodeoxyribonucleotides (ISS-ODNs) stimulated PDC/MDC mixtures to up-regulate co-stimulatory molecule expression and to secrete both IFN-alpha and IL-12. |
| 1015 | 16672547 | Additionally, ISS-ODNs augmented SIV-specific IFN-gamma responses induced by virus-bearing DCs. |
| 1016 | 16690948 | We hypothesized that plasmacytoid dendritic cells, the cells that provide large amounts of IFN-alpha in response to Toll-like receptor 9 (TLR9) agonists, are defective in neonates. |
| 1017 | 16690948 | TLR9-stimulation of whole blood from adults and neonates resulted in comparable amounts of IFN-alpha production. |
| 1018 | 16690948 | However, we observed small but significant differences in IFN-alpha production from purified CD123+ plasmacytoid dendritic cells from neonates after stimulation with the TLR9 ligand CpG-DNA. |
| 1019 | 16690948 | While purified CD123+ plasmacytoid dendritic cells from adults up-regulated co-stimulatory molecules CD80 and CD86 with IL-3 alone those from neonates required the addition of CpG-DNA to reach adult levels. |
| 1020 | 16690948 | We hypothesized that plasmacytoid dendritic cells, the cells that provide large amounts of IFN-alpha in response to Toll-like receptor 9 (TLR9) agonists, are defective in neonates. |
| 1021 | 16690948 | TLR9-stimulation of whole blood from adults and neonates resulted in comparable amounts of IFN-alpha production. |
| 1022 | 16690948 | However, we observed small but significant differences in IFN-alpha production from purified CD123+ plasmacytoid dendritic cells from neonates after stimulation with the TLR9 ligand CpG-DNA. |
| 1023 | 16690948 | While purified CD123+ plasmacytoid dendritic cells from adults up-regulated co-stimulatory molecules CD80 and CD86 with IL-3 alone those from neonates required the addition of CpG-DNA to reach adult levels. |
| 1024 | 16690948 | We hypothesized that plasmacytoid dendritic cells, the cells that provide large amounts of IFN-alpha in response to Toll-like receptor 9 (TLR9) agonists, are defective in neonates. |
| 1025 | 16690948 | TLR9-stimulation of whole blood from adults and neonates resulted in comparable amounts of IFN-alpha production. |
| 1026 | 16690948 | However, we observed small but significant differences in IFN-alpha production from purified CD123+ plasmacytoid dendritic cells from neonates after stimulation with the TLR9 ligand CpG-DNA. |
| 1027 | 16690948 | While purified CD123+ plasmacytoid dendritic cells from adults up-regulated co-stimulatory molecules CD80 and CD86 with IL-3 alone those from neonates required the addition of CpG-DNA to reach adult levels. |
| 1028 | 16704888 | 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. |
| 1029 | 16704888 | Poly (I:C), a TLR3 ligand, has shown promise as a vaccine adjuvant to CD8(+) T cell responses. |
| 1030 | 16704888 | 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. |
| 1031 | 16704888 | 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. |
| 1032 | 16704888 | 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. |
| 1033 | 16704888 | IFN-alpha and IFN-beta, but not TNF-alpha or IL-6, were able to mimic the adjuvant effects of poly (I:C). |
| 1034 | 16704888 | 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. |
| 1035 | 16704888 | Poly (I:C), a TLR3 ligand, has shown promise as a vaccine adjuvant to CD8(+) T cell responses. |
| 1036 | 16704888 | 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. |
| 1037 | 16704888 | 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. |
| 1038 | 16704888 | 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. |
| 1039 | 16704888 | IFN-alpha and IFN-beta, but not TNF-alpha or IL-6, were able to mimic the adjuvant effects of poly (I:C). |
| 1040 | 16725231 | Because viral infections are known to trigger innate immune responses that lead to the rapid production of Type I Interferons (IFNs), namely IFN-alpha and IFN-beta, we investigated the role of Type I IFNs in the enhanced immunogenicity of replicase-based DNA vaccines. |
| 1041 | 16775317 | The NS1 protein is an important virulence factor associated with the suppression of innate immunity via the inhibition of type I interferon (IFN) production in infected cells. |
| 1042 | 16775317 | Among the genes affected by NS1 are those coding for macrophage inflammatory protein 1beta, interleukin-12 p35 (IL-12 p35), IL-23 p19, RANTES, IL-8, IFN-alpha/beta, and CCR7. |
| 1043 | 16775317 | These results indicate that the influenza A virus NS1 protein is a bifunctional viral immunosuppressor which inhibits innate immunity by preventing type I IFN release and inhibits adaptive immunity by attenuating human DC maturation and the capacity of DCs to induce T-cell responses. |
| 1044 | 16783851 | Modification of TLR-induced activation of human dendritic cells by type I IFN: synergistic interaction with TLR4 but not TLR3 agonists. |
| 1045 | 16783851 | Type I interferon (IFN-alpha/beta), which includes a large family of closely related infection-inducible cytokines, represents one indirect signal that can act as a DC stimulus. |
| 1046 | 16783851 | We have investigated the ability of IFN-alpha/beta subtypes to affect DC function and to influence DC responses to Toll-like receptor (TLR) agonists (i.e., direct infection-associated signals). |
| 1047 | 16783851 | Subtle differences were observed among 15 subtypes of IFN-alpha/beta in the ability to stimulate expression of maturation markers and chemokines by human monocyte-derived DC, with IFN-omega being the most unique in its effects. |
| 1048 | 16783851 | Pre-treatment with IFN-alpha/beta did not alter the ability of DC to mature in response to subsequent contact with TLR agonists, but did modulate their secretion of chemokines. |
| 1049 | 16783851 | Conversely, IFN-alpha/beta was shown to act synergistically with TLR4 but not TLR3 agonists for the induction of maturation and chemokine production when DC were exposed to IFN-alpha/beta and TLR ligands simultaneously. |
| 1050 | 16783851 | Taken together, these results indicate a complex role for IFN-alpha/beta in regulating DC function during the course an infection, which varies according to IFN-alpha/beta subtype and the timing of exposure to other stimuli. |
| 1051 | 16783851 | Modification of TLR-induced activation of human dendritic cells by type I IFN: synergistic interaction with TLR4 but not TLR3 agonists. |
| 1052 | 16783851 | Type I interferon (IFN-alpha/beta), which includes a large family of closely related infection-inducible cytokines, represents one indirect signal that can act as a DC stimulus. |
| 1053 | 16783851 | We have investigated the ability of IFN-alpha/beta subtypes to affect DC function and to influence DC responses to Toll-like receptor (TLR) agonists (i.e., direct infection-associated signals). |
| 1054 | 16783851 | Subtle differences were observed among 15 subtypes of IFN-alpha/beta in the ability to stimulate expression of maturation markers and chemokines by human monocyte-derived DC, with IFN-omega being the most unique in its effects. |
| 1055 | 16783851 | Pre-treatment with IFN-alpha/beta did not alter the ability of DC to mature in response to subsequent contact with TLR agonists, but did modulate their secretion of chemokines. |
| 1056 | 16783851 | Conversely, IFN-alpha/beta was shown to act synergistically with TLR4 but not TLR3 agonists for the induction of maturation and chemokine production when DC were exposed to IFN-alpha/beta and TLR ligands simultaneously. |
| 1057 | 16783851 | Taken together, these results indicate a complex role for IFN-alpha/beta in regulating DC function during the course an infection, which varies according to IFN-alpha/beta subtype and the timing of exposure to other stimuli. |
| 1058 | 16783851 | Modification of TLR-induced activation of human dendritic cells by type I IFN: synergistic interaction with TLR4 but not TLR3 agonists. |
| 1059 | 16783851 | Type I interferon (IFN-alpha/beta), which includes a large family of closely related infection-inducible cytokines, represents one indirect signal that can act as a DC stimulus. |
| 1060 | 16783851 | We have investigated the ability of IFN-alpha/beta subtypes to affect DC function and to influence DC responses to Toll-like receptor (TLR) agonists (i.e., direct infection-associated signals). |
| 1061 | 16783851 | Subtle differences were observed among 15 subtypes of IFN-alpha/beta in the ability to stimulate expression of maturation markers and chemokines by human monocyte-derived DC, with IFN-omega being the most unique in its effects. |
| 1062 | 16783851 | Pre-treatment with IFN-alpha/beta did not alter the ability of DC to mature in response to subsequent contact with TLR agonists, but did modulate their secretion of chemokines. |
| 1063 | 16783851 | Conversely, IFN-alpha/beta was shown to act synergistically with TLR4 but not TLR3 agonists for the induction of maturation and chemokine production when DC were exposed to IFN-alpha/beta and TLR ligands simultaneously. |
| 1064 | 16783851 | Taken together, these results indicate a complex role for IFN-alpha/beta in regulating DC function during the course an infection, which varies according to IFN-alpha/beta subtype and the timing of exposure to other stimuli. |
| 1065 | 16783851 | Modification of TLR-induced activation of human dendritic cells by type I IFN: synergistic interaction with TLR4 but not TLR3 agonists. |
| 1066 | 16783851 | Type I interferon (IFN-alpha/beta), which includes a large family of closely related infection-inducible cytokines, represents one indirect signal that can act as a DC stimulus. |
| 1067 | 16783851 | We have investigated the ability of IFN-alpha/beta subtypes to affect DC function and to influence DC responses to Toll-like receptor (TLR) agonists (i.e., direct infection-associated signals). |
| 1068 | 16783851 | Subtle differences were observed among 15 subtypes of IFN-alpha/beta in the ability to stimulate expression of maturation markers and chemokines by human monocyte-derived DC, with IFN-omega being the most unique in its effects. |
| 1069 | 16783851 | Pre-treatment with IFN-alpha/beta did not alter the ability of DC to mature in response to subsequent contact with TLR agonists, but did modulate their secretion of chemokines. |
| 1070 | 16783851 | Conversely, IFN-alpha/beta was shown to act synergistically with TLR4 but not TLR3 agonists for the induction of maturation and chemokine production when DC were exposed to IFN-alpha/beta and TLR ligands simultaneously. |
| 1071 | 16783851 | Taken together, these results indicate a complex role for IFN-alpha/beta in regulating DC function during the course an infection, which varies according to IFN-alpha/beta subtype and the timing of exposure to other stimuli. |
| 1072 | 16783851 | Modification of TLR-induced activation of human dendritic cells by type I IFN: synergistic interaction with TLR4 but not TLR3 agonists. |
| 1073 | 16783851 | Type I interferon (IFN-alpha/beta), which includes a large family of closely related infection-inducible cytokines, represents one indirect signal that can act as a DC stimulus. |
| 1074 | 16783851 | We have investigated the ability of IFN-alpha/beta subtypes to affect DC function and to influence DC responses to Toll-like receptor (TLR) agonists (i.e., direct infection-associated signals). |
| 1075 | 16783851 | Subtle differences were observed among 15 subtypes of IFN-alpha/beta in the ability to stimulate expression of maturation markers and chemokines by human monocyte-derived DC, with IFN-omega being the most unique in its effects. |
| 1076 | 16783851 | Pre-treatment with IFN-alpha/beta did not alter the ability of DC to mature in response to subsequent contact with TLR agonists, but did modulate their secretion of chemokines. |
| 1077 | 16783851 | Conversely, IFN-alpha/beta was shown to act synergistically with TLR4 but not TLR3 agonists for the induction of maturation and chemokine production when DC were exposed to IFN-alpha/beta and TLR ligands simultaneously. |
| 1078 | 16783851 | Taken together, these results indicate a complex role for IFN-alpha/beta in regulating DC function during the course an infection, which varies according to IFN-alpha/beta subtype and the timing of exposure to other stimuli. |
| 1079 | 16783851 | Modification of TLR-induced activation of human dendritic cells by type I IFN: synergistic interaction with TLR4 but not TLR3 agonists. |
| 1080 | 16783851 | Type I interferon (IFN-alpha/beta), which includes a large family of closely related infection-inducible cytokines, represents one indirect signal that can act as a DC stimulus. |
| 1081 | 16783851 | We have investigated the ability of IFN-alpha/beta subtypes to affect DC function and to influence DC responses to Toll-like receptor (TLR) agonists (i.e., direct infection-associated signals). |
| 1082 | 16783851 | Subtle differences were observed among 15 subtypes of IFN-alpha/beta in the ability to stimulate expression of maturation markers and chemokines by human monocyte-derived DC, with IFN-omega being the most unique in its effects. |
| 1083 | 16783851 | Pre-treatment with IFN-alpha/beta did not alter the ability of DC to mature in response to subsequent contact with TLR agonists, but did modulate their secretion of chemokines. |
| 1084 | 16783851 | Conversely, IFN-alpha/beta was shown to act synergistically with TLR4 but not TLR3 agonists for the induction of maturation and chemokine production when DC were exposed to IFN-alpha/beta and TLR ligands simultaneously. |
| 1085 | 16783851 | Taken together, these results indicate a complex role for IFN-alpha/beta in regulating DC function during the course an infection, which varies according to IFN-alpha/beta subtype and the timing of exposure to other stimuli. |
| 1086 | 16809315 | In contrast, the adjuvant effect of rSFV on coimmunized protein was completely abolished in mice lacking the alpha/beta interferon (IFN-alpha/beta) receptor (IFN-AR1), demonstrating that IFN-alpha/beta signaling was critical for mediating this effect. |
| 1087 | 16810633 | A role for the transcription factor RelB in IFN-alpha production and in IFN-alpha-stimulated cross-priming. |
| 1088 | 16810633 | Although plasmacytoid dendritic cell numbers were similar, serum interferon (IFN)-alpha levels in RelB(-/-) and RelB(+/-) chimeras were markedly lower than in RelB(+/+) chimeras during early LCMV infection. |
| 1089 | 16810633 | Further, both RelB(-/-) and RelB(+/-) chimeras mounted a lower-magnitude LCMV-specific CD8(+) T cell response than their RelB(+/+) counterparts, although the LCMV-specific CD8(+) T cells present were differentiated into functional cytotoxic cells. |
| 1090 | 16810633 | In LCMV-infected RelB(-/-) mice, induction of cross-priming to an independently injected soluble protein, which depends on the IFN-alpha/beta made during the viral infection, was also impaired. |
| 1091 | 16810633 | Notably, provision of exogenous IFN-alpha did not restore the ability of RelB(-/-) mice to cross-prime. |
| 1092 | 16810633 | In summary, these results show that the RelB/NF-kappaB pathway is required for optimal IFN-alpha production after LCMV infection and suggest a crucial role for RelB in IFN-alpha-stimulated cross-priming of CD8(+) T cell responses. |
| 1093 | 16810633 | A role for the transcription factor RelB in IFN-alpha production and in IFN-alpha-stimulated cross-priming. |
| 1094 | 16810633 | Although plasmacytoid dendritic cell numbers were similar, serum interferon (IFN)-alpha levels in RelB(-/-) and RelB(+/-) chimeras were markedly lower than in RelB(+/+) chimeras during early LCMV infection. |
| 1095 | 16810633 | Further, both RelB(-/-) and RelB(+/-) chimeras mounted a lower-magnitude LCMV-specific CD8(+) T cell response than their RelB(+/+) counterparts, although the LCMV-specific CD8(+) T cells present were differentiated into functional cytotoxic cells. |
| 1096 | 16810633 | In LCMV-infected RelB(-/-) mice, induction of cross-priming to an independently injected soluble protein, which depends on the IFN-alpha/beta made during the viral infection, was also impaired. |
| 1097 | 16810633 | Notably, provision of exogenous IFN-alpha did not restore the ability of RelB(-/-) mice to cross-prime. |
| 1098 | 16810633 | In summary, these results show that the RelB/NF-kappaB pathway is required for optimal IFN-alpha production after LCMV infection and suggest a crucial role for RelB in IFN-alpha-stimulated cross-priming of CD8(+) T cell responses. |
| 1099 | 16810633 | A role for the transcription factor RelB in IFN-alpha production and in IFN-alpha-stimulated cross-priming. |
| 1100 | 16810633 | Although plasmacytoid dendritic cell numbers were similar, serum interferon (IFN)-alpha levels in RelB(-/-) and RelB(+/-) chimeras were markedly lower than in RelB(+/+) chimeras during early LCMV infection. |
| 1101 | 16810633 | Further, both RelB(-/-) and RelB(+/-) chimeras mounted a lower-magnitude LCMV-specific CD8(+) T cell response than their RelB(+/+) counterparts, although the LCMV-specific CD8(+) T cells present were differentiated into functional cytotoxic cells. |
| 1102 | 16810633 | In LCMV-infected RelB(-/-) mice, induction of cross-priming to an independently injected soluble protein, which depends on the IFN-alpha/beta made during the viral infection, was also impaired. |
| 1103 | 16810633 | Notably, provision of exogenous IFN-alpha did not restore the ability of RelB(-/-) mice to cross-prime. |
| 1104 | 16810633 | In summary, these results show that the RelB/NF-kappaB pathway is required for optimal IFN-alpha production after LCMV infection and suggest a crucial role for RelB in IFN-alpha-stimulated cross-priming of CD8(+) T cell responses. |
| 1105 | 16810633 | A role for the transcription factor RelB in IFN-alpha production and in IFN-alpha-stimulated cross-priming. |
| 1106 | 16810633 | Although plasmacytoid dendritic cell numbers were similar, serum interferon (IFN)-alpha levels in RelB(-/-) and RelB(+/-) chimeras were markedly lower than in RelB(+/+) chimeras during early LCMV infection. |
| 1107 | 16810633 | Further, both RelB(-/-) and RelB(+/-) chimeras mounted a lower-magnitude LCMV-specific CD8(+) T cell response than their RelB(+/+) counterparts, although the LCMV-specific CD8(+) T cells present were differentiated into functional cytotoxic cells. |
| 1108 | 16810633 | In LCMV-infected RelB(-/-) mice, induction of cross-priming to an independently injected soluble protein, which depends on the IFN-alpha/beta made during the viral infection, was also impaired. |
| 1109 | 16810633 | Notably, provision of exogenous IFN-alpha did not restore the ability of RelB(-/-) mice to cross-prime. |
| 1110 | 16810633 | In summary, these results show that the RelB/NF-kappaB pathway is required for optimal IFN-alpha production after LCMV infection and suggest a crucial role for RelB in IFN-alpha-stimulated cross-priming of CD8(+) T cell responses. |
| 1111 | 16810633 | A role for the transcription factor RelB in IFN-alpha production and in IFN-alpha-stimulated cross-priming. |
| 1112 | 16810633 | Although plasmacytoid dendritic cell numbers were similar, serum interferon (IFN)-alpha levels in RelB(-/-) and RelB(+/-) chimeras were markedly lower than in RelB(+/+) chimeras during early LCMV infection. |
| 1113 | 16810633 | Further, both RelB(-/-) and RelB(+/-) chimeras mounted a lower-magnitude LCMV-specific CD8(+) T cell response than their RelB(+/+) counterparts, although the LCMV-specific CD8(+) T cells present were differentiated into functional cytotoxic cells. |
| 1114 | 16810633 | In LCMV-infected RelB(-/-) mice, induction of cross-priming to an independently injected soluble protein, which depends on the IFN-alpha/beta made during the viral infection, was also impaired. |
| 1115 | 16810633 | Notably, provision of exogenous IFN-alpha did not restore the ability of RelB(-/-) mice to cross-prime. |
| 1116 | 16810633 | In summary, these results show that the RelB/NF-kappaB pathway is required for optimal IFN-alpha production after LCMV infection and suggest a crucial role for RelB in IFN-alpha-stimulated cross-priming of CD8(+) T cell responses. |
| 1117 | 16823922 | The use of transgenic mice expressing a green fluorescent protein reporter gene regulated by an IFN responsive element has shown that IFN-activated cells are present in the peripheral circulation of influenza vaccinated mice as early as 4 h after initiation of IFNalpha treatment and that the principal cell populations activated by IFN treatment included B220 (-) Ly6c (-), CD11c (high), CD11b (high), CD8 (+) cells, and B220 (high), Ly6c (high), CD11c (low), CD11b (-), CD4 (+), CD19 (-) cells. |
| 1118 | 16823922 | Differential display analysis showed that numerous IFN responsive genes were induced in the lymphoid tissue of IFN treated animals together with a number of genes not previously shown to be induced by IFNalpha including Crg2 and other chemokines, proteases associated with antigen processing, and genes involved in lymphocyte activation, apoptosis, and protein degradation. |
| 1119 | 16823922 | The use of transgenic mice expressing a green fluorescent protein reporter gene regulated by an IFN responsive element has shown that IFN-activated cells are present in the peripheral circulation of influenza vaccinated mice as early as 4 h after initiation of IFNalpha treatment and that the principal cell populations activated by IFN treatment included B220 (-) Ly6c (-), CD11c (high), CD11b (high), CD8 (+) cells, and B220 (high), Ly6c (high), CD11c (low), CD11b (-), CD4 (+), CD19 (-) cells. |
| 1120 | 16823922 | Differential display analysis showed that numerous IFN responsive genes were induced in the lymphoid tissue of IFN treated animals together with a number of genes not previously shown to be induced by IFNalpha including Crg2 and other chemokines, proteases associated with antigen processing, and genes involved in lymphocyte activation, apoptosis, and protein degradation. |
| 1121 | 16843517 | Expression of replicon RNA was significantly reduced in the presence of interferon (IFN)-alpha in a dose-dependent manner in the NV replicon-bearing cells, suggesting a role for innate immunity in the control of human norovirus replication. |
| 1122 | 16958969 | Therapy consisted of inoculation of 20 x 10(6) SV-BR-1-GM cells, a unique breast cancer cell line transfected to release sargramostim (granulocyte macrophage colony-stimulating factor [GM-CSF]). |
| 1123 | 16958969 | Interferon (IFN)-alpha, 20,000 IU, was injected into each inoculation site at 48 and 96 hours postinoculation to provide an additional "danger signal." |
| 1124 | 16972041 | Respiratory syncytial virus(RSV)-induced allergy may be controlled by IL-4 and CX3C fractalkine antagonists and CpG ODN as adjuvant: hypothesis and implications for treatment. |
| 1125 | 16972041 | Together with CpG ODNs that induce Toll-like receptor 9(+) (TLR9(+)) plasmacytoid dendritic cells to release type I IFN-alpha and -beta will reactivate the inhibited Th1 cells and the antiviral cytotoxic T leukocytes. |
| 1126 | 17008080 | It was observed that despite differential induction of Interleukin(IL)-12 and IL-10 production, identical IL-12/IL-10 concentration ratio was obtained by all Brucella strains DNAs that was 2 after 24 h and 4 after 5 days of incubation. |
| 1127 | 17008080 | In addition, IL-2 and Interferon(IFN)-gamma production were profoundly increased compared to the medium at day 3 and 5 respectively but IFN-alpha was not induced. |
| 1128 | 17067685 | All three classes of CpG induced IFNalpha and IFNgamma in LNC. |
| 1129 | 17067685 | In contrast, only A and C-class ODN induced IFNalpha and IFNgamma in PBMC. |
| 1130 | 17067685 | All three classes of CpG induced IFNalpha and IFNgamma in LNC. |
| 1131 | 17067685 | In contrast, only A and C-class ODN induced IFNalpha and IFNgamma in PBMC. |
| 1132 | 17068156 | Noninfectious papilloma virus-like particles inhibit HIV-1 replication: implications for immune control of HIV-1 infection by IL-27. |
| 1133 | 17068156 | Recent studies demonstrate that VLPs bind to dendritic cells and induce the expression of antiviral cytokines such as interferon-alpha (IFN-alpha), interleukin-10 (IL-10) and IFN-gamma. |
| 1134 | 17068156 | Here, we show that VLPs suppress the replication of both X4 and R5 HIV-1 without affecting the expression of CD4, CXCR4, and CCR5. |
| 1135 | 17068156 | VLPs induced the genes associated with IFN induction, immune responses, and antiviral responses, among with the recently described cytokine IL-27. |
| 1136 | 17068156 | Subsequently, IL-27 was found to be a potent inhibitor of HIV-1 replication in PBMCs, CD4+ T cells, and macrophages. |
| 1137 | 17068156 | Taken together, our studies identify a novel role of IL-27 in restricting HIV-1 replication and suggest that further examination of the inhibitory property of IL-27 may pave the way for a novel therapy for HIV-1 infection. |
| 1138 | 17092567 | Lack of IFN-alpha/betaR signaling also blocked production of IFN-gamma and TNF-alpha in response to TLR9 activation. |
| 1139 | 17108047 | While the majority of serotypes utilize coxsackievirus-adenovirus receptor (CAR) as their primary attachment receptor, subgroup B and subgroup D Ad37 serotypes use CD46. |
| 1140 | 17108047 | We found that CD46 Ads were capable of alpha interferon (IFN-alpha) induction by peripheral blood mononuclear cells and that plasmacytoid dendritic cells (pDCs) were the principal producers of this cytokine. |
| 1141 | 17108047 | IFN-alpha induction correlated with the permissivity of pDCs to CD46- but not CAR-utilizing Ad serotypes. |
| 1142 | 17108047 | A role for Toll-like receptor 9 (TLR9) recognition of Ad was supported by the requirement for viral DNA and efficient endosomal acidification and by the ability of a TLR9-inhibitory oligonucleotide to attenuate IFN-alpha induction. |
| 1143 | 17108047 | Cell lines expressing TLR9 that are permissive to infection by both CAR- and CD46-utilizing serotypes showed a preferential induction of TLR9-mediated events by CD46-utilizing Ads. |
| 1144 | 17108047 | Specifically, the latter virus types induced higher levels of cytokine expression and NF-kappaB activation in HeLa cells than CAR-dependent Ad types, despite equivalent infection rates. |
| 1145 | 17108047 | While the majority of serotypes utilize coxsackievirus-adenovirus receptor (CAR) as their primary attachment receptor, subgroup B and subgroup D Ad37 serotypes use CD46. |
| 1146 | 17108047 | We found that CD46 Ads were capable of alpha interferon (IFN-alpha) induction by peripheral blood mononuclear cells and that plasmacytoid dendritic cells (pDCs) were the principal producers of this cytokine. |
| 1147 | 17108047 | IFN-alpha induction correlated with the permissivity of pDCs to CD46- but not CAR-utilizing Ad serotypes. |
| 1148 | 17108047 | A role for Toll-like receptor 9 (TLR9) recognition of Ad was supported by the requirement for viral DNA and efficient endosomal acidification and by the ability of a TLR9-inhibitory oligonucleotide to attenuate IFN-alpha induction. |
| 1149 | 17108047 | Cell lines expressing TLR9 that are permissive to infection by both CAR- and CD46-utilizing serotypes showed a preferential induction of TLR9-mediated events by CD46-utilizing Ads. |
| 1150 | 17108047 | Specifically, the latter virus types induced higher levels of cytokine expression and NF-kappaB activation in HeLa cells than CAR-dependent Ad types, despite equivalent infection rates. |
| 1151 | 17108047 | While the majority of serotypes utilize coxsackievirus-adenovirus receptor (CAR) as their primary attachment receptor, subgroup B and subgroup D Ad37 serotypes use CD46. |
| 1152 | 17108047 | We found that CD46 Ads were capable of alpha interferon (IFN-alpha) induction by peripheral blood mononuclear cells and that plasmacytoid dendritic cells (pDCs) were the principal producers of this cytokine. |
| 1153 | 17108047 | IFN-alpha induction correlated with the permissivity of pDCs to CD46- but not CAR-utilizing Ad serotypes. |
| 1154 | 17108047 | A role for Toll-like receptor 9 (TLR9) recognition of Ad was supported by the requirement for viral DNA and efficient endosomal acidification and by the ability of a TLR9-inhibitory oligonucleotide to attenuate IFN-alpha induction. |
| 1155 | 17108047 | Cell lines expressing TLR9 that are permissive to infection by both CAR- and CD46-utilizing serotypes showed a preferential induction of TLR9-mediated events by CD46-utilizing Ads. |
| 1156 | 17108047 | Specifically, the latter virus types induced higher levels of cytokine expression and NF-kappaB activation in HeLa cells than CAR-dependent Ad types, despite equivalent infection rates. |
| 1157 | 17142751 | We have shown that the CpG-C ISS-ODN C274 stimulates macaque blood dendritic cells (DCs) and B cells and augments SIV-specific IFN-gamma responses in vitro. |
| 1158 | 17142751 | This was particularly apparent at the level of CD80 (less so CD86) expression by CD123(+) plasmacytoid DCs and was further boosted in the presence of additional C274 in vitro. |
| 1159 | 17142751 | This was more pronounced when cells were exposed to additional stimuli in vitro, producing IFN-alpha, IL-3, IL-6, IL-12, TNF-alpha, CCL2, CCL3, CCL5, and CXCL8. |
| 1160 | 17142751 | Elevated IFN-alpha, CCL2, and CCL5 were also detected in the plasma after C274 injection. |
| 1161 | 17142751 | We have shown that the CpG-C ISS-ODN C274 stimulates macaque blood dendritic cells (DCs) and B cells and augments SIV-specific IFN-gamma responses in vitro. |
| 1162 | 17142751 | This was particularly apparent at the level of CD80 (less so CD86) expression by CD123(+) plasmacytoid DCs and was further boosted in the presence of additional C274 in vitro. |
| 1163 | 17142751 | This was more pronounced when cells were exposed to additional stimuli in vitro, producing IFN-alpha, IL-3, IL-6, IL-12, TNF-alpha, CCL2, CCL3, CCL5, and CXCL8. |
| 1164 | 17142751 | Elevated IFN-alpha, CCL2, and CCL5 were also detected in the plasma after C274 injection. |
| 1165 | 17143781 | Of the genes tested, 21 genes (IRF-1, IFN 1-2 promoter, IFNAR-1, IRF-10, IFN-gamma, 2',5'-OAS, IAP-1, caspase 8, TRAIL-like, STAT-3, IL-6, IL-8, MIP-3 alpha, MHC-I, MHC-II, TVB, GLVR-1, OTF, IL-13R alpha, ST3GAL-VI and PGK) showed an increased expression. |
| 1166 | 17143781 | The remaining seven genes (IFNAR-2, IFN-alpha, NF-kappaB subunit p65, BLRcp38, DDX1, G6PDH and UB) showed a constant expression or only slight alteration. |
| 1167 | 17198082 | Defining the ability of cyclophosphamide preconditioning to enhance the antigen-specific CD8+ T-cell response to peptide vaccination: creation of a beneficial host microenvironment involving type I IFNs and myeloid cells. |
| 1168 | 17198082 | CTX therapy increased the relative number and activation status of myeloid dendritic cells, and was associated with the induction of significant levels of the inflammatory cytokines interferon-alpha, monocyte chemoattractant protein-1, and IL-6. |
| 1169 | 17198082 | CTX decreased the absolute, but not relative number of CD4+CD25+ Treg cells, consistent with the possibility that regulatory T cells may be targeted by CTX therapy. |
| 1170 | 17240000 | Differences in antiviral efficacy were found among the subtypes with IFNA5 and IFNA6 being most effective, while IFNA1 was the least effective in reducing lung virus replication. |
| 1171 | 17266439 | IFN-alpha-induced murine B16 melanoma cancer vaccine cells: induction and accumulation of cell-associated IL-15. |
| 1172 | 17266439 | Long-term IFN-alpha treatment of B16alpha vaccine cells induced both interleukin-15 (IL-15) mRNA and IL-15 protein. |
| 1173 | 17266439 | These observations suggest that long-term IFN-alpha treatment may induce primarily the truncated isoform of IL-15. |
| 1174 | 17266439 | IFN-alpha-induced murine B16 melanoma cancer vaccine cells: induction and accumulation of cell-associated IL-15. |
| 1175 | 17266439 | Long-term IFN-alpha treatment of B16alpha vaccine cells induced both interleukin-15 (IL-15) mRNA and IL-15 protein. |
| 1176 | 17266439 | These observations suggest that long-term IFN-alpha treatment may induce primarily the truncated isoform of IL-15. |
| 1177 | 17266439 | IFN-alpha-induced murine B16 melanoma cancer vaccine cells: induction and accumulation of cell-associated IL-15. |
| 1178 | 17266439 | Long-term IFN-alpha treatment of B16alpha vaccine cells induced both interleukin-15 (IL-15) mRNA and IL-15 protein. |
| 1179 | 17266439 | These observations suggest that long-term IFN-alpha treatment may induce primarily the truncated isoform of IL-15. |
| 1180 | 17428947 | Five days after infection, these animals produced a potent, innate antiviral immune response by inducing the transcription of signature genes from the interferon (IFN) pathway with demonstrated antiviral activity, such as myxoprotein, 2',5'-oligoadenylate synthetase, phospholipid scramblase 1, and viperin. |
| 1181 | 17428947 | Unexpectedly, no up-regulation of IFN-alpha, -beta, or -gamma genes was detected. |
| 1182 | 17428947 | Transcription of the genes of interleukin-10 (IL-10), IL-8, IL-6, and tumor necrosis factor alpha was neither up-regulated nor down-regulated. |
| 1183 | 17555848 | Our studies indicate that porcine IFN-alpha is a powerful adjuvant for recombinant FMD protein vaccine and could aid in vaccination against FMDV in swine. |
| 1184 | 17590425 | More than 120 primary immunodeficiencies were defined at a molecular level, and biological agents such as TNF-alpha antagonists and IFN-alpha were shown to have therapeutic use. |
| 1185 | 17644436 | The virus inhibits key cytokines, such as IFN-alpha, and may induce regulatory cytokines, such as interleukin (IL)-10. |
| 1186 | 17714025 | In this review, the authors discuss a number of novel biological response modifiers that work as general stimulants of the immune system, through varied mechanisms including induction of stimulatory cytokines (such as IFN-alpha, TNF-alpha and IL-12) and activation of T cells and the antigen-presenting dendritic cells. |
| 1187 | 17855554 | MVA stimulation of bone marrow-derived dendritic cells (DC) showed that plasmacytoid DC were main alpha IFN (IFN-alpha) producers that were triggered independently of productive infection, viral replication, or intermediate and late viral gene expression. |
| 1188 | 17855554 | Increased IFN-alpha levels were induced upon treatment with mildly UV-irradiated MVA, suggesting that a virus-encoded immune modulator(s) interfered with the host cytokine response. |
| 1189 | 17855554 | Mice devoid of Toll-like receptor 9 (TLR9), the receptor for double-stranded DNA, mounted normal IFN-alpha responses upon MVA treatment. |
| 1190 | 17855554 | Furthermore, mice devoid of the adaptors of TLR signaling MyD88 and TRIF and mice deficient in protein kinase R (PKR) showed IFN-alpha responses that were only slightly reduced compared to those of wild-type mice. |
| 1191 | 17855554 | MVA-induced IFN-alpha responses were critically dependent on autocrine/paracrine triggering of the IFN-alpha/beta receptor and were independent of IFN-beta, thus involving "one-half" of a positive-feedback loop. |
| 1192 | 17855554 | MVA stimulation of bone marrow-derived dendritic cells (DC) showed that plasmacytoid DC were main alpha IFN (IFN-alpha) producers that were triggered independently of productive infection, viral replication, or intermediate and late viral gene expression. |
| 1193 | 17855554 | Increased IFN-alpha levels were induced upon treatment with mildly UV-irradiated MVA, suggesting that a virus-encoded immune modulator(s) interfered with the host cytokine response. |
| 1194 | 17855554 | Mice devoid of Toll-like receptor 9 (TLR9), the receptor for double-stranded DNA, mounted normal IFN-alpha responses upon MVA treatment. |
| 1195 | 17855554 | Furthermore, mice devoid of the adaptors of TLR signaling MyD88 and TRIF and mice deficient in protein kinase R (PKR) showed IFN-alpha responses that were only slightly reduced compared to those of wild-type mice. |
| 1196 | 17855554 | MVA-induced IFN-alpha responses were critically dependent on autocrine/paracrine triggering of the IFN-alpha/beta receptor and were independent of IFN-beta, thus involving "one-half" of a positive-feedback loop. |
| 1197 | 17855554 | MVA stimulation of bone marrow-derived dendritic cells (DC) showed that plasmacytoid DC were main alpha IFN (IFN-alpha) producers that were triggered independently of productive infection, viral replication, or intermediate and late viral gene expression. |
| 1198 | 17855554 | Increased IFN-alpha levels were induced upon treatment with mildly UV-irradiated MVA, suggesting that a virus-encoded immune modulator(s) interfered with the host cytokine response. |
| 1199 | 17855554 | Mice devoid of Toll-like receptor 9 (TLR9), the receptor for double-stranded DNA, mounted normal IFN-alpha responses upon MVA treatment. |
| 1200 | 17855554 | Furthermore, mice devoid of the adaptors of TLR signaling MyD88 and TRIF and mice deficient in protein kinase R (PKR) showed IFN-alpha responses that were only slightly reduced compared to those of wild-type mice. |
| 1201 | 17855554 | MVA-induced IFN-alpha responses were critically dependent on autocrine/paracrine triggering of the IFN-alpha/beta receptor and were independent of IFN-beta, thus involving "one-half" of a positive-feedback loop. |
| 1202 | 17855554 | MVA stimulation of bone marrow-derived dendritic cells (DC) showed that plasmacytoid DC were main alpha IFN (IFN-alpha) producers that were triggered independently of productive infection, viral replication, or intermediate and late viral gene expression. |
| 1203 | 17855554 | Increased IFN-alpha levels were induced upon treatment with mildly UV-irradiated MVA, suggesting that a virus-encoded immune modulator(s) interfered with the host cytokine response. |
| 1204 | 17855554 | Mice devoid of Toll-like receptor 9 (TLR9), the receptor for double-stranded DNA, mounted normal IFN-alpha responses upon MVA treatment. |
| 1205 | 17855554 | Furthermore, mice devoid of the adaptors of TLR signaling MyD88 and TRIF and mice deficient in protein kinase R (PKR) showed IFN-alpha responses that were only slightly reduced compared to those of wild-type mice. |
| 1206 | 17855554 | MVA-induced IFN-alpha responses were critically dependent on autocrine/paracrine triggering of the IFN-alpha/beta receptor and were independent of IFN-beta, thus involving "one-half" of a positive-feedback loop. |
| 1207 | 17855554 | MVA stimulation of bone marrow-derived dendritic cells (DC) showed that plasmacytoid DC were main alpha IFN (IFN-alpha) producers that were triggered independently of productive infection, viral replication, or intermediate and late viral gene expression. |
| 1208 | 17855554 | Increased IFN-alpha levels were induced upon treatment with mildly UV-irradiated MVA, suggesting that a virus-encoded immune modulator(s) interfered with the host cytokine response. |
| 1209 | 17855554 | Mice devoid of Toll-like receptor 9 (TLR9), the receptor for double-stranded DNA, mounted normal IFN-alpha responses upon MVA treatment. |
| 1210 | 17855554 | Furthermore, mice devoid of the adaptors of TLR signaling MyD88 and TRIF and mice deficient in protein kinase R (PKR) showed IFN-alpha responses that were only slightly reduced compared to those of wild-type mice. |
| 1211 | 17855554 | MVA-induced IFN-alpha responses were critically dependent on autocrine/paracrine triggering of the IFN-alpha/beta receptor and were independent of IFN-beta, thus involving "one-half" of a positive-feedback loop. |
| 1212 | 17914407 | The gene encoding granulocyte/macrophage colony-stimulating factor (GM-CSF) was inserted as an additional transcription unit at two different positions into the NDV genome. |
| 1213 | 17914407 | Furthermore, rec(GM-CSF) led to a much higher interferon-alpha (IFN-alpha) production than rec(-) when added as virus or as virus-modified vaccine to PBMC. |
| 1214 | 18164612 | In the first study, 60 patients in France and the UK received injections of SRL172, and their survival was compared with that of historical controls who had been treated either with biological response modifiers (IL-2, IFN-alpha) or chemotherapy. |
| 1215 | 18164612 | The first study showed that those treated with SRL172 alone survived equally as long as those receiving IL-2 or IFN-alpha and both treatment groups survived longer than those on chemotherapy (p<0.001), a result supported by Cox's proportional hazards regression analysis. |
| 1216 | 18164612 | In the first study, 60 patients in France and the UK received injections of SRL172, and their survival was compared with that of historical controls who had been treated either with biological response modifiers (IL-2, IFN-alpha) or chemotherapy. |
| 1217 | 18164612 | The first study showed that those treated with SRL172 alone survived equally as long as those receiving IL-2 or IFN-alpha and both treatment groups survived longer than those on chemotherapy (p<0.001), a result supported by Cox's proportional hazards regression analysis. |
| 1218 | 18317362 | Given the perceived need to augment antitumor type-1 immunity (TC1 and Th1) as a therapeutic end point, and the known functional plasticity of DC populations that may display heterogeneous capacity to promote T-cell responses, we sought to identify a preferred DC preparation with this capacity. |
| 1219 | 18317362 | We compared 2 different preparations of monocyte-derived DC using interferon-alpha (IFN-alpha) (IFN-DC and alphaDC1) with classic DCs "matured" (mDCs) using interleukin-1beta/interleukin-6/tumor necrosis factor-alpha/prostaglandin E2, for their ability to promote autologous TC1 antitumor responses from RCC patients in vitro. |
| 1220 | 18317362 | IFN-alpha-conditioned DC promoted significantly higher numbers of RCC-specific CD8+ T cells exhibiting a cytotoxic phenotype after in vitro stimulation (IVS) than cytokine cocktail-mDCs. |
| 1221 | 18317362 | Given the perceived need to augment antitumor type-1 immunity (TC1 and Th1) as a therapeutic end point, and the known functional plasticity of DC populations that may display heterogeneous capacity to promote T-cell responses, we sought to identify a preferred DC preparation with this capacity. |
| 1222 | 18317362 | We compared 2 different preparations of monocyte-derived DC using interferon-alpha (IFN-alpha) (IFN-DC and alphaDC1) with classic DCs "matured" (mDCs) using interleukin-1beta/interleukin-6/tumor necrosis factor-alpha/prostaglandin E2, for their ability to promote autologous TC1 antitumor responses from RCC patients in vitro. |
| 1223 | 18317362 | IFN-alpha-conditioned DC promoted significantly higher numbers of RCC-specific CD8+ T cells exhibiting a cytotoxic phenotype after in vitro stimulation (IVS) than cytokine cocktail-mDCs. |
| 1224 | 18351335 | In addition, T cells from surviving-immunized animals secreted IFNgamma when were co-cultured with IFNalpha-treated B16 melanoma cells or DCs pulsed with melanoma extract. |
| 1225 | 18377354 | The current paper under evaluation described one randomized Phase III trial of the therapeutic vaccine Melacine plus low-dose IFN-alpha(2b), which had an effect comparable to standard high-dose interferon-alpha(2b) but with less toxicity. |
| 1226 | 18400516 | Analysis of the promoters of the salmon IFN-alpha1 and IFN-alpha2 genes shows that activation is dependent on both NFkappaB and IRFs similar to human IFN-beta. |
| 1227 | 18450338 | The current "gold standard" for generation of dendritic cell (DC) used in DC-based cancer vaccine studies is maturation of monocyte-derived DCs with tumor necrosis factor-alpha (TNF-alpha)/IL-1beta/IL-6 and prostaglandin E(2) (PGE(2)). |
| 1228 | 18450338 | Recently, a protocol for producing so-called alpha-Type-1 polarized dendritic cells (alphaDC1) in serum-free medium was published based on maturation of monocyte-derived DCs with TNF-alpha/IL-1-beta/polyinosinic:polycytidylic acid (poly-I:C)/interferon (IFN)-alpha and IFN-gamma. |
| 1229 | 18450338 | We showed that alphaDC1 in this protocol induce lower up-regulation of CD83 and several other maturation markers, co-stimulatory molecules and CCR7 together with higher up-regulation of inhibitory molecules such as PD-L1, ILT2, ILT3 as compared to sDC. |
| 1230 | 18490712 | Here we show that treatment of murine fetal thymic organ cultures (FTOCs) with TLR3 or TLR7 ligands induced rapid expression of IFN-alpha and -beta mRNA, hallmarks of acute and chronic viral infections. |
| 1231 | 18490712 | Down-regulation of IL-7R alpha-chain expression, together with an increased expression of suppressor of cytokine signaling-1 and a concomitant decreased expression of the transcriptional regulator growth factor independence 1 were observed in TLR ligands or IFN-treated FTOCs. |
| 1232 | 18490712 | Because TLR ligands are widely used as vaccine adjuvants, their immunomodulatory actions mediated mainly by IFN-alpha suggested by our results should be taken in consideration. |
| 1233 | 18490712 | Here we show that treatment of murine fetal thymic organ cultures (FTOCs) with TLR3 or TLR7 ligands induced rapid expression of IFN-alpha and -beta mRNA, hallmarks of acute and chronic viral infections. |
| 1234 | 18490712 | Down-regulation of IL-7R alpha-chain expression, together with an increased expression of suppressor of cytokine signaling-1 and a concomitant decreased expression of the transcriptional regulator growth factor independence 1 were observed in TLR ligands or IFN-treated FTOCs. |
| 1235 | 18490712 | Because TLR ligands are widely used as vaccine adjuvants, their immunomodulatory actions mediated mainly by IFN-alpha suggested by our results should be taken in consideration. |
| 1236 | 18490714 | To study this further, we have constructed recombinant vaccinia viruses expressing HIV or hemagglutinin (HA) Ags along with murine type I IFNs, IFN-alpha(4) (HA-VV-IFN-alpha(4)), IFN-beta (HA-VV-IFN-beta), or IFN-epsilon (HIV-VV-IFN-epsilon), a recently discovered member of this family. |
| 1237 | 18490714 | Flow cytofluorometric analysis of B lymphocytes incubated with virally encoded IFN-epsilon showed up-regulation of activation markers CD69 and CD86, while RT-PCR of IFN-epsilon-treated cells revealed that gene expression levels of antiviral proteins were elevated, indicating the induction of an antiviral state. |
| 1238 | 18579593 | The V protein of measles virus is an important virulence factor that can interfere with host innate immunity by inactivating alpha/beta interferon (IFN-alpha/beta) and IFN-gamma signaling through protein interactions with signal transducer and activator of transcription proteins STAT1 and STAT2. |
| 1239 | 18579593 | Here we demonstrate that although STAT1 interference results from protein interactions within a V protein N-terminal region encompassed by amino acids 110 to 130, detection of STAT1 interaction and IFN-gamma signaling inhibition requires the presence of cellular STAT2. |
| 1240 | 18579593 | A more direct target for measles virus V protein-mediated IFN-alpha/beta evasion is STAT2. |
| 1241 | 18579593 | Results indicate that the widely conserved C-terminal zinc finger domain of measles virus V protein is both necessary and sufficient to bind STAT2 and disrupt IFN-alpha/beta signal transduction. |
| 1242 | 18579593 | Mutagenesis and molecular modeling define a contact surface for STAT2 association that includes aspartic acid residue 248 as critical for STAT2 interference and IFN antiviral immune suppression. |
| 1243 | 18579593 | The V protein of measles virus is an important virulence factor that can interfere with host innate immunity by inactivating alpha/beta interferon (IFN-alpha/beta) and IFN-gamma signaling through protein interactions with signal transducer and activator of transcription proteins STAT1 and STAT2. |
| 1244 | 18579593 | Here we demonstrate that although STAT1 interference results from protein interactions within a V protein N-terminal region encompassed by amino acids 110 to 130, detection of STAT1 interaction and IFN-gamma signaling inhibition requires the presence of cellular STAT2. |
| 1245 | 18579593 | A more direct target for measles virus V protein-mediated IFN-alpha/beta evasion is STAT2. |
| 1246 | 18579593 | Results indicate that the widely conserved C-terminal zinc finger domain of measles virus V protein is both necessary and sufficient to bind STAT2 and disrupt IFN-alpha/beta signal transduction. |
| 1247 | 18579593 | Mutagenesis and molecular modeling define a contact surface for STAT2 association that includes aspartic acid residue 248 as critical for STAT2 interference and IFN antiviral immune suppression. |
| 1248 | 18579593 | The V protein of measles virus is an important virulence factor that can interfere with host innate immunity by inactivating alpha/beta interferon (IFN-alpha/beta) and IFN-gamma signaling through protein interactions with signal transducer and activator of transcription proteins STAT1 and STAT2. |
| 1249 | 18579593 | Here we demonstrate that although STAT1 interference results from protein interactions within a V protein N-terminal region encompassed by amino acids 110 to 130, detection of STAT1 interaction and IFN-gamma signaling inhibition requires the presence of cellular STAT2. |
| 1250 | 18579593 | A more direct target for measles virus V protein-mediated IFN-alpha/beta evasion is STAT2. |
| 1251 | 18579593 | Results indicate that the widely conserved C-terminal zinc finger domain of measles virus V protein is both necessary and sufficient to bind STAT2 and disrupt IFN-alpha/beta signal transduction. |
| 1252 | 18579593 | Mutagenesis and molecular modeling define a contact surface for STAT2 association that includes aspartic acid residue 248 as critical for STAT2 interference and IFN antiviral immune suppression. |
| 1253 | 18602433 | When combining them a synergistic up-regulation of the genes interferon (IFN)-alpha1/alpha2, Mx, CXCL10, IL-1beta, IFN-gamma and CD83 was detected. |
| 1254 | 18602433 | Interestingly, synergies between two different CpG ODNs classes also resulted in pronounced IFN-alpha1/alpha2 and IFN-gamma transcripts levels. |
| 1255 | 18632652 | Here, we show that monocyte-derived immature human DCs stimulated with polyinosinic acid:polycytidylic acid, IFN-alpha, tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and IFN-gamma, alpha-type 1-polarized DC (alpha DC1), secrete profuse amounts of the CXCR3 ligand CXCL9/MIG and substantial amounts of CXCL10/IP-10 and CXCL11/I-TAC after withdrawal of maturation stimuli. |
| 1256 | 18632652 | In sharp contrast, no measurable production of these chemokines was found in DCs after maturation with the current gold standard maturation cocktail for human DC-based cancer vaccines consisting of TNF-alpha, IL-1 beta, IL-6, and prostaglandin-E(2) (PGE(2)-DC). |
| 1257 | 18632652 | PGE(2)-DCs preferentially produced the Th2 and regulatory T-cell-attracting chemokines CCL17/TARC and CCL22/MDC, whereas only marginal levels of these chemokines were produced by alpha DC1s. |
| 1258 | 18632652 | Functional studies in vitro showed that supernatants from mature alpha DC1s actively recruited CD3(-)CD56(+) NK cells and that adding anti-CXCL9/MIG antibodies to the alpha DC1 supernatant substantially reduced this recruitment. |
| 1259 | 18632652 | Finally, alpha DC1s were able to induce IFN-gamma production when cocultured with resting autologous NK cells, but only if concurrent CD40 ligation was provided. |
| 1260 | 18632653 | This PGE(2)-induced overproduction of CCL22 and the resulting attraction of FOXP3(+) Tregs are counteracted by IFN alpha, a mediator of acute inflammation, which also restores the ability of the PGE(2)-exposed DC to secrete the Th1-attracting chemokines: CXCL9, CXCL10, CXCL11, and CCL5. |
| 1261 | 18758466 | Inhibition of mTOR or its 'downstream' mediators, the p70 ribosomal S6 protein kinases p70S6K1 and p70S6K2, during pDC activation by Toll-like receptor 9 (TLR9) blocked the interaction of TLR9 with the adaptor MyD88 and subsequent activation of the interferon-regulatory factor IRF7, which resulted in impaired IFN-alpha/beta production. |
| 1262 | 18953536 | Short activation of FL-DC for as little as 4 h induced fully functional DC that rapidly secreted IL-12p70 and IFN-alpha, expressed high levels of costimulatory and MHC molecules and efficiently presented antigen to CD4 and CD8 T cells. |
| 1263 | 18989354 | To further enhance the efficacy of DNA-EP, we have evaluated the toll-like receptor7 (TLR7) agonist-2, 9, substituted 8-hydroxyadenosine derivative or SM360320--as an adjuvant to vaccines against HER2/neu and CEA in BALB-neuT and CEA transgenic mice (CEA.Tg), respectively. |
| 1264 | 18989354 | SM360320 induced in vivo secretion of interferon alpha (IFNalpha) and exerted a significant antitumor effect in CEA.Tg mice challenged with a syngenic tumor cell line expressing CEA and an additive effect with a CEA vaccine. |
| 1265 | 18989354 | These data demonstrate that SM360320 exerts significant antitumor effects and can act in association with DNA-EP for CEA-positive colon cancer and HER2-positive mammary carcinoma. |
| 1266 | 19017955 | Targeting poly(I:C) to the TLR3-independent pathway boosts effector CD8 T cell differentiation through IFN-alpha/beta. |
| 1267 | 19017955 | A higher percentage of Ag-specific CD8 T cells became IFN-gamma and TNF-alpha producers in the absence of TLR3 signaling. |
| 1268 | 19017955 | Ultimately, however, the fundamental mechanism of CD8 effector T cell differentiation through the TLR3-independent pathway was shown to be completely IFN-alpha/beta-dependent. |
| 1269 | 19017955 | Targeting poly(I:C) to the TLR3-independent pathway boosts effector CD8 T cell differentiation through IFN-alpha/beta. |
| 1270 | 19017955 | A higher percentage of Ag-specific CD8 T cells became IFN-gamma and TNF-alpha producers in the absence of TLR3 signaling. |
| 1271 | 19017955 | Ultimately, however, the fundamental mechanism of CD8 effector T cell differentiation through the TLR3-independent pathway was shown to be completely IFN-alpha/beta-dependent. |
| 1272 | 19027322 | Peripheral blood samples were measured by ELISA for plasma levels of IL-2, IL-6, TNF-alpha, IFN-gamma, and IFN-alpha. |
| 1273 | 19027322 | The pattern of production of IFN-gamma was opposite to that of TNF-alpha, but statistical significance was stronger in patients receiving ATT and Dzherelo+Anemin than in Dzherelo group: -34% (P=0.004), +31.9% (P=0.008), and +17.3% (P=0.33), respectively. |
| 1274 | 19054578 | In this study, we evaluated the patterns of TLR2-, TLR3- and TLR9-expressing antigen presenting cells (APCs) in spleen and blood of gnotobiotic (Gn) pigs after colonization with a mixture of two strains of lactic acid bacteria (LAB), Lactobacillus acidophilus and Lactobacillus reuteri or infection with the virulent human rotavirus (HRV) Wa strain. |
| 1275 | 19054578 | We demonstrated that LAB induced strong TLR2-expressing APC responses in blood and spleen, HRV induced a TLR3 response in spleen, and TLR9 responses were induced by either HRV (in spleen) or LAB (in blood). |
| 1276 | 19054578 | LAB and HRV have an additive effect on TLR2- and TLR9-expressing APC responses, consistent with the adjuvant effect of LAB. |
| 1277 | 19054578 | LAB enhanced the IFN-gamma and IL-4 responses in serum, but it had a suppressive effect on the TLR3- and TLR9-expressing CD14- APC responses in spleen and the serum IFN-alpha response induced by HRV. |
| 1278 | 19054578 | These results elucidated the systemic TLR2-, TLR3-, and TLR9-expressing monocyte/macrophage and cDC responses after HRV infection, LAB colonization, and the two combined. |
| 1279 | 19157569 | Of 11 vaccine adjuvants tested, five (i.e. interleukin-2 (IL-2), IL-12, interferon alpha (IFNalpha), polyinosinic and polycytidylic acid, and cytidine-phosphate-guanosine oligodeoxynucleotides (CpG ODN)) significantly enhance CMI response to PRRSV vaccines. |
| 1280 | 19196197 | Role of IL-15 and IL-21 in viral immunity: applications for vaccines and therapies. |
| 1281 | 19196197 | Two recently discovered cytokines (IL-15 and IL-21) appear to be key regulators in this process. |
| 1282 | 19196197 | IL-15 induces an antiviral state during innate immunity through the regulation of IFN-alpha/beta production and natural killer cell proliferation. |
| 1283 | 19196197 | During the memory phase, antigen-specific CD8(+) T cells are highly dependent on IL-15 signaling. |
| 1284 | 19196197 | IL-21 induces natural killer cell maturation and IFN-gamma production and acts to enhance the proliferation of memory CD8(+) T cells, its effects being more pronounced when combined with IL-15. |
| 1285 | 19262501 | A novel regulatory B-cell population in sheep Peyer's patches spontaneously secretes IL-10 and downregulates TLR9-induced IFNalpha responses. |
| 1286 | 19262501 | Peripheral blood mononuclear cells and lymph node cells secreted significant amounts of interferon (IFN)-alpha, IFNgamma, and interleukin (IL)-12 following stimulation with CpG ODN. |
| 1287 | 19262501 | PP cells spontaneously secreted high levels of IL-10, and the primary source of the IL-10 was resting CD5(-)CD11c(-)CD21(+) B cells. |
| 1288 | 19262501 | A novel regulatory B-cell population in sheep Peyer's patches spontaneously secretes IL-10 and downregulates TLR9-induced IFNalpha responses. |
| 1289 | 19262501 | Peripheral blood mononuclear cells and lymph node cells secreted significant amounts of interferon (IFN)-alpha, IFNgamma, and interleukin (IL)-12 following stimulation with CpG ODN. |
| 1290 | 19262501 | PP cells spontaneously secreted high levels of IL-10, and the primary source of the IL-10 was resting CD5(-)CD11c(-)CD21(+) B cells. |
| 1291 | 19342665 | S221 did not replicate well in wild-type mice, but did induce a CD8(+) T cell response, whereas viral replication and a robust CD8(+) T cell response were observed after infection of IFN-alpha/betaR(-/-) mice. |
| 1292 | 19342665 | Depletion of CD8(+) T cells from IFN-alpha/betaR(-/-) mice before infection resulted in significantly higher viral loads compared with undepleted mice. |
| 1293 | 19342665 | Mapping the specificity of the CD8(+) T cell response led to the identification of 12 epitopes derived from 6 of the 10 DENV proteins, with a similar immunodominance hierarchy observed in wild-type and IFN-alpha/betaR(-/-) mice. |
| 1294 | 19342665 | DENV-specific CD8(+) T cells produced IFN-gamma, TNF-alpha, expressed cell surface CD107a, and exhibited cytotoxic activity in vivo. |
| 1295 | 19342665 | S221 did not replicate well in wild-type mice, but did induce a CD8(+) T cell response, whereas viral replication and a robust CD8(+) T cell response were observed after infection of IFN-alpha/betaR(-/-) mice. |
| 1296 | 19342665 | Depletion of CD8(+) T cells from IFN-alpha/betaR(-/-) mice before infection resulted in significantly higher viral loads compared with undepleted mice. |
| 1297 | 19342665 | Mapping the specificity of the CD8(+) T cell response led to the identification of 12 epitopes derived from 6 of the 10 DENV proteins, with a similar immunodominance hierarchy observed in wild-type and IFN-alpha/betaR(-/-) mice. |
| 1298 | 19342665 | DENV-specific CD8(+) T cells produced IFN-gamma, TNF-alpha, expressed cell surface CD107a, and exhibited cytotoxic activity in vivo. |
| 1299 | 19342665 | S221 did not replicate well in wild-type mice, but did induce a CD8(+) T cell response, whereas viral replication and a robust CD8(+) T cell response were observed after infection of IFN-alpha/betaR(-/-) mice. |
| 1300 | 19342665 | Depletion of CD8(+) T cells from IFN-alpha/betaR(-/-) mice before infection resulted in significantly higher viral loads compared with undepleted mice. |
| 1301 | 19342665 | Mapping the specificity of the CD8(+) T cell response led to the identification of 12 epitopes derived from 6 of the 10 DENV proteins, with a similar immunodominance hierarchy observed in wild-type and IFN-alpha/betaR(-/-) mice. |
| 1302 | 19342665 | DENV-specific CD8(+) T cells produced IFN-gamma, TNF-alpha, expressed cell surface CD107a, and exhibited cytotoxic activity in vivo. |
| 1303 | 19428829 | Furthermore, the addition of polyphosphazene to CpG ODN and indolicidin dose-dependently enhanced the secretion of the cytokines IFN-alpha, TNF-alpha and IFN-gammain vitro, indicating that polyphosphazene can also synergize with CpG ODN and indolicidin to stimulate innate immune responses. |
| 1304 | 19428835 | In order to obtain full functional capacity, these DCs need to be maturated, and the current "gold standard" for this process is maturation with TNF-alpha, IL-1beta, IL-6 and PGE(2) used for generating standard DCs (sDC). |
| 1305 | 19428835 | We observed that maturation by IFN-alpha differs from sDC maturation: The major phenotypic change after IFN-alpha maturation was dose-dependent up-regulation of CD38 but not CD83, while sDCs expressed the opposite profile with low CD38 and high CD83 expression. |
| 1306 | 19428835 | Similarly, maturation by Poly I:C leads to CD38high, CD83low DCs indicating a functional relationship between CD38, IFN-alpha and TLR3. |
| 1307 | 19428835 | Thus, CD38 appear to be a relevant marker for activation by TLR3 or IFN-alpha. |
| 1308 | 19428835 | Addition of IFN-alpha to the sDC cocktail results in up-regulation of both CD38 and CD83 and improved capacity for induction of autologous T-cell responses despite few other changes in DC phenotype and cytokine secretion. |
| 1309 | 19428835 | Our observations suggest that IFN-alpha could be included in maturation protocols for clinical grade DCs used for immunotherapy against cancer and should be included if DCs are used for CD8+ T-cell stimulation in vitro. |
| 1310 | 19428835 | In order to obtain full functional capacity, these DCs need to be maturated, and the current "gold standard" for this process is maturation with TNF-alpha, IL-1beta, IL-6 and PGE(2) used for generating standard DCs (sDC). |
| 1311 | 19428835 | We observed that maturation by IFN-alpha differs from sDC maturation: The major phenotypic change after IFN-alpha maturation was dose-dependent up-regulation of CD38 but not CD83, while sDCs expressed the opposite profile with low CD38 and high CD83 expression. |
| 1312 | 19428835 | Similarly, maturation by Poly I:C leads to CD38high, CD83low DCs indicating a functional relationship between CD38, IFN-alpha and TLR3. |
| 1313 | 19428835 | Thus, CD38 appear to be a relevant marker for activation by TLR3 or IFN-alpha. |
| 1314 | 19428835 | Addition of IFN-alpha to the sDC cocktail results in up-regulation of both CD38 and CD83 and improved capacity for induction of autologous T-cell responses despite few other changes in DC phenotype and cytokine secretion. |
| 1315 | 19428835 | Our observations suggest that IFN-alpha could be included in maturation protocols for clinical grade DCs used for immunotherapy against cancer and should be included if DCs are used for CD8+ T-cell stimulation in vitro. |
| 1316 | 19428835 | In order to obtain full functional capacity, these DCs need to be maturated, and the current "gold standard" for this process is maturation with TNF-alpha, IL-1beta, IL-6 and PGE(2) used for generating standard DCs (sDC). |
| 1317 | 19428835 | We observed that maturation by IFN-alpha differs from sDC maturation: The major phenotypic change after IFN-alpha maturation was dose-dependent up-regulation of CD38 but not CD83, while sDCs expressed the opposite profile with low CD38 and high CD83 expression. |
| 1318 | 19428835 | Similarly, maturation by Poly I:C leads to CD38high, CD83low DCs indicating a functional relationship between CD38, IFN-alpha and TLR3. |
| 1319 | 19428835 | Thus, CD38 appear to be a relevant marker for activation by TLR3 or IFN-alpha. |
| 1320 | 19428835 | Addition of IFN-alpha to the sDC cocktail results in up-regulation of both CD38 and CD83 and improved capacity for induction of autologous T-cell responses despite few other changes in DC phenotype and cytokine secretion. |
| 1321 | 19428835 | Our observations suggest that IFN-alpha could be included in maturation protocols for clinical grade DCs used for immunotherapy against cancer and should be included if DCs are used for CD8+ T-cell stimulation in vitro. |
| 1322 | 19428835 | In order to obtain full functional capacity, these DCs need to be maturated, and the current "gold standard" for this process is maturation with TNF-alpha, IL-1beta, IL-6 and PGE(2) used for generating standard DCs (sDC). |
| 1323 | 19428835 | We observed that maturation by IFN-alpha differs from sDC maturation: The major phenotypic change after IFN-alpha maturation was dose-dependent up-regulation of CD38 but not CD83, while sDCs expressed the opposite profile with low CD38 and high CD83 expression. |
| 1324 | 19428835 | Similarly, maturation by Poly I:C leads to CD38high, CD83low DCs indicating a functional relationship between CD38, IFN-alpha and TLR3. |
| 1325 | 19428835 | Thus, CD38 appear to be a relevant marker for activation by TLR3 or IFN-alpha. |
| 1326 | 19428835 | Addition of IFN-alpha to the sDC cocktail results in up-regulation of both CD38 and CD83 and improved capacity for induction of autologous T-cell responses despite few other changes in DC phenotype and cytokine secretion. |
| 1327 | 19428835 | Our observations suggest that IFN-alpha could be included in maturation protocols for clinical grade DCs used for immunotherapy against cancer and should be included if DCs are used for CD8+ T-cell stimulation in vitro. |
| 1328 | 19428835 | In order to obtain full functional capacity, these DCs need to be maturated, and the current "gold standard" for this process is maturation with TNF-alpha, IL-1beta, IL-6 and PGE(2) used for generating standard DCs (sDC). |
| 1329 | 19428835 | We observed that maturation by IFN-alpha differs from sDC maturation: The major phenotypic change after IFN-alpha maturation was dose-dependent up-regulation of CD38 but not CD83, while sDCs expressed the opposite profile with low CD38 and high CD83 expression. |
| 1330 | 19428835 | Similarly, maturation by Poly I:C leads to CD38high, CD83low DCs indicating a functional relationship between CD38, IFN-alpha and TLR3. |
| 1331 | 19428835 | Thus, CD38 appear to be a relevant marker for activation by TLR3 or IFN-alpha. |
| 1332 | 19428835 | Addition of IFN-alpha to the sDC cocktail results in up-regulation of both CD38 and CD83 and improved capacity for induction of autologous T-cell responses despite few other changes in DC phenotype and cytokine secretion. |
| 1333 | 19428835 | Our observations suggest that IFN-alpha could be included in maturation protocols for clinical grade DCs used for immunotherapy against cancer and should be included if DCs are used for CD8+ T-cell stimulation in vitro. |
| 1334 | 19464538 | Moreover, splenocytes of immunized mice exhibited natural killer cell activity accompanied by the production of IFN-alpha and IFN-gamma. |
| 1335 | 19494262 | IFN-alpha enhances peptide vaccine-induced CD8+ T cell numbers, effector function, and antitumor activity. |
| 1336 | 19494262 | Type I IFNs, including IFN-alpha, enhance Ag presentation and promote the expansion, survival, and effector function of CD8(+) CTL during viral infection. |
| 1337 | 19494262 | IFN-alpha dramatically increased the accumulation of gp100-specific, IFN-gamma-secreting, CD8(+) T cells in the tumor through reduced apoptosis and enhanced proliferation of Ag-specific CD8(+) T cells. |
| 1338 | 19494262 | IFN-alpha treatment also greatly increased the long-term maintenance of pmel-1 CD8(+) T cells with an effector memory phenotype, a process that required expression of IFN-alpha receptor on the T cells and IL-15 in the host. |
| 1339 | 19494262 | IFN-alpha enhances peptide vaccine-induced CD8+ T cell numbers, effector function, and antitumor activity. |
| 1340 | 19494262 | Type I IFNs, including IFN-alpha, enhance Ag presentation and promote the expansion, survival, and effector function of CD8(+) CTL during viral infection. |
| 1341 | 19494262 | IFN-alpha dramatically increased the accumulation of gp100-specific, IFN-gamma-secreting, CD8(+) T cells in the tumor through reduced apoptosis and enhanced proliferation of Ag-specific CD8(+) T cells. |
| 1342 | 19494262 | IFN-alpha treatment also greatly increased the long-term maintenance of pmel-1 CD8(+) T cells with an effector memory phenotype, a process that required expression of IFN-alpha receptor on the T cells and IL-15 in the host. |
| 1343 | 19494262 | IFN-alpha enhances peptide vaccine-induced CD8+ T cell numbers, effector function, and antitumor activity. |
| 1344 | 19494262 | Type I IFNs, including IFN-alpha, enhance Ag presentation and promote the expansion, survival, and effector function of CD8(+) CTL during viral infection. |
| 1345 | 19494262 | IFN-alpha dramatically increased the accumulation of gp100-specific, IFN-gamma-secreting, CD8(+) T cells in the tumor through reduced apoptosis and enhanced proliferation of Ag-specific CD8(+) T cells. |
| 1346 | 19494262 | IFN-alpha treatment also greatly increased the long-term maintenance of pmel-1 CD8(+) T cells with an effector memory phenotype, a process that required expression of IFN-alpha receptor on the T cells and IL-15 in the host. |
| 1347 | 19494262 | IFN-alpha enhances peptide vaccine-induced CD8+ T cell numbers, effector function, and antitumor activity. |
| 1348 | 19494262 | Type I IFNs, including IFN-alpha, enhance Ag presentation and promote the expansion, survival, and effector function of CD8(+) CTL during viral infection. |
| 1349 | 19494262 | IFN-alpha dramatically increased the accumulation of gp100-specific, IFN-gamma-secreting, CD8(+) T cells in the tumor through reduced apoptosis and enhanced proliferation of Ag-specific CD8(+) T cells. |
| 1350 | 19494262 | IFN-alpha treatment also greatly increased the long-term maintenance of pmel-1 CD8(+) T cells with an effector memory phenotype, a process that required expression of IFN-alpha receptor on the T cells and IL-15 in the host. |
| 1351 | 19494321 | Bone marrow-derived mesenchymal stromal cells (MSC) possess an immune plasticity manifested by either an immunosuppressive or, when activated with IFN-gamma, an APC phenotype. |
| 1352 | 19494321 | We observed that human MSC and macrophages expressed TLR3 and TLR4 at comparable levels and TLR-mediated activation of MSC resulted in the production of inflammatory mediators such as IL-1beta, IL-6, IL-8/CXCL8, and CCL5. |
| 1353 | 19494321 | IFN-alpha or IFN-gamma priming up-regulated production of these inflammatory mediators and expression of IFNB, inducible NO synthase (iNOS), and TRAIL upon TLR activation in MSC and macrophages, but failed to induce IL-12 and TNF-alpha production in MSC. |
| 1354 | 19494321 | In addition, IFN priming combined with TLR activation may increase immune responses induced by Ag-presenting MSC through presentation of Ag in an inflammatory context, a mechanism that could be applied in a cell-based vaccine. |
| 1355 | 19549606 | Compared to the vaccination with rHBsAg alone, LMS could up-regulate the expressions of TLR7&8, MyD88, IRF7 and their downstream pro-inflammatory cytokines including IFN-alpha and TNF-alpha, which promote DCs activation. |
| 1356 | 19549606 | Strikingly, we find that the combination of LMS and alum adjuvant synergistically enhances immunogenicity of rHBsAg and leads to a robust cell-mediated response demonstrated by the higher level of IgG2a/IgG1, T cell proliferation, and importantly, a high level of antigen-specific CTL and IFN-gamma production within these activated CD8(+) T cells. |
| 1357 | 19561532 | Vaccination of renal cell cancer patients with modified vaccinia Ankara delivering the tumor antigen 5T4 (TroVax) alone or administered in combination with interferon-alpha (IFN-alpha): a phase 2 trial. |
| 1358 | 19561532 | MVA-5T4 has been evaluated in an open-label phase 2 trial in metastatic renal cell cancer patients in which the vaccine was administered alone or in combination with interferon-alpha-2b (IFN-alpha). |
| 1359 | 19561532 | The safety, immunologic, and clinical efficacy of MVA-5T4 with or without IFN-alpha was determined. |
| 1360 | 19561532 | Twenty-eight patients with metastatic renal cell cancer were treated with MVA-5T4 alone (13) or plus IFN-alpha (15). |
| 1361 | 19561532 | One patient treated with MVA-5T4 plus IFN-alpha showed a partial response for >7 months, whereas an additional 14 patients (7 receiving MVA-5T4 plus IFN and 7 receiving MVA-5T4 alone) showed periods of disease stabilization ranging from 1.73 to 9.60 months. |
| 1362 | 19561532 | MVA-5T4 administered alone or in combination with IFN-alpha was well tolerated in all patients. |
| 1363 | 19561532 | Vaccination of renal cell cancer patients with modified vaccinia Ankara delivering the tumor antigen 5T4 (TroVax) alone or administered in combination with interferon-alpha (IFN-alpha): a phase 2 trial. |
| 1364 | 19561532 | MVA-5T4 has been evaluated in an open-label phase 2 trial in metastatic renal cell cancer patients in which the vaccine was administered alone or in combination with interferon-alpha-2b (IFN-alpha). |
| 1365 | 19561532 | The safety, immunologic, and clinical efficacy of MVA-5T4 with or without IFN-alpha was determined. |
| 1366 | 19561532 | Twenty-eight patients with metastatic renal cell cancer were treated with MVA-5T4 alone (13) or plus IFN-alpha (15). |
| 1367 | 19561532 | One patient treated with MVA-5T4 plus IFN-alpha showed a partial response for >7 months, whereas an additional 14 patients (7 receiving MVA-5T4 plus IFN and 7 receiving MVA-5T4 alone) showed periods of disease stabilization ranging from 1.73 to 9.60 months. |
| 1368 | 19561532 | MVA-5T4 administered alone or in combination with IFN-alpha was well tolerated in all patients. |
| 1369 | 19561532 | Vaccination of renal cell cancer patients with modified vaccinia Ankara delivering the tumor antigen 5T4 (TroVax) alone or administered in combination with interferon-alpha (IFN-alpha): a phase 2 trial. |
| 1370 | 19561532 | MVA-5T4 has been evaluated in an open-label phase 2 trial in metastatic renal cell cancer patients in which the vaccine was administered alone or in combination with interferon-alpha-2b (IFN-alpha). |
| 1371 | 19561532 | The safety, immunologic, and clinical efficacy of MVA-5T4 with or without IFN-alpha was determined. |
| 1372 | 19561532 | Twenty-eight patients with metastatic renal cell cancer were treated with MVA-5T4 alone (13) or plus IFN-alpha (15). |
| 1373 | 19561532 | One patient treated with MVA-5T4 plus IFN-alpha showed a partial response for >7 months, whereas an additional 14 patients (7 receiving MVA-5T4 plus IFN and 7 receiving MVA-5T4 alone) showed periods of disease stabilization ranging from 1.73 to 9.60 months. |
| 1374 | 19561532 | MVA-5T4 administered alone or in combination with IFN-alpha was well tolerated in all patients. |
| 1375 | 19561532 | Vaccination of renal cell cancer patients with modified vaccinia Ankara delivering the tumor antigen 5T4 (TroVax) alone or administered in combination with interferon-alpha (IFN-alpha): a phase 2 trial. |
| 1376 | 19561532 | MVA-5T4 has been evaluated in an open-label phase 2 trial in metastatic renal cell cancer patients in which the vaccine was administered alone or in combination with interferon-alpha-2b (IFN-alpha). |
| 1377 | 19561532 | The safety, immunologic, and clinical efficacy of MVA-5T4 with or without IFN-alpha was determined. |
| 1378 | 19561532 | Twenty-eight patients with metastatic renal cell cancer were treated with MVA-5T4 alone (13) or plus IFN-alpha (15). |
| 1379 | 19561532 | One patient treated with MVA-5T4 plus IFN-alpha showed a partial response for >7 months, whereas an additional 14 patients (7 receiving MVA-5T4 plus IFN and 7 receiving MVA-5T4 alone) showed periods of disease stabilization ranging from 1.73 to 9.60 months. |
| 1380 | 19561532 | MVA-5T4 administered alone or in combination with IFN-alpha was well tolerated in all patients. |
| 1381 | 19561532 | Vaccination of renal cell cancer patients with modified vaccinia Ankara delivering the tumor antigen 5T4 (TroVax) alone or administered in combination with interferon-alpha (IFN-alpha): a phase 2 trial. |
| 1382 | 19561532 | MVA-5T4 has been evaluated in an open-label phase 2 trial in metastatic renal cell cancer patients in which the vaccine was administered alone or in combination with interferon-alpha-2b (IFN-alpha). |
| 1383 | 19561532 | The safety, immunologic, and clinical efficacy of MVA-5T4 with or without IFN-alpha was determined. |
| 1384 | 19561532 | Twenty-eight patients with metastatic renal cell cancer were treated with MVA-5T4 alone (13) or plus IFN-alpha (15). |
| 1385 | 19561532 | One patient treated with MVA-5T4 plus IFN-alpha showed a partial response for >7 months, whereas an additional 14 patients (7 receiving MVA-5T4 plus IFN and 7 receiving MVA-5T4 alone) showed periods of disease stabilization ranging from 1.73 to 9.60 months. |
| 1386 | 19561532 | MVA-5T4 administered alone or in combination with IFN-alpha was well tolerated in all patients. |
| 1387 | 19561532 | Vaccination of renal cell cancer patients with modified vaccinia Ankara delivering the tumor antigen 5T4 (TroVax) alone or administered in combination with interferon-alpha (IFN-alpha): a phase 2 trial. |
| 1388 | 19561532 | MVA-5T4 has been evaluated in an open-label phase 2 trial in metastatic renal cell cancer patients in which the vaccine was administered alone or in combination with interferon-alpha-2b (IFN-alpha). |
| 1389 | 19561532 | The safety, immunologic, and clinical efficacy of MVA-5T4 with or without IFN-alpha was determined. |
| 1390 | 19561532 | Twenty-eight patients with metastatic renal cell cancer were treated with MVA-5T4 alone (13) or plus IFN-alpha (15). |
| 1391 | 19561532 | One patient treated with MVA-5T4 plus IFN-alpha showed a partial response for >7 months, whereas an additional 14 patients (7 receiving MVA-5T4 plus IFN and 7 receiving MVA-5T4 alone) showed periods of disease stabilization ranging from 1.73 to 9.60 months. |
| 1392 | 19561532 | MVA-5T4 administered alone or in combination with IFN-alpha was well tolerated in all patients. |
| 1393 | 19642895 | In comparison to B16alpha vaccine cells, long-term IFN-alpha-treated RM-1 cells (RM-1alpha vaccine cells) showed significant IL-15 mRNA induction but relatively low IL-15 protein up-regulation. |
| 1394 | 19667099 | Type I interferon (IFN alpha) acts directly on human memory CD4+ T cells altering their response to antigen. |
| 1395 | 19667099 | The aim of this study was to examine the impact of IFNalpha on the function of human memory CD4(+) T cells using the recall Ags purified protein derivative, tetanus toxoid, and hemagglutinin. |
| 1396 | 19667099 | Purifying the memory CD4(+)CD45RO(+) T cells confirmed IFNalpha acted directly on these cells and not via an intermediate. |
| 1397 | 19667099 | The T cells could be divided into two broad categories depending on how IFNalpha effected their responses to cognate Ag: 1) enhanced proliferation and a striking increase in IFNgamma-production compared with smaller increases in IL-10 (increased ratio of IFNgamma:IL-10), and 2) neutral or diminished proliferation coupled with a smaller increase in IFNgamma relative to the increase in IL-10 (reduced IFNgamma:IL-10 ratio). |
| 1398 | 19730851 | The presence of an anti-interferon (IFN)-alpha antibody resulted in enhanced NDV production kinetics in a dose-dependent manner by blocking binding of NDV-induced IFN to its receptor. |
| 1399 | 19733573 | In this study, we assessed the relationship between stimulation of human purified resting peripheral blood NK cells with one (tumor cell or IFN-alpha) and two (tumor cell+IFN-alpha) signals by measuring IFN-gamma using three different assays. |
| 1400 | 19759147 | The mRNA expression of four immune modulators-alpha interferon (IFN-alpha), oligoadenylate synthetase (OAS), CXCL9, and CXCL10-was positively associated with disease progression within LN tissue. |
| 1401 | 19759147 | Our results indicate that higher IFN-alpha, OAS, CXCL9, and CXCL10 mRNA expression in LN was associated with rapid disease progression and a LN environment that may favor SIV replication. |
| 1402 | 19759147 | The mRNA expression of four immune modulators-alpha interferon (IFN-alpha), oligoadenylate synthetase (OAS), CXCL9, and CXCL10-was positively associated with disease progression within LN tissue. |
| 1403 | 19759147 | Our results indicate that higher IFN-alpha, OAS, CXCL9, and CXCL10 mRNA expression in LN was associated with rapid disease progression and a LN environment that may favor SIV replication. |
| 1404 | 19769732 | Based on our recent studies, efficient CNS tumor homing is a characteristic of cytotoxic T lymphocytes (CTLs) with a type 1 phenotype (Tc1), and this appears to be related to the Tc1 response to the type 1 CXC chemokine ligand (CXCL) 10 [also known as interferon (IFN)-inducible protein (IP)-10] and expression of an integrin receptor very late antigen (VLA)-4 on Tc1. |
| 1405 | 19769732 | In addition, we have previously shown that direct intratumoral delivery of dendritic cells (DCs) ex vivo engineered to secrete IFN-alpha further enhances Tc1 homing via upregulation of CXCL10/IP-10 in the tumor microenvironment. |
| 1406 | 19769732 | As a means to induce IFN-alpha and CXCL10/IP-10 in the CNS tumor microenvironment in a clinically feasible manner, we used administration of polyinosinic-polycytidylic acid stabilized by lysine and carboxymethylcellulose (poly-ICLC), a ligand for toll-like receptor 3 and melanoma differentiation-associated gene 5 (MDA5) in combination with vaccinations targeting CTL epitopes derived from glioma-associated antigens (GAAs). |
| 1407 | 19769732 | Based on our recent studies, efficient CNS tumor homing is a characteristic of cytotoxic T lymphocytes (CTLs) with a type 1 phenotype (Tc1), and this appears to be related to the Tc1 response to the type 1 CXC chemokine ligand (CXCL) 10 [also known as interferon (IFN)-inducible protein (IP)-10] and expression of an integrin receptor very late antigen (VLA)-4 on Tc1. |
| 1408 | 19769732 | In addition, we have previously shown that direct intratumoral delivery of dendritic cells (DCs) ex vivo engineered to secrete IFN-alpha further enhances Tc1 homing via upregulation of CXCL10/IP-10 in the tumor microenvironment. |
| 1409 | 19769732 | As a means to induce IFN-alpha and CXCL10/IP-10 in the CNS tumor microenvironment in a clinically feasible manner, we used administration of polyinosinic-polycytidylic acid stabilized by lysine and carboxymethylcellulose (poly-ICLC), a ligand for toll-like receptor 3 and melanoma differentiation-associated gene 5 (MDA5) in combination with vaccinations targeting CTL epitopes derived from glioma-associated antigens (GAAs). |
| 1410 | 19793807 | Type I interferon (IFN-beta and IFN-alpha) was poorly expressed and gamma IFN (IFN-gamma) potently induced during time periods in which we detected abundant amounts of HSV-2 antigens and HSV-2 RNA. |
| 1411 | 19793807 | IFN-stimulated genes were also markedly upregulated, with expression patterns that more closely matched those in primary human fibroblasts treated by IFN-gamma than those in fibroblasts treated by IFN-beta. |
| 1412 | 19793807 | Transcriptional arrays of the same lesional biopsy sites during healing and at 2 and 4 weeks posthealing revealed no HSV nucleic acids or antigen; however, there was persistent expression of IFN-gamma, with very low levels of IFN-beta and IFN-alpha. |
| 1413 | 19793807 | The findings of extremely low levels of IFN-alpha and IFN-beta, despite the presence of a large number of cells capable of synthesizing these substances, suggest a potent alteration in host defense during HSV-2 infection in vivo. |
| 1414 | 19793807 | Type I interferon (IFN-beta and IFN-alpha) was poorly expressed and gamma IFN (IFN-gamma) potently induced during time periods in which we detected abundant amounts of HSV-2 antigens and HSV-2 RNA. |
| 1415 | 19793807 | IFN-stimulated genes were also markedly upregulated, with expression patterns that more closely matched those in primary human fibroblasts treated by IFN-gamma than those in fibroblasts treated by IFN-beta. |
| 1416 | 19793807 | Transcriptional arrays of the same lesional biopsy sites during healing and at 2 and 4 weeks posthealing revealed no HSV nucleic acids or antigen; however, there was persistent expression of IFN-gamma, with very low levels of IFN-beta and IFN-alpha. |
| 1417 | 19793807 | The findings of extremely low levels of IFN-alpha and IFN-beta, despite the presence of a large number of cells capable of synthesizing these substances, suggest a potent alteration in host defense during HSV-2 infection in vivo. |
| 1418 | 19793807 | Type I interferon (IFN-beta and IFN-alpha) was poorly expressed and gamma IFN (IFN-gamma) potently induced during time periods in which we detected abundant amounts of HSV-2 antigens and HSV-2 RNA. |
| 1419 | 19793807 | IFN-stimulated genes were also markedly upregulated, with expression patterns that more closely matched those in primary human fibroblasts treated by IFN-gamma than those in fibroblasts treated by IFN-beta. |
| 1420 | 19793807 | Transcriptional arrays of the same lesional biopsy sites during healing and at 2 and 4 weeks posthealing revealed no HSV nucleic acids or antigen; however, there was persistent expression of IFN-gamma, with very low levels of IFN-beta and IFN-alpha. |
| 1421 | 19793807 | The findings of extremely low levels of IFN-alpha and IFN-beta, despite the presence of a large number of cells capable of synthesizing these substances, suggest a potent alteration in host defense during HSV-2 infection in vivo. |
| 1422 | 19816561 | Investigation of the role of type I interferon (IFN-alpha/beta) in protection of mice from viscerotropic YFV infection revealed that mice deficient in the IFN-alpha/beta receptor (A129) or the STAT1 signaling molecule (STAT129) were highly susceptible to infection and disease, succumbing within 6-7 days. |
| 1423 | 19816561 | Rapid viremic dissemination and extensive replication in visceral organs, spleen and liver, was associated with severe pathologies in these tissues and dramatically elevated MCP-1 and IL-6 levels, suggestive of a cytokine storm. |
| 1424 | 19819211 | Consistent with this model, mice vaccinated with the specific vaccine rVSV HA had high levels of IFN-alpha in the serum by 24h after challenge/vaccination, developed serum neutralizing Ab to influenza 2 days prior to control animals, and had detectable anti-HA CD8 T cells present in the peripheral blood 3 days prior to control mice. |
| 1425 | 19880818 | Focusing on type I interferon (IFN) expression, we observed that influenza-infected NECs from smokers produced significantly less IFN-alpha than NECs from nonsmokers. |
| 1426 | 19880818 | Similarly, the expression of IRF7, a key transcription factor controlling the expression of IFN-alpha, was significantly decreased in influenza-infected and IFN-beta-stimulated NECs from smokers. |
| 1427 | 19880818 | Furthermore, our data indicate that the DNA methylation of the IRF7 gene and expression of the DNA (cytosine-5-)-methyltransferase 1 was enhanced in NECs from smokers. |
| 1428 | 19880818 | Focusing on type I interferon (IFN) expression, we observed that influenza-infected NECs from smokers produced significantly less IFN-alpha than NECs from nonsmokers. |
| 1429 | 19880818 | Similarly, the expression of IRF7, a key transcription factor controlling the expression of IFN-alpha, was significantly decreased in influenza-infected and IFN-beta-stimulated NECs from smokers. |
| 1430 | 19880818 | Furthermore, our data indicate that the DNA methylation of the IRF7 gene and expression of the DNA (cytosine-5-)-methyltransferase 1 was enhanced in NECs from smokers. |
| 1431 | 19895246 | In the past decade progress has been made, ranging from rather nonspecific stimulations of the immune system with IL-2 and IFN-alpha to more specific approaches based on vaccination with tumor antigens. |
| 1432 | 19896784 | Finally, an inverse correlation seemed to exist between early induction of IFN-alpha and the protection observed, while IL-10 seemed to be differentially regulated in vaccinated and non-vaccinated animals. |
| 1433 | 20028856 | Anti-murine CCL2/CCL12 monoclonal antibodies were administered in three immunotherapy models: one aimed at the human papillomavirus E7 antigen expressed by a non-small cell lung cancer (NSCLC) line, one targeted to mesothelin expressed by a mesothelioma cell line, and one using an adenovirus-expressing IFN-alpha to treat a nonimmunogenic NSCLC line. |
| 1434 | 20042593 | Cell type-specific recognition of human metapneumoviruses (HMPVs) by retinoic acid-inducible gene I (RIG-I) and TLR7 and viral interference of RIG-I ligand recognition by HMPV-B1 phosphoprotein. |
| 1435 | 20042593 | In this study, we investigated the abilities of two prototype strains of HMPV (A1 [NL1 0] and B1 [NL199]) to activate RIG-I and induce type I IFNs. |
| 1436 | 20042593 | Despite the abilities of both HMPV-A1 and HMPV-B1 to infect and replicate in cell lines and primary cells, only the HMPV-A1 strain triggered RIG-I to induce IFNA/B gene transcription. |
| 1437 | 20042593 | The failure of the HMPV-B1 strain to elicit type I IFN production was dependent on the B1 phosphoprotein, which specifically prevented RIG-I-mediated sensing of HMPV viral 5' triphosphate RNA. |
| 1438 | 20042593 | Cell type-specific recognition of human metapneumoviruses (HMPVs) by retinoic acid-inducible gene I (RIG-I) and TLR7 and viral interference of RIG-I ligand recognition by HMPV-B1 phosphoprotein. |
| 1439 | 20042593 | In this study, we investigated the abilities of two prototype strains of HMPV (A1 [NL1 0] and B1 [NL199]) to activate RIG-I and induce type I IFNs. |
| 1440 | 20042593 | Despite the abilities of both HMPV-A1 and HMPV-B1 to infect and replicate in cell lines and primary cells, only the HMPV-A1 strain triggered RIG-I to induce IFNA/B gene transcription. |
| 1441 | 20042593 | The failure of the HMPV-B1 strain to elicit type I IFN production was dependent on the B1 phosphoprotein, which specifically prevented RIG-I-mediated sensing of HMPV viral 5' triphosphate RNA. |
| 1442 | 20042593 | Cell type-specific recognition of human metapneumoviruses (HMPVs) by retinoic acid-inducible gene I (RIG-I) and TLR7 and viral interference of RIG-I ligand recognition by HMPV-B1 phosphoprotein. |
| 1443 | 20042593 | In this study, we investigated the abilities of two prototype strains of HMPV (A1 [NL1 0] and B1 [NL199]) to activate RIG-I and induce type I IFNs. |
| 1444 | 20042593 | Despite the abilities of both HMPV-A1 and HMPV-B1 to infect and replicate in cell lines and primary cells, only the HMPV-A1 strain triggered RIG-I to induce IFNA/B gene transcription. |
| 1445 | 20042593 | The failure of the HMPV-B1 strain to elicit type I IFN production was dependent on the B1 phosphoprotein, which specifically prevented RIG-I-mediated sensing of HMPV viral 5' triphosphate RNA. |
| 1446 | 20051938 | The P/V/C protein of wild-type MV was shown to resist the antiviral effects of interferon (IFN)-alpha. |
| 1447 | 20051938 | IFN-alpha effectively inhibited the replication of MV-Etag and MV-P, but not MV-NPL. |
| 1448 | 20051938 | MV-NPL more efficiently induced cytopathic effects (CPEs) in OS-RC-2 cells, even in the presence of human IFN-alpha. |
| 1449 | 20051938 | The P/V/C protein of wild-type MV was shown to resist the antiviral effects of interferon (IFN)-alpha. |
| 1450 | 20051938 | IFN-alpha effectively inhibited the replication of MV-Etag and MV-P, but not MV-NPL. |
| 1451 | 20051938 | MV-NPL more efficiently induced cytopathic effects (CPEs) in OS-RC-2 cells, even in the presence of human IFN-alpha. |
| 1452 | 20051938 | The P/V/C protein of wild-type MV was shown to resist the antiviral effects of interferon (IFN)-alpha. |
| 1453 | 20051938 | IFN-alpha effectively inhibited the replication of MV-Etag and MV-P, but not MV-NPL. |
| 1454 | 20051938 | MV-NPL more efficiently induced cytopathic effects (CPEs) in OS-RC-2 cells, even in the presence of human IFN-alpha. |
| 1455 | 20099135 | The activity of several potent adjuvants, including incomplete Freund's adjuvant, CpG oligodeoxynucleotides, and alum, has been shown to be due at least in part to the induction of cytokines, including type I interferons (IFNs), IFN-gamma, interleukin-2 (IL-2), and IL-12, that play key roles in the regulation of innate and adaptive immunity. |
| 1456 | 20099135 | Although a number of cytokines including IFN-alpha, IFN-gamma, IL-2, IL-12, IL-15, IL-18, IL-21, GM-CSF, and Flt-3 ligand have been shown to potentiate the immune response to vaccination in various experimental models, the full potential of cytokines as vaccine adjuvants remains to be established. |
| 1457 | 20100933 | We used multicolor flow cytometry and intracellular cytokine staining of myeloid DCs (mDCs) and plasmacytoid DCs (pDCs) and found substantial decreases in older compared with young individuals in TNF-alpha, IL-6, and/or IL-12 (p40) production in mDCs and in TNF-alpha and IFN-alpha production in pDCs in response to TLR1/2, TLR2/6, TLR3, TLR5, and TLR8 engagement in mDCs and TLR7 and TLR9 in pDCs. |
| 1458 | 20117268 | BTV-1 vaccination induced significant cell-mediated immunity (CMI) as determined by lymphoproliferative responses, and increased CD8 T cell, IL-2 and IFN-gamma responses. |
| 1459 | 20117268 | Both naïve and immunized sheep also showed increased CD4 T cell, IL-12 and IFN-alpha responses. |
| 1460 | 20178101 | We have recently proposed that the progression or regression of a tumor lesion in cancer patients undergoing immunotherapy could be predetermined by the molecular mechanism responsible for the MHC Class I alteration and not by the type of immunotherapy used, i.e., interleukin-2 (IL-2), Bacillus Calmette-Guèrin (BCG), interferon-alpha (IFN-alpha), peptides alone, dendritic cells loaded with peptides, protein-bound polysaccharide etc. |
| 1461 | 20219878 | Compared to the levels in the controls, the levels of alpha interferon (IFN-alpha), interleukin-1beta (IL-1beta), IL-12, and IFN-gamma were increased in TBLN homogenates from PRV-infected pigs at 1 dpi, whereas the IL-18 levels were decreased from 3 to 6 dpi. |
| 1462 | 20219878 | The protein levels of IL-4 and IL-10 did not differ between the controls and the PRV-infected pigs at any time point. |
| 1463 | 20219878 | Flow cytometric analysis of TBLN homogenates of PRV-infected pigs and the controls revealed increases in the percentages of B cells at 6 dpi, CD4(+) cells at 14 dpi, and CD25 expression in TBLN homogenates (in the total mononuclear fraction and on B cells) in the PRV-infected pigs. |
| 1464 | 20238400 | This review discusses the impact of alcohol metabolism on HCV replication and the negative impact on interferon (IFN)-alpha treatment, with a particular focus on how alcohol and HCV act synergistically to increase oxidative stress, ultimately leading to exacerbated liver disease and a reduction in the efficacy of IFN-alpha treatment. |
| 1465 | 20390417 | Evidence for this came from the marked increase in the IFN-gamma mRNA expression in CD4+ T cells in the draining inguinal lymph nodes, an increase in the number of functional HER-2/neu-specific CTLs, and the increased tumor infiltration of both CD4+ and CD8+ T cells, depletion of which abolishes the antitumor effect of the HER-2/neu DNA vaccine-AC therapy. |
| 1466 | 20390417 | IL-12, and IFN-alpha) in the draining lymph nodes, which were sufficient to directly stimulate T cell proliferation and higher IFN-gamma production in response to ErbB2. |
| 1467 | 20419155 | The decrease in platelet release was also TfR1-dependent, mimicked by poly(I:C), and type I interferon (IFN alpha/beta) was implicated as a key paracrine mediator. |
| 1468 | 20419155 | Among the relevant molecules studied, only the transcription factor NF-E2 showed a moderate decrease in expression in megakaryocytes from either infected cultures or after type I IFN treatment. |
| 1469 | 20419155 | Moreover, type I IFN-treated megakaryocytes presented ultrastructural abnormalities resembling the reported thrombocytopenic NF-E2(-/-) mouse phenotype. |
| 1470 | 20444892 | To test whether the initial host immune response limits the capacity of mLANA-null virus to traffic to and establish latency in the spleen, we infected type I interferon receptor knockout (IFN-alpha/betaR(-/-)) mice via intranasal inoculation and observed the presence of viral genome-positive splenocytes at day 18 postinfection at approximately 10-fold-lower levels than in the genetically repaired marker rescue-infected mice. |
| 1471 | 20463102 | Peripheral blood mononuclear cells (PBMCs) and cord blood pDCs were stimulated with resiquimod, and alpha interferon (IFN-alpha) production and the pDC phenotype were assessed. |
| 1472 | 20463102 | RV infection did not induce pDC maturation until the age of 6 months, and it reduced TLR7-dependent resiquimod-induced IFN-alpha production similarly in both groups. |
| 1473 | 20463102 | RV is a weak inducer of IFN-alpha production until the age of 6 months and inhibits IFN-alpha responses triggered by the TLR7 pathway. |
| 1474 | 20463102 | Peripheral blood mononuclear cells (PBMCs) and cord blood pDCs were stimulated with resiquimod, and alpha interferon (IFN-alpha) production and the pDC phenotype were assessed. |
| 1475 | 20463102 | RV infection did not induce pDC maturation until the age of 6 months, and it reduced TLR7-dependent resiquimod-induced IFN-alpha production similarly in both groups. |
| 1476 | 20463102 | RV is a weak inducer of IFN-alpha production until the age of 6 months and inhibits IFN-alpha responses triggered by the TLR7 pathway. |
| 1477 | 20463102 | Peripheral blood mononuclear cells (PBMCs) and cord blood pDCs were stimulated with resiquimod, and alpha interferon (IFN-alpha) production and the pDC phenotype were assessed. |
| 1478 | 20463102 | RV infection did not induce pDC maturation until the age of 6 months, and it reduced TLR7-dependent resiquimod-induced IFN-alpha production similarly in both groups. |
| 1479 | 20463102 | RV is a weak inducer of IFN-alpha production until the age of 6 months and inhibits IFN-alpha responses triggered by the TLR7 pathway. |
| 1480 | 20488263 | This FMIA simultaneously detects innate (IL-1 beta, IL-8, IFN-alpha, TNF-alpha, IL-12), regulatory (IL-10), Th1 (IFN-gamma) and Th2 (IL-4) cytokines. |
| 1481 | 20502631 | Furthermore, persistent viral growth was achieved after passaging through IFN-alpha/beta-deficient VeroE6 cells for 2 years. |
| 1482 | 20549206 | Poly-ICLC promotes the infiltration of effector T cells into intracranial gliomas via induction of CXCL10 in IFN-alpha and IFN-gamma dependent manners. |
| 1483 | 20549206 | In this study, we sought to determine critical roles of host IFN-alpha and IFN-gamma pathways in the enhanced therapeutic efficacy mediated by peptide vaccines and polyinosinic-polycytidylic acid [poly(I:C)] stabilized by lysine and carboxymethylcellulose (poly-ICLC) in the murine central nervous system (CNS) GL261 glioma. |
| 1484 | 20549206 | C57BL/6-background wild type (WT), IFN-alpha receptor-1 (IFN-alphaR1)(-/-) or IFN-gamma(-/-) mice bearing syngeneic CNS GL261 glioma received subcutaneous (s.c.) vaccinations with synthetic peptides encoding CTL epitopes with or without intramuscular (i.m.) injections of poly-ICLC. |
| 1485 | 20549206 | Both IFN-alphaR(-/-) and IFN-gamma(-/-) hosts failed to up-regulate the CXCL10 mRNA and recruit Tc1 cells to the tumor site, indicating non-redundant roles of type-1 and type-2 IFNs in the effects of poly-ICLC-assisted vaccines. |
| 1486 | 20549206 | The efficient trafficking of Tc1 also required Tc1-derived IFN-gamma. |
| 1487 | 20549206 | Our data point to critical roles of the host-IFN-alpha and IFN-gamma pathways in the modulation of CNS glioma microenvironment, and the therapeutic effectiveness of poly-ICLC-assisted glioma vaccines. |
| 1488 | 20549206 | Poly-ICLC promotes the infiltration of effector T cells into intracranial gliomas via induction of CXCL10 in IFN-alpha and IFN-gamma dependent manners. |
| 1489 | 20549206 | In this study, we sought to determine critical roles of host IFN-alpha and IFN-gamma pathways in the enhanced therapeutic efficacy mediated by peptide vaccines and polyinosinic-polycytidylic acid [poly(I:C)] stabilized by lysine and carboxymethylcellulose (poly-ICLC) in the murine central nervous system (CNS) GL261 glioma. |
| 1490 | 20549206 | C57BL/6-background wild type (WT), IFN-alpha receptor-1 (IFN-alphaR1)(-/-) or IFN-gamma(-/-) mice bearing syngeneic CNS GL261 glioma received subcutaneous (s.c.) vaccinations with synthetic peptides encoding CTL epitopes with or without intramuscular (i.m.) injections of poly-ICLC. |
| 1491 | 20549206 | Both IFN-alphaR(-/-) and IFN-gamma(-/-) hosts failed to up-regulate the CXCL10 mRNA and recruit Tc1 cells to the tumor site, indicating non-redundant roles of type-1 and type-2 IFNs in the effects of poly-ICLC-assisted vaccines. |
| 1492 | 20549206 | The efficient trafficking of Tc1 also required Tc1-derived IFN-gamma. |
| 1493 | 20549206 | Our data point to critical roles of the host-IFN-alpha and IFN-gamma pathways in the modulation of CNS glioma microenvironment, and the therapeutic effectiveness of poly-ICLC-assisted glioma vaccines. |
| 1494 | 20549206 | Poly-ICLC promotes the infiltration of effector T cells into intracranial gliomas via induction of CXCL10 in IFN-alpha and IFN-gamma dependent manners. |
| 1495 | 20549206 | In this study, we sought to determine critical roles of host IFN-alpha and IFN-gamma pathways in the enhanced therapeutic efficacy mediated by peptide vaccines and polyinosinic-polycytidylic acid [poly(I:C)] stabilized by lysine and carboxymethylcellulose (poly-ICLC) in the murine central nervous system (CNS) GL261 glioma. |
| 1496 | 20549206 | C57BL/6-background wild type (WT), IFN-alpha receptor-1 (IFN-alphaR1)(-/-) or IFN-gamma(-/-) mice bearing syngeneic CNS GL261 glioma received subcutaneous (s.c.) vaccinations with synthetic peptides encoding CTL epitopes with or without intramuscular (i.m.) injections of poly-ICLC. |
| 1497 | 20549206 | Both IFN-alphaR(-/-) and IFN-gamma(-/-) hosts failed to up-regulate the CXCL10 mRNA and recruit Tc1 cells to the tumor site, indicating non-redundant roles of type-1 and type-2 IFNs in the effects of poly-ICLC-assisted vaccines. |
| 1498 | 20549206 | The efficient trafficking of Tc1 also required Tc1-derived IFN-gamma. |
| 1499 | 20549206 | Our data point to critical roles of the host-IFN-alpha and IFN-gamma pathways in the modulation of CNS glioma microenvironment, and the therapeutic effectiveness of poly-ICLC-assisted glioma vaccines. |
| 1500 | 20549206 | Poly-ICLC promotes the infiltration of effector T cells into intracranial gliomas via induction of CXCL10 in IFN-alpha and IFN-gamma dependent manners. |
| 1501 | 20549206 | In this study, we sought to determine critical roles of host IFN-alpha and IFN-gamma pathways in the enhanced therapeutic efficacy mediated by peptide vaccines and polyinosinic-polycytidylic acid [poly(I:C)] stabilized by lysine and carboxymethylcellulose (poly-ICLC) in the murine central nervous system (CNS) GL261 glioma. |
| 1502 | 20549206 | C57BL/6-background wild type (WT), IFN-alpha receptor-1 (IFN-alphaR1)(-/-) or IFN-gamma(-/-) mice bearing syngeneic CNS GL261 glioma received subcutaneous (s.c.) vaccinations with synthetic peptides encoding CTL epitopes with or without intramuscular (i.m.) injections of poly-ICLC. |
| 1503 | 20549206 | Both IFN-alphaR(-/-) and IFN-gamma(-/-) hosts failed to up-regulate the CXCL10 mRNA and recruit Tc1 cells to the tumor site, indicating non-redundant roles of type-1 and type-2 IFNs in the effects of poly-ICLC-assisted vaccines. |
| 1504 | 20549206 | The efficient trafficking of Tc1 also required Tc1-derived IFN-gamma. |
| 1505 | 20549206 | Our data point to critical roles of the host-IFN-alpha and IFN-gamma pathways in the modulation of CNS glioma microenvironment, and the therapeutic effectiveness of poly-ICLC-assisted glioma vaccines. |
| 1506 | 20600391 | While the antiviral response during measles virus (MeV) infection is documented, the contribution of the hosting cell type to the type I interferon (IFN-alpha/beta) response is still not clearly established. |
| 1507 | 20600391 | Here, we report that a signature heterogeneity of the IFN-alpha/beta response according to the cell type. |
| 1508 | 20600391 | In response to both wild type MeV isolates and laboratory/vaccine strains, immature cDCs produced higher levels of IFN-alpha than mature cDCs, despite the reduced expression levels of both CD46 and CD150 receptors by the former ones. |
| 1509 | 20600391 | While in epithelial cells and cDCs the MeV transcription was required to activate the IFN-alpha/beta response, plasmacytoid DCs (pDCs) rapidly produced large amounts of IFN-alpha mostly independently of the viral infection cycle. |
| 1510 | 20600391 | While the antiviral response during measles virus (MeV) infection is documented, the contribution of the hosting cell type to the type I interferon (IFN-alpha/beta) response is still not clearly established. |
| 1511 | 20600391 | Here, we report that a signature heterogeneity of the IFN-alpha/beta response according to the cell type. |
| 1512 | 20600391 | In response to both wild type MeV isolates and laboratory/vaccine strains, immature cDCs produced higher levels of IFN-alpha than mature cDCs, despite the reduced expression levels of both CD46 and CD150 receptors by the former ones. |
| 1513 | 20600391 | While in epithelial cells and cDCs the MeV transcription was required to activate the IFN-alpha/beta response, plasmacytoid DCs (pDCs) rapidly produced large amounts of IFN-alpha mostly independently of the viral infection cycle. |
| 1514 | 20600391 | While the antiviral response during measles virus (MeV) infection is documented, the contribution of the hosting cell type to the type I interferon (IFN-alpha/beta) response is still not clearly established. |
| 1515 | 20600391 | Here, we report that a signature heterogeneity of the IFN-alpha/beta response according to the cell type. |
| 1516 | 20600391 | In response to both wild type MeV isolates and laboratory/vaccine strains, immature cDCs produced higher levels of IFN-alpha than mature cDCs, despite the reduced expression levels of both CD46 and CD150 receptors by the former ones. |
| 1517 | 20600391 | While in epithelial cells and cDCs the MeV transcription was required to activate the IFN-alpha/beta response, plasmacytoid DCs (pDCs) rapidly produced large amounts of IFN-alpha mostly independently of the viral infection cycle. |
| 1518 | 20600391 | While the antiviral response during measles virus (MeV) infection is documented, the contribution of the hosting cell type to the type I interferon (IFN-alpha/beta) response is still not clearly established. |
| 1519 | 20600391 | Here, we report that a signature heterogeneity of the IFN-alpha/beta response according to the cell type. |
| 1520 | 20600391 | In response to both wild type MeV isolates and laboratory/vaccine strains, immature cDCs produced higher levels of IFN-alpha than mature cDCs, despite the reduced expression levels of both CD46 and CD150 receptors by the former ones. |
| 1521 | 20600391 | While in epithelial cells and cDCs the MeV transcription was required to activate the IFN-alpha/beta response, plasmacytoid DCs (pDCs) rapidly produced large amounts of IFN-alpha mostly independently of the viral infection cycle. |
| 1522 | 20631336 | Moreover, the levels of interleukin 1 (IL-1), IL-6, tumor necrosis factor alpha (TNF-alpha), and alpha interferon (IFN-alpha) in peripheral blood were upregulated 7 days postinoculation with HuN4, which was earlier than in the HuN4-F112 group. |
| 1523 | 20635977 | Immunotherapeutic approaches with IL-2 and/or IFN-alpha have become standard regimens in treating metastatic renal cell cancer. |
| 1524 | 20660347 | In these studies we observed that M. tuberculosis, which expresses agonists of both TLR9 and TLR2, did not induce production of IFN-alpha/beta or cross processing by murine DCs. |
| 1525 | 20660347 | Inhibition of the response to one TLR by another may affect the ultimate response to pathogens like M. tuberculosis that express agonists of multiple TLRs, including TLR2 and TLR9. |
| 1526 | 21074276 | Regulation of IgA production in cattle is not completely understood and thus we have focused in part on highly conserved factors such as transforming growth factor beta, Type I and Type 2 interferons, neuropeptides which interdigitate mucosal tissues (vasoactive intestinal peptide or VIP), and a small peptide (IgA inducing peptide or IGIP) which can serve as targets for modulation and increasing SIgA virus-specific antibodies. |
| 1527 | 21074276 | In previous studies in cattle, IgA has been shown to be regulated by several cytokines including IFN-gamma, Type I interferons such as IFN-alpha and IFN-tau, transforming growth factor beta, IgA inducing peptide and other potential factors such as APRIL and BlyS which have not yet been fully evaluated in cattle. |
| 1528 | 21074276 | Many of these factors, namely TGF-beta and Type I interferons block cell cycle progression which is an essential component of Ig class switching and thus these factors require additional regulatory factors such as IL-2 to drive cells through cell cycle resulting in class switch recombination. |
| 1529 | 21556623 | Tumor response and 4 year survival-data of patients with advanced renal-cell carcinoma treated with autologous tumor vaccine and subcutaneous R-IL-2 and IFN-alpha(2b). |
| 1530 | 21556623 | The present analysis was designed to assess the effects of concomitant application of renal cancer vaccine and cytokines on DTH skin responses to tumor cell challenge, clinical remissions and patients survival. 40 patients with advanced RCC, all with distant metastases in at least one organ, were entered after nephrectomy into a protocol involving multiple vaccinations with Newcastle disease virus (NDV)-infected autologous irradiated tumor cells, with subsequent repetitive 3 bi-weekly cycles of low dose interleukin-2 (r-IL-2) and interferon-alpha(2b)/rIFN-alpha(2) s.c. (1.5 million r-IL-2 Cetus units/m(2)/day and 3 million IFN-alpha IU/m(2)/day). |
| 1531 | 21556623 | While the multi-modality treatment with autologous tumor vaccine and s.c. administration of IL-2 and IFN-alpha appears to be effective in advanced RCC, a randomized trial (ASI-IL-2/IFN-alpha vs IL-2/IFN-alpha without ASI) is now set up to help assess the role of ASI within the combined treatment regimen. |
| 1532 | 21556623 | Tumor response and 4 year survival-data of patients with advanced renal-cell carcinoma treated with autologous tumor vaccine and subcutaneous R-IL-2 and IFN-alpha(2b). |
| 1533 | 21556623 | The present analysis was designed to assess the effects of concomitant application of renal cancer vaccine and cytokines on DTH skin responses to tumor cell challenge, clinical remissions and patients survival. 40 patients with advanced RCC, all with distant metastases in at least one organ, were entered after nephrectomy into a protocol involving multiple vaccinations with Newcastle disease virus (NDV)-infected autologous irradiated tumor cells, with subsequent repetitive 3 bi-weekly cycles of low dose interleukin-2 (r-IL-2) and interferon-alpha(2b)/rIFN-alpha(2) s.c. (1.5 million r-IL-2 Cetus units/m(2)/day and 3 million IFN-alpha IU/m(2)/day). |
| 1534 | 21556623 | While the multi-modality treatment with autologous tumor vaccine and s.c. administration of IL-2 and IFN-alpha appears to be effective in advanced RCC, a randomized trial (ASI-IL-2/IFN-alpha vs IL-2/IFN-alpha without ASI) is now set up to help assess the role of ASI within the combined treatment regimen. |
| 1535 | 21556623 | Tumor response and 4 year survival-data of patients with advanced renal-cell carcinoma treated with autologous tumor vaccine and subcutaneous R-IL-2 and IFN-alpha(2b). |
| 1536 | 21556623 | The present analysis was designed to assess the effects of concomitant application of renal cancer vaccine and cytokines on DTH skin responses to tumor cell challenge, clinical remissions and patients survival. 40 patients with advanced RCC, all with distant metastases in at least one organ, were entered after nephrectomy into a protocol involving multiple vaccinations with Newcastle disease virus (NDV)-infected autologous irradiated tumor cells, with subsequent repetitive 3 bi-weekly cycles of low dose interleukin-2 (r-IL-2) and interferon-alpha(2b)/rIFN-alpha(2) s.c. (1.5 million r-IL-2 Cetus units/m(2)/day and 3 million IFN-alpha IU/m(2)/day). |
| 1537 | 21556623 | While the multi-modality treatment with autologous tumor vaccine and s.c. administration of IL-2 and IFN-alpha appears to be effective in advanced RCC, a randomized trial (ASI-IL-2/IFN-alpha vs IL-2/IFN-alpha without ASI) is now set up to help assess the role of ASI within the combined treatment regimen. |
| 1538 | 22083261 | NSs induces a shut-off of host transcription including interferon (IFN)-beta mRNA and promotes degradation of double-stranded RNA-dependent protein kinase (PKR) at the post-translational level. |
| 1539 | 22083261 | IFN-beta is transcriptionally upregulated by interferon regulatory factor 3 (IRF-3), NF-kB and activator protein-1 (AP-1), and the binding of IFN-beta to IFN-alpha/beta receptor (IFNAR) stimulates the transcription of IFN-alpha genes or other interferon stimulated genes (ISGs), which induces host antiviral activities, whereas host transcription suppression including IFN-beta gene by NSs prevents the gene upregulations of those ISGs in response to viral replication although IRF-3, NF-kB and activator protein-1 (AP-1) can be activated by RVFV7. |
| 1540 | 22790963 | In this study, we evaluated the efficacy of the combination of IFN-α-transduced tumor cell vaccines and programmed cell death 1 (PD-1) blockade, and investigated the mechanisms of the antitumor effects of the combined therapy. |
| 1541 | 22790963 | Immunohistochemical analyses of the therapeutic model showed marked infiltration of CD4(+) cells and CD8(+) cells in the established MC38 tumors of mice treated with both IFN-α and anti-PD-1. |
| 1542 | 23050463 | In all three duck species, there was up-regulation of IFN-alpha, IFN-gamma, IL-6, CCL19, RIG-I, and MHC class I and down-regulation of MHC class II, but variable expression of IL-18 and TLR7. |
| 1543 | 24296439 | Inferring from the known organization of IFN pathways, the reason for the more IFN-a production in the HIGH pigs was likely due to the enhanced expression of IRF-7 in TLR or RIG- I/MDA5 signaling pathways. |
| 1544 | 24363758 | We previously identified a human leukocyte antigen (HLA)-A24-restricted antigenic peptide, survivin-2B80-88, a member of the inhibitor of apoptosis protein family, recognized by CD8+cytotoxic T lymphocytes (CTL). |
| 1545 | 24363758 | Therefore, we started a new phase I clinical trial of survivin-2B80-88 vaccination with IFN α for MUC patients. |
| 1546 | 25865470 | Salmon presmolts were injected with a plasmid encoding HE alone or together with a plasmid encoding Atlantic salmon type I IFN (IFNa1, IFNb or IFNc). |
| 1547 | 24743339 | Transcription factors IRF3 (IFN regulatory factor 3) and IRF7, and the positive feedback loop mediated by IFNAR1 (IFN alpha/beta receptor 1), are required for the induction. |
| 1548 | 24743339 | MVA infection of cDCs triggers phosphorylation of TBK1 (Tank-binding kinase 1) and IRF3, which is abolished in the absence of cGAS and STING. |
| 1549 | 24743339 | Furthermore, intravenous delivery of MVA induces type I IFN in wild-type mice, but not in mice lacking STING or IRF3. |
| 1550 | 24743339 | Treatment of cDCs with inhibitors of endosomal and lysosomal acidification or the lysosomal enzyme Cathepsin B attenuated MVA-induced type I IFN production, indicating that lysosomal enzymatic processing of virions is important for MVA sensing. |
| 1551 | 24743339 | We present evidence that vaccinia virulence factors E3 and N1 inhibit the activation of IRF3 and the induction of IFNB gene in MVA-infected cDCs. |