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Gene Information
Gene symbol: TNF
Gene name: tumor necrosis factor
HGNC ID: 11892
Synonyms: TNFSF2, DIF, TNF-alpha
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 1358619 | Intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-asociated antigen-1 (LFA-1) are cell surface adhesion receptors that bind to one another and promote a variety of effector/target cell interactions in tissues affected by inflammatory or immune processes. |
| 2 | 1358619 | As determined by immunocytochemistry and immunoprecipitation using a monoclonal anti-ICAM-1 antibody, interleukin-1-alpha (IL-1a), tumour necrosis factor-alpha (TNFa) and interferon-gamma (IFNg) strongly enhanced surface expression of ICAM-1 in both GO- and normal OF. |
| 3 | 1358619 | No effect was observed in either cell type with interleukin-2, transforming growth factor-beta, or IgGs from patients with HT, RA and normal individuals. |
| 4 | 1358619 | Using phorbol ester-activated, 51Cr-labelled peripheral blood mononuclear cells (PBMCs) in a cell adhesion assay, we demonstrated potent adhesive activity of ICAM-1 in GO-OF pretreated with IL-1a, TNFa, IFNg or Graves' IgGs, while all other compounds did not affect PBMC adhesion to GO-OF. |
| 5 | 1358619 | Intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-asociated antigen-1 (LFA-1) are cell surface adhesion receptors that bind to one another and promote a variety of effector/target cell interactions in tissues affected by inflammatory or immune processes. |
| 6 | 1358619 | As determined by immunocytochemistry and immunoprecipitation using a monoclonal anti-ICAM-1 antibody, interleukin-1-alpha (IL-1a), tumour necrosis factor-alpha (TNFa) and interferon-gamma (IFNg) strongly enhanced surface expression of ICAM-1 in both GO- and normal OF. |
| 7 | 1358619 | No effect was observed in either cell type with interleukin-2, transforming growth factor-beta, or IgGs from patients with HT, RA and normal individuals. |
| 8 | 1358619 | Using phorbol ester-activated, 51Cr-labelled peripheral blood mononuclear cells (PBMCs) in a cell adhesion assay, we demonstrated potent adhesive activity of ICAM-1 in GO-OF pretreated with IL-1a, TNFa, IFNg or Graves' IgGs, while all other compounds did not affect PBMC adhesion to GO-OF. |
| 9 | 1371640 | CD4/CD8 ratio and percentage CD4 were normal in peripheral blood. |
| 10 | 1371640 | Analysis of the pleural effusion revealed an increased CD4/CD8 ratio because of an increased percentage of CD4+CD29+ helper memory T cells, lack of expression of the resting B-cell marker CD21, immune complex deposition and complement consumption, increased relative levels of ANA, abnormally high levels of IL-6 and soluble IL-2R, and detectable levels of IL-1b, IFN-g and TNF-a. |
| 11 | 1399092 | Serial measurements were made during each treatment of interleukin-1 beta (II-1 beta), TNF, soluble IL-2 receptor (sII-2r), soluble CD4 (sCD4), soluble CD8 (sCD8), interferon gamma (IFNg) and neopterin. |
| 12 | 1399092 | In contrast to the known increase of IL-1 beta, IL-2r and TNF with cuprophane membranes, none of the modern high-flux dialyzers stimulated the production of these factors. |
| 13 | 1399092 | Serial measurements were made during each treatment of interleukin-1 beta (II-1 beta), TNF, soluble IL-2 receptor (sII-2r), soluble CD4 (sCD4), soluble CD8 (sCD8), interferon gamma (IFNg) and neopterin. |
| 14 | 1399092 | In contrast to the known increase of IL-1 beta, IL-2r and TNF with cuprophane membranes, none of the modern high-flux dialyzers stimulated the production of these factors. |
| 15 | 1404261 | Cytokines assessed in this study included interleukin-1, IL-1, and tumor necrosis factor (TNF) alpha produced by macrophages, and interleukin-2, IL-2, and gamma interferon (IFN-G) secreted by T-lymphocytes. |
| 16 | 1404261 | Production of IL-2 was suppressed by 14.1-31.9%, and IFN-G was reduced by 8.7-57.0%. |
| 17 | 1404261 | Both IL-1 and TNF are endogenous pyrogens and activate polymorphonuclear leukocytes. |
| 18 | 1404261 | Activities of TNF and IFN-G include antiviral properties and induction of expression of class I and II major histocompatibility complex molecules, which are critical components in the recognition of antigen by T-lymphocytes. |
| 19 | 1404261 | Cytokines assessed in this study included interleukin-1, IL-1, and tumor necrosis factor (TNF) alpha produced by macrophages, and interleukin-2, IL-2, and gamma interferon (IFN-G) secreted by T-lymphocytes. |
| 20 | 1404261 | Production of IL-2 was suppressed by 14.1-31.9%, and IFN-G was reduced by 8.7-57.0%. |
| 21 | 1404261 | Both IL-1 and TNF are endogenous pyrogens and activate polymorphonuclear leukocytes. |
| 22 | 1404261 | Activities of TNF and IFN-G include antiviral properties and induction of expression of class I and II major histocompatibility complex molecules, which are critical components in the recognition of antigen by T-lymphocytes. |
| 23 | 1404261 | Cytokines assessed in this study included interleukin-1, IL-1, and tumor necrosis factor (TNF) alpha produced by macrophages, and interleukin-2, IL-2, and gamma interferon (IFN-G) secreted by T-lymphocytes. |
| 24 | 1404261 | Production of IL-2 was suppressed by 14.1-31.9%, and IFN-G was reduced by 8.7-57.0%. |
| 25 | 1404261 | Both IL-1 and TNF are endogenous pyrogens and activate polymorphonuclear leukocytes. |
| 26 | 1404261 | Activities of TNF and IFN-G include antiviral properties and induction of expression of class I and II major histocompatibility complex molecules, which are critical components in the recognition of antigen by T-lymphocytes. |
| 27 | 1414596 | TNF, IFNg, and GMCSF, to activate neutrophil function against C. albicans. |
| 28 | 1414596 | The cytokine-producing LGL differs from the spontaneous tumoricidal LGL by being DR+; otherwise other markers are identical, i.e., CD2(+)-CD16+CD4-CD8-CD15-. |
| 29 | 1414596 | It is of importance to note that TNF and GMCSF have also been shown to have chemotactic properties on neutrophils (27,28). |
| 30 | 1414596 | Since TNF is a neutrophil activating factor, this implies that neutrophils may self-regulate function in an autocrine manner or utilize released TNF to recruit neighboring PMN. |
| 31 | 1414596 | TNF, IFNg, and GMCSF, to activate neutrophil function against C. albicans. |
| 32 | 1414596 | The cytokine-producing LGL differs from the spontaneous tumoricidal LGL by being DR+; otherwise other markers are identical, i.e., CD2(+)-CD16+CD4-CD8-CD15-. |
| 33 | 1414596 | It is of importance to note that TNF and GMCSF have also been shown to have chemotactic properties on neutrophils (27,28). |
| 34 | 1414596 | Since TNF is a neutrophil activating factor, this implies that neutrophils may self-regulate function in an autocrine manner or utilize released TNF to recruit neighboring PMN. |
| 35 | 1414596 | TNF, IFNg, and GMCSF, to activate neutrophil function against C. albicans. |
| 36 | 1414596 | The cytokine-producing LGL differs from the spontaneous tumoricidal LGL by being DR+; otherwise other markers are identical, i.e., CD2(+)-CD16+CD4-CD8-CD15-. |
| 37 | 1414596 | It is of importance to note that TNF and GMCSF have also been shown to have chemotactic properties on neutrophils (27,28). |
| 38 | 1414596 | Since TNF is a neutrophil activating factor, this implies that neutrophils may self-regulate function in an autocrine manner or utilize released TNF to recruit neighboring PMN. |
| 39 | 1724447 | The 52 kD myeloid membrane glycoprotein CD14 represents the receptor for complexes of lipopolysaccharide (LPS) and LPS binding protein (LBP); it is involved in LPS induced tumor necrosis factor-alpha production. |
| 40 | 1724447 | The effect of rIFNg on CD14 in PBL cultures was dose-dependently inhibited by rIL-4 and this inhibition is probably due to an IL-4 mediated blockade of IFNg secretion. |
| 41 | 1724447 | The results, showing that CD14 antigen expression is upregulated by LPS and downregulated by rIFNg and rIL-4, suggest that the LPS-LBP receptor is involved in the feedback response of IFNg and IL-4 to LPS stimulation. |
| 42 | 1906659 | Differential sensitivity of renal cell carcinoma xenografts towards therapy with interferon-alpha, interferon-gamma, tumor necrosis factor and their combinations. |
| 43 | 1906659 | In the present study we evaluated the antiproliferative effects of human recombinant alpha-interferon (IFN), gamma-interferon and tumor necrosis factor-alpha (TNF) on eight human RCC xenografts. |
| 44 | 1906659 | After 6 weeks of therapy consisting of 150 or 1,500 units IFN/g given s.c. peritumorally three times a week or 30,000 units TNF/g given five times a week, alpha-IFN treatment resulted in 2%-100% growth inhibition; gamma-IFN, in 7%-80%; and TNF, in 35%-75% as compared with the untreated control. |
| 45 | 1906659 | Growth of five of eight tumor lines could be inhibited completely by combinations of IFN and TNF, whereby the tumor dimensions at the beginning of therapy were decisive for the results. |
| 46 | 1906659 | In some cases IFNs had optimal doses; however, the antitumor effects of TNF were always dose-dependent. |
| 47 | 1906659 | Differential sensitivity of renal cell carcinoma xenografts towards therapy with interferon-alpha, interferon-gamma, tumor necrosis factor and their combinations. |
| 48 | 1906659 | In the present study we evaluated the antiproliferative effects of human recombinant alpha-interferon (IFN), gamma-interferon and tumor necrosis factor-alpha (TNF) on eight human RCC xenografts. |
| 49 | 1906659 | After 6 weeks of therapy consisting of 150 or 1,500 units IFN/g given s.c. peritumorally three times a week or 30,000 units TNF/g given five times a week, alpha-IFN treatment resulted in 2%-100% growth inhibition; gamma-IFN, in 7%-80%; and TNF, in 35%-75% as compared with the untreated control. |
| 50 | 1906659 | Growth of five of eight tumor lines could be inhibited completely by combinations of IFN and TNF, whereby the tumor dimensions at the beginning of therapy were decisive for the results. |
| 51 | 1906659 | In some cases IFNs had optimal doses; however, the antitumor effects of TNF were always dose-dependent. |
| 52 | 1906659 | Differential sensitivity of renal cell carcinoma xenografts towards therapy with interferon-alpha, interferon-gamma, tumor necrosis factor and their combinations. |
| 53 | 1906659 | In the present study we evaluated the antiproliferative effects of human recombinant alpha-interferon (IFN), gamma-interferon and tumor necrosis factor-alpha (TNF) on eight human RCC xenografts. |
| 54 | 1906659 | After 6 weeks of therapy consisting of 150 or 1,500 units IFN/g given s.c. peritumorally three times a week or 30,000 units TNF/g given five times a week, alpha-IFN treatment resulted in 2%-100% growth inhibition; gamma-IFN, in 7%-80%; and TNF, in 35%-75% as compared with the untreated control. |
| 55 | 1906659 | Growth of five of eight tumor lines could be inhibited completely by combinations of IFN and TNF, whereby the tumor dimensions at the beginning of therapy were decisive for the results. |
| 56 | 1906659 | In some cases IFNs had optimal doses; however, the antitumor effects of TNF were always dose-dependent. |
| 57 | 1906659 | Differential sensitivity of renal cell carcinoma xenografts towards therapy with interferon-alpha, interferon-gamma, tumor necrosis factor and their combinations. |
| 58 | 1906659 | In the present study we evaluated the antiproliferative effects of human recombinant alpha-interferon (IFN), gamma-interferon and tumor necrosis factor-alpha (TNF) on eight human RCC xenografts. |
| 59 | 1906659 | After 6 weeks of therapy consisting of 150 or 1,500 units IFN/g given s.c. peritumorally three times a week or 30,000 units TNF/g given five times a week, alpha-IFN treatment resulted in 2%-100% growth inhibition; gamma-IFN, in 7%-80%; and TNF, in 35%-75% as compared with the untreated control. |
| 60 | 1906659 | Growth of five of eight tumor lines could be inhibited completely by combinations of IFN and TNF, whereby the tumor dimensions at the beginning of therapy were decisive for the results. |
| 61 | 1906659 | In some cases IFNs had optimal doses; however, the antitumor effects of TNF were always dose-dependent. |
| 62 | 1906659 | Differential sensitivity of renal cell carcinoma xenografts towards therapy with interferon-alpha, interferon-gamma, tumor necrosis factor and their combinations. |
| 63 | 1906659 | In the present study we evaluated the antiproliferative effects of human recombinant alpha-interferon (IFN), gamma-interferon and tumor necrosis factor-alpha (TNF) on eight human RCC xenografts. |
| 64 | 1906659 | After 6 weeks of therapy consisting of 150 or 1,500 units IFN/g given s.c. peritumorally three times a week or 30,000 units TNF/g given five times a week, alpha-IFN treatment resulted in 2%-100% growth inhibition; gamma-IFN, in 7%-80%; and TNF, in 35%-75% as compared with the untreated control. |
| 65 | 1906659 | Growth of five of eight tumor lines could be inhibited completely by combinations of IFN and TNF, whereby the tumor dimensions at the beginning of therapy were decisive for the results. |
| 66 | 1906659 | In some cases IFNs had optimal doses; however, the antitumor effects of TNF were always dose-dependent. |
| 67 | 1974278 | Human melanocyte expression of intercellular adhesion molecule-1 (ICAM-1) with or without stimulation by interferon gamma (IFN-G), tumor necrosis factor alpha (TNF-alpha), or interleukin-1-alpha (IL-1 alpha), was measured utilizing direct immunofluorescence and fluorescence-activated cell sorting (FACS). |
| 68 | 1974278 | Melanocytes grown in vitro expressed low levels of ICAM-1, which could be increased by exposing the cells to IFN-G, TNF-alpha, or IL-1 alpha. |
| 69 | 1974278 | The lowest dose necessary to cause a significant increase in melanocyte ICAM-1 expression was 1 U/ml IFN-G, 0.3 ng/ml TNF-alpha, or 3 U/ml IL-1 alpha. |
| 70 | 1974278 | Melanocytes were most sensitive to TNF-alpha stimulation, with the greatest levels of ICAM-1 expression following 30 ng/ml or more TNF-alpha. |
| 71 | 1974278 | When IFN-G was added to melanocyte cultures in combination with TNF-alpha or IL-1 alpha, there was an additive increase in ICAM-1 expression but no synergy was noted with the combined cytokines. |
| 72 | 1974278 | To our knowledge, this is the first report of melanocyte ICAM-1 induction by TNF-alpha and IL-1 alpha and by physiologically relevant doses of IFN-G. |
| 73 | 1974278 | Human melanocyte expression of intercellular adhesion molecule-1 (ICAM-1) with or without stimulation by interferon gamma (IFN-G), tumor necrosis factor alpha (TNF-alpha), or interleukin-1-alpha (IL-1 alpha), was measured utilizing direct immunofluorescence and fluorescence-activated cell sorting (FACS). |
| 74 | 1974278 | Melanocytes grown in vitro expressed low levels of ICAM-1, which could be increased by exposing the cells to IFN-G, TNF-alpha, or IL-1 alpha. |
| 75 | 1974278 | The lowest dose necessary to cause a significant increase in melanocyte ICAM-1 expression was 1 U/ml IFN-G, 0.3 ng/ml TNF-alpha, or 3 U/ml IL-1 alpha. |
| 76 | 1974278 | Melanocytes were most sensitive to TNF-alpha stimulation, with the greatest levels of ICAM-1 expression following 30 ng/ml or more TNF-alpha. |
| 77 | 1974278 | When IFN-G was added to melanocyte cultures in combination with TNF-alpha or IL-1 alpha, there was an additive increase in ICAM-1 expression but no synergy was noted with the combined cytokines. |
| 78 | 1974278 | To our knowledge, this is the first report of melanocyte ICAM-1 induction by TNF-alpha and IL-1 alpha and by physiologically relevant doses of IFN-G. |
| 79 | 1974278 | Human melanocyte expression of intercellular adhesion molecule-1 (ICAM-1) with or without stimulation by interferon gamma (IFN-G), tumor necrosis factor alpha (TNF-alpha), or interleukin-1-alpha (IL-1 alpha), was measured utilizing direct immunofluorescence and fluorescence-activated cell sorting (FACS). |
| 80 | 1974278 | Melanocytes grown in vitro expressed low levels of ICAM-1, which could be increased by exposing the cells to IFN-G, TNF-alpha, or IL-1 alpha. |
| 81 | 1974278 | The lowest dose necessary to cause a significant increase in melanocyte ICAM-1 expression was 1 U/ml IFN-G, 0.3 ng/ml TNF-alpha, or 3 U/ml IL-1 alpha. |
| 82 | 1974278 | Melanocytes were most sensitive to TNF-alpha stimulation, with the greatest levels of ICAM-1 expression following 30 ng/ml or more TNF-alpha. |
| 83 | 1974278 | When IFN-G was added to melanocyte cultures in combination with TNF-alpha or IL-1 alpha, there was an additive increase in ICAM-1 expression but no synergy was noted with the combined cytokines. |
| 84 | 1974278 | To our knowledge, this is the first report of melanocyte ICAM-1 induction by TNF-alpha and IL-1 alpha and by physiologically relevant doses of IFN-G. |
| 85 | 1974278 | Human melanocyte expression of intercellular adhesion molecule-1 (ICAM-1) with or without stimulation by interferon gamma (IFN-G), tumor necrosis factor alpha (TNF-alpha), or interleukin-1-alpha (IL-1 alpha), was measured utilizing direct immunofluorescence and fluorescence-activated cell sorting (FACS). |
| 86 | 1974278 | Melanocytes grown in vitro expressed low levels of ICAM-1, which could be increased by exposing the cells to IFN-G, TNF-alpha, or IL-1 alpha. |
| 87 | 1974278 | The lowest dose necessary to cause a significant increase in melanocyte ICAM-1 expression was 1 U/ml IFN-G, 0.3 ng/ml TNF-alpha, or 3 U/ml IL-1 alpha. |
| 88 | 1974278 | Melanocytes were most sensitive to TNF-alpha stimulation, with the greatest levels of ICAM-1 expression following 30 ng/ml or more TNF-alpha. |
| 89 | 1974278 | When IFN-G was added to melanocyte cultures in combination with TNF-alpha or IL-1 alpha, there was an additive increase in ICAM-1 expression but no synergy was noted with the combined cytokines. |
| 90 | 1974278 | To our knowledge, this is the first report of melanocyte ICAM-1 induction by TNF-alpha and IL-1 alpha and by physiologically relevant doses of IFN-G. |
| 91 | 1974278 | Human melanocyte expression of intercellular adhesion molecule-1 (ICAM-1) with or without stimulation by interferon gamma (IFN-G), tumor necrosis factor alpha (TNF-alpha), or interleukin-1-alpha (IL-1 alpha), was measured utilizing direct immunofluorescence and fluorescence-activated cell sorting (FACS). |
| 92 | 1974278 | Melanocytes grown in vitro expressed low levels of ICAM-1, which could be increased by exposing the cells to IFN-G, TNF-alpha, or IL-1 alpha. |
| 93 | 1974278 | The lowest dose necessary to cause a significant increase in melanocyte ICAM-1 expression was 1 U/ml IFN-G, 0.3 ng/ml TNF-alpha, or 3 U/ml IL-1 alpha. |
| 94 | 1974278 | Melanocytes were most sensitive to TNF-alpha stimulation, with the greatest levels of ICAM-1 expression following 30 ng/ml or more TNF-alpha. |
| 95 | 1974278 | When IFN-G was added to melanocyte cultures in combination with TNF-alpha or IL-1 alpha, there was an additive increase in ICAM-1 expression but no synergy was noted with the combined cytokines. |
| 96 | 1974278 | To our knowledge, this is the first report of melanocyte ICAM-1 induction by TNF-alpha and IL-1 alpha and by physiologically relevant doses of IFN-G. |
| 97 | 1974278 | Human melanocyte expression of intercellular adhesion molecule-1 (ICAM-1) with or without stimulation by interferon gamma (IFN-G), tumor necrosis factor alpha (TNF-alpha), or interleukin-1-alpha (IL-1 alpha), was measured utilizing direct immunofluorescence and fluorescence-activated cell sorting (FACS). |
| 98 | 1974278 | Melanocytes grown in vitro expressed low levels of ICAM-1, which could be increased by exposing the cells to IFN-G, TNF-alpha, or IL-1 alpha. |
| 99 | 1974278 | The lowest dose necessary to cause a significant increase in melanocyte ICAM-1 expression was 1 U/ml IFN-G, 0.3 ng/ml TNF-alpha, or 3 U/ml IL-1 alpha. |
| 100 | 1974278 | Melanocytes were most sensitive to TNF-alpha stimulation, with the greatest levels of ICAM-1 expression following 30 ng/ml or more TNF-alpha. |
| 101 | 1974278 | When IFN-G was added to melanocyte cultures in combination with TNF-alpha or IL-1 alpha, there was an additive increase in ICAM-1 expression but no synergy was noted with the combined cytokines. |
| 102 | 1974278 | To our knowledge, this is the first report of melanocyte ICAM-1 induction by TNF-alpha and IL-1 alpha and by physiologically relevant doses of IFN-G. |
| 103 | 2056245 | Developmental regulation of the cytokine repertoire in human macrophages: IL-1, IL-6, TNF-alpha, and M-CSF. |
| 104 | 2056245 | For each of the cytokines tested, interleukin (IL)-1 beta, IL-6, tumor necrosis factor (TNF)-alpha, and macrophage colony-stimulating factor (M-CSF), a different pattern of regulation was observed. |
| 105 | 2056245 | From the LPS-dependent cytokines, IL-1 beta and IL-6 were downregulated whereas TNF-alpha levels increased severalfold. |
| 106 | 2056245 | For the release of IL-1 beta, IL-6, and TNF-alpha a synergistic effect of interferon-gamma (IFN-g) and lipopolysaccharide (LPS) was observed. |
| 107 | 2056245 | Upon further cultivation of MAC up to 28 days, LPS-induced IL-1 beta levels remained very low, but IL-6 levels increased again reaching that of blood MO, and TNF-alpha continued to rise reaching levels up to 30-fold higher than in blood MO. |
| 108 | 2056245 | Long-term cultured MAC started to release IL-6 and TNF-alpha also in the absence of a stimulus and, furthermore, became responsive to IFN-g alone. |
| 109 | 2056245 | Developmental regulation of the cytokine repertoire in human macrophages: IL-1, IL-6, TNF-alpha, and M-CSF. |
| 110 | 2056245 | For each of the cytokines tested, interleukin (IL)-1 beta, IL-6, tumor necrosis factor (TNF)-alpha, and macrophage colony-stimulating factor (M-CSF), a different pattern of regulation was observed. |
| 111 | 2056245 | From the LPS-dependent cytokines, IL-1 beta and IL-6 were downregulated whereas TNF-alpha levels increased severalfold. |
| 112 | 2056245 | For the release of IL-1 beta, IL-6, and TNF-alpha a synergistic effect of interferon-gamma (IFN-g) and lipopolysaccharide (LPS) was observed. |
| 113 | 2056245 | Upon further cultivation of MAC up to 28 days, LPS-induced IL-1 beta levels remained very low, but IL-6 levels increased again reaching that of blood MO, and TNF-alpha continued to rise reaching levels up to 30-fold higher than in blood MO. |
| 114 | 2056245 | Long-term cultured MAC started to release IL-6 and TNF-alpha also in the absence of a stimulus and, furthermore, became responsive to IFN-g alone. |
| 115 | 2056245 | Developmental regulation of the cytokine repertoire in human macrophages: IL-1, IL-6, TNF-alpha, and M-CSF. |
| 116 | 2056245 | For each of the cytokines tested, interleukin (IL)-1 beta, IL-6, tumor necrosis factor (TNF)-alpha, and macrophage colony-stimulating factor (M-CSF), a different pattern of regulation was observed. |
| 117 | 2056245 | From the LPS-dependent cytokines, IL-1 beta and IL-6 were downregulated whereas TNF-alpha levels increased severalfold. |
| 118 | 2056245 | For the release of IL-1 beta, IL-6, and TNF-alpha a synergistic effect of interferon-gamma (IFN-g) and lipopolysaccharide (LPS) was observed. |
| 119 | 2056245 | Upon further cultivation of MAC up to 28 days, LPS-induced IL-1 beta levels remained very low, but IL-6 levels increased again reaching that of blood MO, and TNF-alpha continued to rise reaching levels up to 30-fold higher than in blood MO. |
| 120 | 2056245 | Long-term cultured MAC started to release IL-6 and TNF-alpha also in the absence of a stimulus and, furthermore, became responsive to IFN-g alone. |
| 121 | 2056245 | Developmental regulation of the cytokine repertoire in human macrophages: IL-1, IL-6, TNF-alpha, and M-CSF. |
| 122 | 2056245 | For each of the cytokines tested, interleukin (IL)-1 beta, IL-6, tumor necrosis factor (TNF)-alpha, and macrophage colony-stimulating factor (M-CSF), a different pattern of regulation was observed. |
| 123 | 2056245 | From the LPS-dependent cytokines, IL-1 beta and IL-6 were downregulated whereas TNF-alpha levels increased severalfold. |
| 124 | 2056245 | For the release of IL-1 beta, IL-6, and TNF-alpha a synergistic effect of interferon-gamma (IFN-g) and lipopolysaccharide (LPS) was observed. |
| 125 | 2056245 | Upon further cultivation of MAC up to 28 days, LPS-induced IL-1 beta levels remained very low, but IL-6 levels increased again reaching that of blood MO, and TNF-alpha continued to rise reaching levels up to 30-fold higher than in blood MO. |
| 126 | 2056245 | Long-term cultured MAC started to release IL-6 and TNF-alpha also in the absence of a stimulus and, furthermore, became responsive to IFN-g alone. |
| 127 | 2056245 | Developmental regulation of the cytokine repertoire in human macrophages: IL-1, IL-6, TNF-alpha, and M-CSF. |
| 128 | 2056245 | For each of the cytokines tested, interleukin (IL)-1 beta, IL-6, tumor necrosis factor (TNF)-alpha, and macrophage colony-stimulating factor (M-CSF), a different pattern of regulation was observed. |
| 129 | 2056245 | From the LPS-dependent cytokines, IL-1 beta and IL-6 were downregulated whereas TNF-alpha levels increased severalfold. |
| 130 | 2056245 | For the release of IL-1 beta, IL-6, and TNF-alpha a synergistic effect of interferon-gamma (IFN-g) and lipopolysaccharide (LPS) was observed. |
| 131 | 2056245 | Upon further cultivation of MAC up to 28 days, LPS-induced IL-1 beta levels remained very low, but IL-6 levels increased again reaching that of blood MO, and TNF-alpha continued to rise reaching levels up to 30-fold higher than in blood MO. |
| 132 | 2056245 | Long-term cultured MAC started to release IL-6 and TNF-alpha also in the absence of a stimulus and, furthermore, became responsive to IFN-g alone. |
| 133 | 2056245 | Developmental regulation of the cytokine repertoire in human macrophages: IL-1, IL-6, TNF-alpha, and M-CSF. |
| 134 | 2056245 | For each of the cytokines tested, interleukin (IL)-1 beta, IL-6, tumor necrosis factor (TNF)-alpha, and macrophage colony-stimulating factor (M-CSF), a different pattern of regulation was observed. |
| 135 | 2056245 | From the LPS-dependent cytokines, IL-1 beta and IL-6 were downregulated whereas TNF-alpha levels increased severalfold. |
| 136 | 2056245 | For the release of IL-1 beta, IL-6, and TNF-alpha a synergistic effect of interferon-gamma (IFN-g) and lipopolysaccharide (LPS) was observed. |
| 137 | 2056245 | Upon further cultivation of MAC up to 28 days, LPS-induced IL-1 beta levels remained very low, but IL-6 levels increased again reaching that of blood MO, and TNF-alpha continued to rise reaching levels up to 30-fold higher than in blood MO. |
| 138 | 2056245 | Long-term cultured MAC started to release IL-6 and TNF-alpha also in the absence of a stimulus and, furthermore, became responsive to IFN-g alone. |
| 139 | 2106180 | In this study, we evaluated intragraft mechanisms responsible for these effects by immunoperoxidase localization of relevant humoral mediators (IgG, IgM, C3, cross-linked fibrin), graft infiltrating cells (GIC), and associated cytokines (IL-2, IFN-g, tumor necrosis factor [TNF], or cytokine receptors (IL-2R). |
| 140 | 2106180 | By 18 hr, up to 20% of GIC were IFN-g+, 10% were IL-2R+, and 10% were IL-2+, consistent with labeling of 20% of cells with OX-22. |
| 141 | 2106180 | In addition to the reduction in neutrophils, Ig and C3, fewer IL-2R+ (6%) and OX-22+ (3%) cells, considerably less TNF and TF, and almost no IL-2+ or IFN-g+ GIC (less than 1%) were detected. |
| 142 | 2106180 | In this study, we evaluated intragraft mechanisms responsible for these effects by immunoperoxidase localization of relevant humoral mediators (IgG, IgM, C3, cross-linked fibrin), graft infiltrating cells (GIC), and associated cytokines (IL-2, IFN-g, tumor necrosis factor [TNF], or cytokine receptors (IL-2R). |
| 143 | 2106180 | By 18 hr, up to 20% of GIC were IFN-g+, 10% were IL-2R+, and 10% were IL-2+, consistent with labeling of 20% of cells with OX-22. |
| 144 | 2106180 | In addition to the reduction in neutrophils, Ig and C3, fewer IL-2R+ (6%) and OX-22+ (3%) cells, considerably less TNF and TF, and almost no IL-2+ or IFN-g+ GIC (less than 1%) were detected. |
| 145 | 2113589 | When used in combination with interferon gamma (IFNG) or chemotherapeutic drugs targeted at DNA topoisomerase II, synergistic cytotoxicity has been observed. |
| 146 | 2113589 | The cytotoxicity of TNF and low dose actinomycin-D (AMD) against MBT-2 in vitro was examined alone and following preincubation with IFNG. |
| 147 | 2113589 | The activity of TNF/AMD in vivo utilizing an intravesical implantation mode (MBT-2) was also evaluated. |
| 148 | 2113589 | TNF/AMD was cytotoxic for MBT-2 growth in vitro. |
| 149 | 2113589 | A two hour preincubation with IFNG markedly increased the cytotoxicity of TNF/AMD whereas longer incubations did not enhance cytotoxic activity. |
| 150 | 2113589 | This study demonstrated that TNF/AMD exhibits cytotoxicity for MBT-2 cells in vitro but is ineffective in reducing implantation of intravesical tumors in vivo. |
| 151 | 2113589 | The in vitro data suggest brief exposure of MBT-2 cells to IFNG augments the subsequent anti-tumor activity of TNF/AMD. |
| 152 | 2113589 | When used in combination with interferon gamma (IFNG) or chemotherapeutic drugs targeted at DNA topoisomerase II, synergistic cytotoxicity has been observed. |
| 153 | 2113589 | The cytotoxicity of TNF and low dose actinomycin-D (AMD) against MBT-2 in vitro was examined alone and following preincubation with IFNG. |
| 154 | 2113589 | The activity of TNF/AMD in vivo utilizing an intravesical implantation mode (MBT-2) was also evaluated. |
| 155 | 2113589 | TNF/AMD was cytotoxic for MBT-2 growth in vitro. |
| 156 | 2113589 | A two hour preincubation with IFNG markedly increased the cytotoxicity of TNF/AMD whereas longer incubations did not enhance cytotoxic activity. |
| 157 | 2113589 | This study demonstrated that TNF/AMD exhibits cytotoxicity for MBT-2 cells in vitro but is ineffective in reducing implantation of intravesical tumors in vivo. |
| 158 | 2113589 | The in vitro data suggest brief exposure of MBT-2 cells to IFNG augments the subsequent anti-tumor activity of TNF/AMD. |
| 159 | 2113589 | When used in combination with interferon gamma (IFNG) or chemotherapeutic drugs targeted at DNA topoisomerase II, synergistic cytotoxicity has been observed. |
| 160 | 2113589 | The cytotoxicity of TNF and low dose actinomycin-D (AMD) against MBT-2 in vitro was examined alone and following preincubation with IFNG. |
| 161 | 2113589 | The activity of TNF/AMD in vivo utilizing an intravesical implantation mode (MBT-2) was also evaluated. |
| 162 | 2113589 | TNF/AMD was cytotoxic for MBT-2 growth in vitro. |
| 163 | 2113589 | A two hour preincubation with IFNG markedly increased the cytotoxicity of TNF/AMD whereas longer incubations did not enhance cytotoxic activity. |
| 164 | 2113589 | This study demonstrated that TNF/AMD exhibits cytotoxicity for MBT-2 cells in vitro but is ineffective in reducing implantation of intravesical tumors in vivo. |
| 165 | 2113589 | The in vitro data suggest brief exposure of MBT-2 cells to IFNG augments the subsequent anti-tumor activity of TNF/AMD. |
| 166 | 2113589 | When used in combination with interferon gamma (IFNG) or chemotherapeutic drugs targeted at DNA topoisomerase II, synergistic cytotoxicity has been observed. |
| 167 | 2113589 | The cytotoxicity of TNF and low dose actinomycin-D (AMD) against MBT-2 in vitro was examined alone and following preincubation with IFNG. |
| 168 | 2113589 | The activity of TNF/AMD in vivo utilizing an intravesical implantation mode (MBT-2) was also evaluated. |
| 169 | 2113589 | TNF/AMD was cytotoxic for MBT-2 growth in vitro. |
| 170 | 2113589 | A two hour preincubation with IFNG markedly increased the cytotoxicity of TNF/AMD whereas longer incubations did not enhance cytotoxic activity. |
| 171 | 2113589 | This study demonstrated that TNF/AMD exhibits cytotoxicity for MBT-2 cells in vitro but is ineffective in reducing implantation of intravesical tumors in vivo. |
| 172 | 2113589 | The in vitro data suggest brief exposure of MBT-2 cells to IFNG augments the subsequent anti-tumor activity of TNF/AMD. |
| 173 | 2113589 | When used in combination with interferon gamma (IFNG) or chemotherapeutic drugs targeted at DNA topoisomerase II, synergistic cytotoxicity has been observed. |
| 174 | 2113589 | The cytotoxicity of TNF and low dose actinomycin-D (AMD) against MBT-2 in vitro was examined alone and following preincubation with IFNG. |
| 175 | 2113589 | The activity of TNF/AMD in vivo utilizing an intravesical implantation mode (MBT-2) was also evaluated. |
| 176 | 2113589 | TNF/AMD was cytotoxic for MBT-2 growth in vitro. |
| 177 | 2113589 | A two hour preincubation with IFNG markedly increased the cytotoxicity of TNF/AMD whereas longer incubations did not enhance cytotoxic activity. |
| 178 | 2113589 | This study demonstrated that TNF/AMD exhibits cytotoxicity for MBT-2 cells in vitro but is ineffective in reducing implantation of intravesical tumors in vivo. |
| 179 | 2113589 | The in vitro data suggest brief exposure of MBT-2 cells to IFNG augments the subsequent anti-tumor activity of TNF/AMD. |
| 180 | 2113589 | When used in combination with interferon gamma (IFNG) or chemotherapeutic drugs targeted at DNA topoisomerase II, synergistic cytotoxicity has been observed. |
| 181 | 2113589 | The cytotoxicity of TNF and low dose actinomycin-D (AMD) against MBT-2 in vitro was examined alone and following preincubation with IFNG. |
| 182 | 2113589 | The activity of TNF/AMD in vivo utilizing an intravesical implantation mode (MBT-2) was also evaluated. |
| 183 | 2113589 | TNF/AMD was cytotoxic for MBT-2 growth in vitro. |
| 184 | 2113589 | A two hour preincubation with IFNG markedly increased the cytotoxicity of TNF/AMD whereas longer incubations did not enhance cytotoxic activity. |
| 185 | 2113589 | This study demonstrated that TNF/AMD exhibits cytotoxicity for MBT-2 cells in vitro but is ineffective in reducing implantation of intravesical tumors in vivo. |
| 186 | 2113589 | The in vitro data suggest brief exposure of MBT-2 cells to IFNG augments the subsequent anti-tumor activity of TNF/AMD. |
| 187 | 2125019 | Induction of MHC class II antigen in cultured bovine ciliary epithelial cells. |
| 188 | 2125019 | However, after incubation with bovine gamma-interferon (IFN-G) in concentrations as low as 0.3 units/ml, nearly all cells stained for MHC class II. |
| 189 | 2125019 | Tumor necrosis factor increased IFN-G-induced MHC class II expression. |
| 190 | 2125019 | To test whether MHC class II expression in response to IFN-G was specific for the ciliary epithelium, several intraocular tissues were grown in culture and incubated with IFN-G. |
| 191 | 2125019 | MHC class II expression was observed in all tissues tested for response to IFN-G, but at different sensitivities. |
| 192 | 2219270 | In contrast, suppression in the recipient spleens was donor-specific; both CD4 and CD8 cells prolonged test graft survival. |
| 193 | 2219270 | Immunohistological evaluation of renal allografts revealed that therapy with ART-18 or low-dose CsA alone failed to deplete IL-2R+ cells and prevent production of IL-2, IFN-g, and TNF. |
| 194 | 2493179 | Both CsA and CsG showed very similar dose-dependent inhibition of IFN-G and LT/TNF activity (IC50 CsA for IFN-G = 8.0 ng/ml, for LT/TNF = 9.5 ng/ml; IC50 CsG for IFN-G = 13.0 ng/ml, for LT/TNF = 13.0 ng/ml). |
| 195 | 7584508 | This study details the use of a monovalent anti-CD3 monoclonal antibody in the treatment of allograft rejection in five renal transplant recipients and documents the degree of TNF, IFN-g and IL6 release generated after antibody injection. |
| 196 | 7584508 | TNF, IFN-g and IL6 measurement showed that little pro-inflammatory cytokine release occurred after this drug. |
| 197 | 7584508 | This study details the use of a monovalent anti-CD3 monoclonal antibody in the treatment of allograft rejection in five renal transplant recipients and documents the degree of TNF, IFN-g and IL6 release generated after antibody injection. |
| 198 | 7584508 | TNF, IFN-g and IL6 measurement showed that little pro-inflammatory cytokine release occurred after this drug. |
| 199 | 7616525 | Salivary gland extracts collected daily during engorgement were shown to inhibit normal murine macrophage elaboration of interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF) as well as murine T-lymphocyte production of interleukin-2 (IL-2) and interferon-gamma (IFN-G). |
| 200 | 7683736 | The differentiation inducing effects of interleukins (IL-1 beta, IL-3 and IL-6), colony stimulating factors (GCSF and GMCSF), TNF, LIF and IFNg, were studied either individually or in combination. |
| 201 | 7683736 | IL-3, IL-6, interferon gamma, GCSF and to a smaller extent IL-1 beta and GMCSF synergized the differentiation inducing activity of TNF. |
| 202 | 7683736 | The differentiation inducing effects of interleukins (IL-1 beta, IL-3 and IL-6), colony stimulating factors (GCSF and GMCSF), TNF, LIF and IFNg, were studied either individually or in combination. |
| 203 | 7683736 | IL-3, IL-6, interferon gamma, GCSF and to a smaller extent IL-1 beta and GMCSF synergized the differentiation inducing activity of TNF. |
| 204 | 8018827 | Expression of lymphokine genes including interleukin 2 (IL-2), interleukin 3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon gamma (IFN-g), tumor necrosis factor (TNF) and lymphotoxin (LT) were sequentially monitored in peripheral blood mononuclear cells by Northern blot analysis after stimulation with phytohemagglutinin (PHA). |
| 205 | 8018827 | Lymphokines including IL-2, IL-3 and GM-CSF belong to type 1 and IFN-g, TNF and LT belong to type 2. |
| 206 | 8018827 | Expression of lymphokine genes including interleukin 2 (IL-2), interleukin 3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon gamma (IFN-g), tumor necrosis factor (TNF) and lymphotoxin (LT) were sequentially monitored in peripheral blood mononuclear cells by Northern blot analysis after stimulation with phytohemagglutinin (PHA). |
| 207 | 8018827 | Lymphokines including IL-2, IL-3 and GM-CSF belong to type 1 and IFN-g, TNF and LT belong to type 2. |
| 208 | 8083651 | Tumor necrosis factor, interleukin-2, and interferon-gamma in adult varicella. |
| 209 | 8083651 | This study measured levels of tumor necrosis factor (TNF)-alpha, interleukin-2 (IL-2), and interferon gamma (IFN-G) in a consecutive group of 31 adult varicella patients presenting within 24 hours of rash onset. |
| 210 | 8083651 | There was no correlation between TNF, IL-2, or IFN-G level and clinical severity as determined by duration and severity of cutaneous findings, duration of fever, frequency of hepatitis, or thrombocytopenia. |
| 211 | 8083651 | Tumor necrosis factor, interleukin-2, and interferon-gamma in adult varicella. |
| 212 | 8083651 | This study measured levels of tumor necrosis factor (TNF)-alpha, interleukin-2 (IL-2), and interferon gamma (IFN-G) in a consecutive group of 31 adult varicella patients presenting within 24 hours of rash onset. |
| 213 | 8083651 | There was no correlation between TNF, IL-2, or IFN-G level and clinical severity as determined by duration and severity of cutaneous findings, duration of fever, frequency of hepatitis, or thrombocytopenia. |
| 214 | 8083651 | Tumor necrosis factor, interleukin-2, and interferon-gamma in adult varicella. |
| 215 | 8083651 | This study measured levels of tumor necrosis factor (TNF)-alpha, interleukin-2 (IL-2), and interferon gamma (IFN-G) in a consecutive group of 31 adult varicella patients presenting within 24 hours of rash onset. |
| 216 | 8083651 | There was no correlation between TNF, IL-2, or IFN-G level and clinical severity as determined by duration and severity of cutaneous findings, duration of fever, frequency of hepatitis, or thrombocytopenia. |
| 217 | 8384844 | Expression of calcium-binding proteins MRP8 and MRP14 is associated with distinct monocytic differentiation pathways in HL-60 cells. |
| 218 | 8384844 | MRP8 and MRP14 are two calcium-binding proteins of the S-100 family which are expressed during distinct stages of monocytic maturation. |
| 219 | 8384844 | To further investigate their regulation the human leukemic cell line HL-60 which can be induced to differentiate to monocytes/macrophages by 12-O-tetradecanoylphorbol 13-acetate (TPA), 1,25-(OH)2 Vitamin D3 (VD3), tumor necrosis factor-alpha (TNF-alpha) and interferon-g (IFN-g) were analyzed for expression of MRP8/MRP14. |
| 220 | 8384844 | Employing Northern blotting, a sandwich enzyme-linked immunosorbent assay and immunocytochemical analysis we determined MRP8/MRP14 mRNA and protein levels, which were found to be elevated after VD3 and reduced after TPA treatment. |
| 221 | 8384844 | TNF-alpha and IFN-g did not affect MRP8/MRP14 levels. |
| 222 | 8384844 | Western blot analysis revealed that formation of MRP8/MRP14 to biologically active complexes which has previously been shown to be a calcium-mediated process is not dependent on the differentiation stages of HL-60 cells. |
| 223 | 8384844 | Restriction of MRP8/MRP14 expression to only distinct pathways of monocytic differentiation in HL-60 cells may thus reflect different functional phenotypes of monocytes/macrophages in vivo. |
| 224 | 8384844 | Expression of calcium-binding proteins MRP8 and MRP14 is associated with distinct monocytic differentiation pathways in HL-60 cells. |
| 225 | 8384844 | MRP8 and MRP14 are two calcium-binding proteins of the S-100 family which are expressed during distinct stages of monocytic maturation. |
| 226 | 8384844 | To further investigate their regulation the human leukemic cell line HL-60 which can be induced to differentiate to monocytes/macrophages by 12-O-tetradecanoylphorbol 13-acetate (TPA), 1,25-(OH)2 Vitamin D3 (VD3), tumor necrosis factor-alpha (TNF-alpha) and interferon-g (IFN-g) were analyzed for expression of MRP8/MRP14. |
| 227 | 8384844 | Employing Northern blotting, a sandwich enzyme-linked immunosorbent assay and immunocytochemical analysis we determined MRP8/MRP14 mRNA and protein levels, which were found to be elevated after VD3 and reduced after TPA treatment. |
| 228 | 8384844 | TNF-alpha and IFN-g did not affect MRP8/MRP14 levels. |
| 229 | 8384844 | Western blot analysis revealed that formation of MRP8/MRP14 to biologically active complexes which has previously been shown to be a calcium-mediated process is not dependent on the differentiation stages of HL-60 cells. |
| 230 | 8384844 | Restriction of MRP8/MRP14 expression to only distinct pathways of monocytic differentiation in HL-60 cells may thus reflect different functional phenotypes of monocytes/macrophages in vivo. |
| 231 | 8390714 | The effects of the anti picornaviral drug WIN 54954 (5-(5-(2.6-dichloro-4-(4.5-dihydro-2-oxazolyl)phenoxy)pentyl)-3-me thyl- isoxazole) and the immune modulator LS 2616 (Quinoline-3-carboxamide) on plasma cachectin/TNFa and g-interferon (IFN-g) responses were investigated during the clinical course of a myocarditic coxsackievirus B3 (CB3) infection in the mouse. |
| 232 | 8525128 | Therefore, we decided to analyze interleukin IL-1b, IL-2, IL-4, IL-6, IL-10, tumor necrosis factor-a (TNF-a) and gamma interferon (IFN-g) gene expression in peripheral blood mononuclear cells from 17 women with SLE and 10 normal females by a coupled reverse transcriptase-polymerase chain reaction technique. |
| 233 | 8525128 | High gene expression of IL-4, IL-6, IL-10 and TNF-a was found in SLE patients as compared to normal subjects. |
| 234 | 8525128 | The expression of IL-1b, IL-2 and IFN-g genes was low or undetectable. |
| 235 | 8525128 | Therefore, we decided to analyze interleukin IL-1b, IL-2, IL-4, IL-6, IL-10, tumor necrosis factor-a (TNF-a) and gamma interferon (IFN-g) gene expression in peripheral blood mononuclear cells from 17 women with SLE and 10 normal females by a coupled reverse transcriptase-polymerase chain reaction technique. |
| 236 | 8525128 | High gene expression of IL-4, IL-6, IL-10 and TNF-a was found in SLE patients as compared to normal subjects. |
| 237 | 8525128 | The expression of IL-1b, IL-2 and IFN-g genes was low or undetectable. |
| 238 | 9116875 | In an attempt to understand the mechanism behind these differences we examined age related differences in the phenotype profiles of MNC in parallel with the in vitro production of interleukin IL-6, tumour necrosis factor alpha (TNF alpha) and interferon gamma (IFNg) in neonates, children and adults. |
| 239 | 9116875 | In cultures without added polyclonal activators IL-6 and TNF alpha levels in children were 3-6 times higher than those of umbilical cords and adults. |
| 240 | 9116875 | Flow cytometry analysis of the phenotypic distribution of MNC revealed age related differences in the expression of CD3, CD4, CD8, CD14, CD19, CD45RA, CD45R0, CD2, LFA-1, ICAM-1 and LFA-3. |
| 241 | 9116875 | The TNF alpha levels in suboptimally stimulated cultures correlated negatively with the expression of LFA-3 and positively with CD45RA, while IFNg correlated positively with CD2, LFA-1, CD45R0 and CD8. |
| 242 | 9116875 | In conclusion, the study provides evidence of age related differences in the production of TNF alpha, IL-6 and IFNg among neonates, children and adults. |
| 243 | 9116875 | In an attempt to understand the mechanism behind these differences we examined age related differences in the phenotype profiles of MNC in parallel with the in vitro production of interleukin IL-6, tumour necrosis factor alpha (TNF alpha) and interferon gamma (IFNg) in neonates, children and adults. |
| 244 | 9116875 | In cultures without added polyclonal activators IL-6 and TNF alpha levels in children were 3-6 times higher than those of umbilical cords and adults. |
| 245 | 9116875 | Flow cytometry analysis of the phenotypic distribution of MNC revealed age related differences in the expression of CD3, CD4, CD8, CD14, CD19, CD45RA, CD45R0, CD2, LFA-1, ICAM-1 and LFA-3. |
| 246 | 9116875 | The TNF alpha levels in suboptimally stimulated cultures correlated negatively with the expression of LFA-3 and positively with CD45RA, while IFNg correlated positively with CD2, LFA-1, CD45R0 and CD8. |
| 247 | 9116875 | In conclusion, the study provides evidence of age related differences in the production of TNF alpha, IL-6 and IFNg among neonates, children and adults. |
| 248 | 9116875 | In an attempt to understand the mechanism behind these differences we examined age related differences in the phenotype profiles of MNC in parallel with the in vitro production of interleukin IL-6, tumour necrosis factor alpha (TNF alpha) and interferon gamma (IFNg) in neonates, children and adults. |
| 249 | 9116875 | In cultures without added polyclonal activators IL-6 and TNF alpha levels in children were 3-6 times higher than those of umbilical cords and adults. |
| 250 | 9116875 | Flow cytometry analysis of the phenotypic distribution of MNC revealed age related differences in the expression of CD3, CD4, CD8, CD14, CD19, CD45RA, CD45R0, CD2, LFA-1, ICAM-1 and LFA-3. |
| 251 | 9116875 | The TNF alpha levels in suboptimally stimulated cultures correlated negatively with the expression of LFA-3 and positively with CD45RA, while IFNg correlated positively with CD2, LFA-1, CD45R0 and CD8. |
| 252 | 9116875 | In conclusion, the study provides evidence of age related differences in the production of TNF alpha, IL-6 and IFNg among neonates, children and adults. |
| 253 | 9116875 | In an attempt to understand the mechanism behind these differences we examined age related differences in the phenotype profiles of MNC in parallel with the in vitro production of interleukin IL-6, tumour necrosis factor alpha (TNF alpha) and interferon gamma (IFNg) in neonates, children and adults. |
| 254 | 9116875 | In cultures without added polyclonal activators IL-6 and TNF alpha levels in children were 3-6 times higher than those of umbilical cords and adults. |
| 255 | 9116875 | Flow cytometry analysis of the phenotypic distribution of MNC revealed age related differences in the expression of CD3, CD4, CD8, CD14, CD19, CD45RA, CD45R0, CD2, LFA-1, ICAM-1 and LFA-3. |
| 256 | 9116875 | The TNF alpha levels in suboptimally stimulated cultures correlated negatively with the expression of LFA-3 and positively with CD45RA, while IFNg correlated positively with CD2, LFA-1, CD45R0 and CD8. |
| 257 | 9116875 | In conclusion, the study provides evidence of age related differences in the production of TNF alpha, IL-6 and IFNg among neonates, children and adults. |
| 258 | 9823012 | The production of IFN-g, IL-2, TNF-a (products of TH1 cells) were decreased, whereas the production of IL-4, IL-6 and IL-10 (products of TH2) were not affected during zinc deficiency. |
| 259 | 9823012 | We further documented that zinc deficiency decreased NK cell lytic activity and caused a decrease in the percentage of CD8+ CD73+ T cells which are known to be predominantly precursors of cytotoxic T cells. |
| 260 | 10668244 | The number of cardiac cells displaying intracellular amastigotes was lower in cultures supplemented with IL-1b, TNF-a and IFN-g than with other cytokine combinations and controls. |
| 261 | 11121210 | Radiation of the esophagus of C3H/HeNsd mice with 35 or 37 Gy of 6 MV X rays induces significantly increased RNA transcription for interleukin 1 (Il1), tumor necrosis factor alpha (Tnf), interferon gamma inducing factor (Ifngr), and interferon gamma (Ifng). |
| 262 | 11121210 | An equivalent therapeutic plasmid weight of 10 microgram ALP plasmid in the same 500 microliter of liposomes, correlated to around 52-60% of alkaline phosphatase-positive cells in the squamous layer of the esophagus at 24 h. |
| 263 | 11121210 | Mice with orthotopic thoracic tumors composed of 32D-v-abl cells that received intraesophageal SOD2-PL treatment showed transgenic mRNA in the esophagus at 24 h, but no detectable human SOD2 transgene mRNA in explanted tumors by nested RT-PCR. |
| 264 | 11316066 | In a previous study, we demonstrated a significant association between high IL-10 secretion in mixed lymphocyte culture (MLC), together with HLA mismatching for at least 4-6 antigens, with the occurrence of acute rejection following renal transplantation. |
| 265 | 11316066 | Cytokine protein secretion in MLC for IL-4, IL-6, IL-10 and IFN-gamma was measured by ELISA in 49 patient-donor pairs. |
| 266 | 11316066 | In both patient and control groups, single nucleotide polymorphism analysis for IL-4 G(-590)T, IL-6 G(-174)C, IL-10 G(-1082)A, IL-10 C(-819)T, IL-10 C(-592)A, TNF-alpha G(-308)A and microsatellite analysis for IFNG (CA repeat) was performed. |
| 267 | 11354638 | We investigated, in a random sample of a German population, the association of polymorphisms in the genes encoding the cytokines interleukin 2 (IL-2), interleukin 4 receptor (IL-4R), interleukin 6 (IL-6), interleukin 10, interferon gamma (IFNG), tumor necrosis factor (TNF) and intercellular adhesion molecule 1 (ICAM-1) with (1) secreted levels of the respective proteins after T-cell stimulation and (2) data on selected diseases obtained from a questionnaire. |
| 268 | 11354638 | Furthermore, individuals with a combination of IL2, IL6 and ICAM-1 polymorphisms tended to have higher frequencies of reported common colds than individuals with the alternate genotypes. |
| 269 | 12047360 | Allele frequencies of polymorphisms of TNFA, IL-6, IL-10 and IFNG in an Italian Caucasian population. |
| 270 | 12047360 | The polymorphisms analysed were those of tumour necrosis factor alpha (TNFA), interleukin 6 (IL-6), interleukin 10 (IL-10) and interferon gamma (IFNG). |
| 271 | 12047360 | The frequencies of IL-6 alleles - 174C and -174G were 29.0 and 71.0%, respectively; for IFNG polymorphisms at position -874, in the population under evaluation, the alleles -874T and -874A were present in 44.7 and 55.3% of the subjects, respectively. |
| 272 | 12047360 | Allele frequencies of polymorphisms of TNFA, IL-6, IL-10 and IFNG in an Italian Caucasian population. |
| 273 | 12047360 | The polymorphisms analysed were those of tumour necrosis factor alpha (TNFA), interleukin 6 (IL-6), interleukin 10 (IL-10) and interferon gamma (IFNG). |
| 274 | 12047360 | The frequencies of IL-6 alleles - 174C and -174G were 29.0 and 71.0%, respectively; for IFNG polymorphisms at position -874, in the population under evaluation, the alleles -874T and -874A were present in 44.7 and 55.3% of the subjects, respectively. |
| 275 | 12417450 | Oral terbutaline differentially affects cytokine (IL-10, IL-12, TNF, IFNg) release in multiple sclerosis patients and controls. |
| 276 | 12417450 | In this study, we investigated the effects of terbutaline (5 mg) on IL-10, IL-12, IFN-gamma and TNF-alpha production in whole blood stimulation cultures. |
| 277 | 12417450 | IL-10 and IL-12 production were significantly enhanced in controls but not in MS patients (p=0.03 and p=0.001). |
| 278 | 12417450 | We conclude that administration of terbutaline induces anti-inflammatory (IL-10) as well as IL-12 protein production in healthy controls but not in MS patients. |
| 279 | 12417450 | Oral terbutaline differentially affects cytokine (IL-10, IL-12, TNF, IFNg) release in multiple sclerosis patients and controls. |
| 280 | 12417450 | In this study, we investigated the effects of terbutaline (5 mg) on IL-10, IL-12, IFN-gamma and TNF-alpha production in whole blood stimulation cultures. |
| 281 | 12417450 | IL-10 and IL-12 production were significantly enhanced in controls but not in MS patients (p=0.03 and p=0.001). |
| 282 | 12417450 | We conclude that administration of terbutaline induces anti-inflammatory (IL-10) as well as IL-12 protein production in healthy controls but not in MS patients. |
| 283 | 12548511 | In this article, we analyze the relationship between cytokine gene polymorphisms and in vitro tumor necrosis factor alpha (TNFalpha), interferon gamma (IFNgamma), and interleukin (IL)-10 and IL-13 production, both in liver transplant recipients and in healthy volunteers. |
| 284 | 12548511 | The evaluated cytokine gene polymorphisms involved TNF-A-308; TNF-d3; IFN-G+874; IL-10-1082, -819, and -592; and IL-13+2043, and -1055. |
| 285 | 12548511 | For healthy volunteers, we observed a relationship between polymorphisms of TNF-d3 and IL-10-1082 with in vitro production of TNFalpha and IL-10, respectively, whereas no significant associations were found for the other tested cytokine gene polymorphisms. |
| 286 | 12548511 | In this article, we analyze the relationship between cytokine gene polymorphisms and in vitro tumor necrosis factor alpha (TNFalpha), interferon gamma (IFNgamma), and interleukin (IL)-10 and IL-13 production, both in liver transplant recipients and in healthy volunteers. |
| 287 | 12548511 | The evaluated cytokine gene polymorphisms involved TNF-A-308; TNF-d3; IFN-G+874; IL-10-1082, -819, and -592; and IL-13+2043, and -1055. |
| 288 | 12548511 | For healthy volunteers, we observed a relationship between polymorphisms of TNF-d3 and IL-10-1082 with in vitro production of TNFalpha and IL-10, respectively, whereas no significant associations were found for the other tested cytokine gene polymorphisms. |
| 289 | 12643791 | The NO levels in the cultured salivary gland epithelial cells were increased by treatment with a combination of interferon gamma (Ifng), interleukin 1-beta (Il1b), and tumor necrosis factor alpha (Tnfa). |
| 290 | 12854077 | A tumor necrosis factor-alpha-inducible promoter variant of interferon-gamma accelerates CD4+ T cell depletion in human immunodeficiency virus-1-infected individuals. |
| 291 | 12854077 | A polymorphism, -179G/T, in the promoter of the interferon (IFN)-gamma gene (IFNG) confers differential tumor necrosis factor-alpha (TNF-alpha) inducibility to the IFNG promoter. |
| 292 | 12854077 | In 298 African American human immunodeficiency virus (HIV)-1 seroconverters, the IFNG -179G/T genotype was associated with accelerated progression to CD4 <200 and AIDS-1993, a finding suggesting that IFNG -179T is a risk factor for AIDS progression, as measured by CD4 cell count. |
| 293 | 12854077 | It is possible that increased IFN-gamma production induced by TNF-alpha when -179T is present causes CD4 cell depletion by apoptosis. |
| 294 | 12854077 | A tumor necrosis factor-alpha-inducible promoter variant of interferon-gamma accelerates CD4+ T cell depletion in human immunodeficiency virus-1-infected individuals. |
| 295 | 12854077 | A polymorphism, -179G/T, in the promoter of the interferon (IFN)-gamma gene (IFNG) confers differential tumor necrosis factor-alpha (TNF-alpha) inducibility to the IFNG promoter. |
| 296 | 12854077 | In 298 African American human immunodeficiency virus (HIV)-1 seroconverters, the IFNG -179G/T genotype was associated with accelerated progression to CD4 <200 and AIDS-1993, a finding suggesting that IFNG -179T is a risk factor for AIDS progression, as measured by CD4 cell count. |
| 297 | 12854077 | It is possible that increased IFN-gamma production induced by TNF-alpha when -179T is present causes CD4 cell depletion by apoptosis. |
| 298 | 12854077 | A tumor necrosis factor-alpha-inducible promoter variant of interferon-gamma accelerates CD4+ T cell depletion in human immunodeficiency virus-1-infected individuals. |
| 299 | 12854077 | A polymorphism, -179G/T, in the promoter of the interferon (IFN)-gamma gene (IFNG) confers differential tumor necrosis factor-alpha (TNF-alpha) inducibility to the IFNG promoter. |
| 300 | 12854077 | In 298 African American human immunodeficiency virus (HIV)-1 seroconverters, the IFNG -179G/T genotype was associated with accelerated progression to CD4 <200 and AIDS-1993, a finding suggesting that IFNG -179T is a risk factor for AIDS progression, as measured by CD4 cell count. |
| 301 | 12854077 | It is possible that increased IFN-gamma production induced by TNF-alpha when -179T is present causes CD4 cell depletion by apoptosis. |
| 302 | 12858016 | Induction of nitric oxide synthase (NOS) by soluble glucocorticoid induced tumor necrosis factor receptor (sGITR) is modulated by IFN-gamma in murine macrophage. |
| 303 | 12858016 | Earlier study showed that glucocorticoid induced tumor necrosis factor receptor (GITR), a new TNFR family, activated murine macrophages to express inducible nitric oxide synthase (iNOS) and to generate nitric oxide (NO). |
| 304 | 12858016 | A possible involvement of pro-inflammatory cytokines on NO production by GITR was investigated in vitro systems and signaling molecules contributing to sGITR-induced iNOS production are determined in Raw 264.7 cells, a murine macrophage cell line. |
| 305 | 12858016 | The result showed that the synergy was afforded by the combination of GITR with IFN-g in a dose-dependent manner but IFN-gamma alone was not able to induce NOS. |
| 306 | 12858016 | No effects were observed with TNF-alpha, IL-1beta, or IL-6 co-treated with GITR. |
| 307 | 12858016 | To determine signaling molecules contributing to sGITR-induced iNOS production, a specific inhibitor for signal pathway proteins tested showed that PDTC (NF-kappaB) and genistein (tyrosine kinase) inhibited NOS induction significantly, while sodium orthovanadate (tyrosine phosphatase) potentiated NOS expression. |
| 308 | 12858016 | These results suggest that activations of NF-kappaB were involved in induction of iNOS by GITR and IFN-gamma priming caused earlier and stronger NF-kappaB activation. |
| 309 | 12931271 | IGFs, basic FGF, and glucose modulate proliferation and apoptosis induced by IFNgamma but not by IL-1beta in rat INS-1E beta-cells. |
| 310 | 12931271 | We investigated the effects of glucose and beta-cell growth factors (IGF-I, IGF-II, bFGF) on growth and apoptosis in the presence and absence of apoptosis inducing cytokines (IFNgamma, Il-1beta, TNFalpha). |
| 311 | 12931271 | The cytokines IFNg and IL-1beta, but not TNFalpha strongly induced INS-1E beta-cell apoptosis. |
| 312 | 12931271 | Most importantly, IGF-II and bFGF inhibited apoptosis induced by IFNg, but not by IL-1beta. |
| 313 | 12931271 | Cytokines IFNg and IL-1beta differentially interfere with intracellular signaling cascades stimulated by IGFs and bFGF or glucose, respectively. |
| 314 | 12931271 | IGFs, basic FGF, and glucose modulate proliferation and apoptosis induced by IFNgamma but not by IL-1beta in rat INS-1E beta-cells. |
| 315 | 12931271 | We investigated the effects of glucose and beta-cell growth factors (IGF-I, IGF-II, bFGF) on growth and apoptosis in the presence and absence of apoptosis inducing cytokines (IFNgamma, Il-1beta, TNFalpha). |
| 316 | 12931271 | The cytokines IFNg and IL-1beta, but not TNFalpha strongly induced INS-1E beta-cell apoptosis. |
| 317 | 12931271 | Most importantly, IGF-II and bFGF inhibited apoptosis induced by IFNg, but not by IL-1beta. |
| 318 | 12931271 | Cytokines IFNg and IL-1beta differentially interfere with intracellular signaling cascades stimulated by IGFs and bFGF or glucose, respectively. |
| 319 | 12946285 | The authors have demonstrated recently that acute B19 infection is accompanied by raised circulating levels of IL-1b, IL-6, TNF-a, and IFN-g and that raised circulating levels of TNF-a and IFN-g persist and are accompanied by MCP-1 in those patients who develop CFS. |
| 320 | 15021309 | Among the 3 major ethnic (African-American, Hispanic/Latino, and other) groups involved, HIV-1-seropositive individuals differed significantly from ethnically matched HIV-1-seronegative individuals (odds ratios = 2.13-4.82; P = 0.003-0.05) for several SNPs and haplotypes defined at the IL4, IL4R, IL6, IL10, CCL5 (RANTES), and CXCL12 (SDF1) loci. |
| 321 | 15021309 | No SNPs at IFNG, IL2, IL12B, TNF, or CCL2 (MCP1) showed any association with HIV-related outcomes. |
| 322 | 15021309 | Additional typing for IL1A, IL1B, IL1R1, IL1RN, and TGFB1 SNPs also failed to demonstrate any influence on HIV-1 infection or virologic/immunologic control in more selected patient groups. |
| 323 | 15021309 | Coupled with previous findings, our data suggest that heritable IL4 and IL10 variations may contribute to the acquisition or progression of HIV infection and that the effects of other targeted loci in the cytokine and chemokine system cannot be established unequivocally in the study populations. |
| 324 | 15073568 | Both corticotropin releasing hormone (CRH) and serotonin (5-HT) participate in the stress response and are known to modulate cytokine release by human immune cells. |
| 325 | 15073568 | Extracellular 5-HT concentrations at or above the serum values have negative immunoregulatory effects by inhibiting the production of interferon-gamma (IFNgamma), a pro-inflammatory cytokine produced by Th-1-like lymphocytes, whereas 5-HT has no significant effects on the production of interleukin-10 (IL-10), an anti-inflammatory cytokine. |
| 326 | 15073568 | In one study, CRH significantly decreases IFNgamma production by cultured human peripheral blood immunocytes, whereas in other studies CRH increases the production of cytokines, such as IL-1, IL-2 and IL-6. |
| 327 | 15073568 | The aims of the present study were to examine i) the effects of CRH, 10-9 M, 10(-8) M and 10(-7) M, on the stimulated production of IFNgamma, IL-10 and tumor necrosis factor-alpha (TNFalpha) by human whole blood; and ii) whether CRH, 10(-9) M, 10(-8) M and 10(-7) M, may antagonize some of the negative immunoregulatory effects of 5-HT, 1.5 microg/mL or 15 microg/mL. |
| 328 | 15073568 | We found that CRH, 10(-9) M, 10(-8) M and 10(-7) M, had no significant effects either on the stimulated production of IFNgamma, IL-10 or TNFalpha or on the IFNg/IL-10 production ratio, which reflects the pro-inflammatory capacity of the culture. 5-HT, 1,5 microg/dL and 15 microg/dL, significantly suppressed the production of IFNgamma and TNFalpha and the IFNg/IL-10 production ratio. |
| 329 | 15073568 | CRH, 10(-7) M, significantly reversed the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of IFNg production. |
| 330 | 15073568 | CRH at all concentrations significantly blocked the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of TNFalpha production. |
| 331 | 15073568 | The results suggest that CRH has no significant direct effects on the production of IFNgamma, IL-10 and TNFalpha, but antagonizes the negative immunoregulatory effects of 5-HT on the production of IFNgamma and TNFalpha and on the IFNgamma/IL-10 production ratio. |
| 332 | 15073568 | Both corticotropin releasing hormone (CRH) and serotonin (5-HT) participate in the stress response and are known to modulate cytokine release by human immune cells. |
| 333 | 15073568 | Extracellular 5-HT concentrations at or above the serum values have negative immunoregulatory effects by inhibiting the production of interferon-gamma (IFNgamma), a pro-inflammatory cytokine produced by Th-1-like lymphocytes, whereas 5-HT has no significant effects on the production of interleukin-10 (IL-10), an anti-inflammatory cytokine. |
| 334 | 15073568 | In one study, CRH significantly decreases IFNgamma production by cultured human peripheral blood immunocytes, whereas in other studies CRH increases the production of cytokines, such as IL-1, IL-2 and IL-6. |
| 335 | 15073568 | The aims of the present study were to examine i) the effects of CRH, 10-9 M, 10(-8) M and 10(-7) M, on the stimulated production of IFNgamma, IL-10 and tumor necrosis factor-alpha (TNFalpha) by human whole blood; and ii) whether CRH, 10(-9) M, 10(-8) M and 10(-7) M, may antagonize some of the negative immunoregulatory effects of 5-HT, 1.5 microg/mL or 15 microg/mL. |
| 336 | 15073568 | We found that CRH, 10(-9) M, 10(-8) M and 10(-7) M, had no significant effects either on the stimulated production of IFNgamma, IL-10 or TNFalpha or on the IFNg/IL-10 production ratio, which reflects the pro-inflammatory capacity of the culture. 5-HT, 1,5 microg/dL and 15 microg/dL, significantly suppressed the production of IFNgamma and TNFalpha and the IFNg/IL-10 production ratio. |
| 337 | 15073568 | CRH, 10(-7) M, significantly reversed the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of IFNg production. |
| 338 | 15073568 | CRH at all concentrations significantly blocked the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of TNFalpha production. |
| 339 | 15073568 | The results suggest that CRH has no significant direct effects on the production of IFNgamma, IL-10 and TNFalpha, but antagonizes the negative immunoregulatory effects of 5-HT on the production of IFNgamma and TNFalpha and on the IFNgamma/IL-10 production ratio. |
| 340 | 15073568 | Both corticotropin releasing hormone (CRH) and serotonin (5-HT) participate in the stress response and are known to modulate cytokine release by human immune cells. |
| 341 | 15073568 | Extracellular 5-HT concentrations at or above the serum values have negative immunoregulatory effects by inhibiting the production of interferon-gamma (IFNgamma), a pro-inflammatory cytokine produced by Th-1-like lymphocytes, whereas 5-HT has no significant effects on the production of interleukin-10 (IL-10), an anti-inflammatory cytokine. |
| 342 | 15073568 | In one study, CRH significantly decreases IFNgamma production by cultured human peripheral blood immunocytes, whereas in other studies CRH increases the production of cytokines, such as IL-1, IL-2 and IL-6. |
| 343 | 15073568 | The aims of the present study were to examine i) the effects of CRH, 10-9 M, 10(-8) M and 10(-7) M, on the stimulated production of IFNgamma, IL-10 and tumor necrosis factor-alpha (TNFalpha) by human whole blood; and ii) whether CRH, 10(-9) M, 10(-8) M and 10(-7) M, may antagonize some of the negative immunoregulatory effects of 5-HT, 1.5 microg/mL or 15 microg/mL. |
| 344 | 15073568 | We found that CRH, 10(-9) M, 10(-8) M and 10(-7) M, had no significant effects either on the stimulated production of IFNgamma, IL-10 or TNFalpha or on the IFNg/IL-10 production ratio, which reflects the pro-inflammatory capacity of the culture. 5-HT, 1,5 microg/dL and 15 microg/dL, significantly suppressed the production of IFNgamma and TNFalpha and the IFNg/IL-10 production ratio. |
| 345 | 15073568 | CRH, 10(-7) M, significantly reversed the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of IFNg production. |
| 346 | 15073568 | CRH at all concentrations significantly blocked the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of TNFalpha production. |
| 347 | 15073568 | The results suggest that CRH has no significant direct effects on the production of IFNgamma, IL-10 and TNFalpha, but antagonizes the negative immunoregulatory effects of 5-HT on the production of IFNgamma and TNFalpha and on the IFNgamma/IL-10 production ratio. |
| 348 | 15073568 | Both corticotropin releasing hormone (CRH) and serotonin (5-HT) participate in the stress response and are known to modulate cytokine release by human immune cells. |
| 349 | 15073568 | Extracellular 5-HT concentrations at or above the serum values have negative immunoregulatory effects by inhibiting the production of interferon-gamma (IFNgamma), a pro-inflammatory cytokine produced by Th-1-like lymphocytes, whereas 5-HT has no significant effects on the production of interleukin-10 (IL-10), an anti-inflammatory cytokine. |
| 350 | 15073568 | In one study, CRH significantly decreases IFNgamma production by cultured human peripheral blood immunocytes, whereas in other studies CRH increases the production of cytokines, such as IL-1, IL-2 and IL-6. |
| 351 | 15073568 | The aims of the present study were to examine i) the effects of CRH, 10-9 M, 10(-8) M and 10(-7) M, on the stimulated production of IFNgamma, IL-10 and tumor necrosis factor-alpha (TNFalpha) by human whole blood; and ii) whether CRH, 10(-9) M, 10(-8) M and 10(-7) M, may antagonize some of the negative immunoregulatory effects of 5-HT, 1.5 microg/mL or 15 microg/mL. |
| 352 | 15073568 | We found that CRH, 10(-9) M, 10(-8) M and 10(-7) M, had no significant effects either on the stimulated production of IFNgamma, IL-10 or TNFalpha or on the IFNg/IL-10 production ratio, which reflects the pro-inflammatory capacity of the culture. 5-HT, 1,5 microg/dL and 15 microg/dL, significantly suppressed the production of IFNgamma and TNFalpha and the IFNg/IL-10 production ratio. |
| 353 | 15073568 | CRH, 10(-7) M, significantly reversed the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of IFNg production. |
| 354 | 15073568 | CRH at all concentrations significantly blocked the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of TNFalpha production. |
| 355 | 15073568 | The results suggest that CRH has no significant direct effects on the production of IFNgamma, IL-10 and TNFalpha, but antagonizes the negative immunoregulatory effects of 5-HT on the production of IFNgamma and TNFalpha and on the IFNgamma/IL-10 production ratio. |
| 356 | 15115612 | LIGHT sensitizes IFN-gamma-mediated apoptosis of HT-29 human carcinoma cells through both death receptor and mitochondria pathways. |
| 357 | 15115612 | LIGHT [homologous to lymphotoxins, shows inducible expression, and competes with herpes simplex virus glycoprotein D for herpes virus entry mediator (HVEM/TR2)] is a new member of TNF superfamily. |
| 358 | 15115612 | The HT-29 colon cancer cell line is the most sensitive to LIGHT-induced, IFNg-mediated apoptosis among the cell lines we have examined so far. |
| 359 | 15115612 | Besides downregulation of Bcl-XL, upregulation of Bak, and activation of both PARP [poly (ADP-ribose) polymerase] and DFF45 (DNA fragmentation factor), LIGHT-induced, IFNg-mediated apoptosis of HT-29 cells involves extensive caspase activation. |
| 360 | 15115612 | Caspase-8 and caspase-9 activation, as shown by their cleavages appeared as early as 24 h after treatment, whereas caspase-3 and caspase-7 activation, as shown by their cleavages occurred after 72 h of LIGHT treatment. |
| 361 | 15115612 | Caspase-3 inhibitor Z-DEVD-FMK (benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone) and a broad range caspase inhibitor Z-VAD-FMK (benzyloxycarbonyl-Val-Ala-Asp fluoromethylketone) were able to block LIGHT-induced, IFNg-mediated apoptosis of HT-29 cells. |
| 362 | 15115612 | These results suggest that LIGHT-induced, IFNg-mediated apoptosis of HT-29 cells is caspase-dependent, and LIGHT signaling is mediated through both death receptor and mitochondria pathways. |
| 363 | 15145618 | Treatment with interferon-gamma (IFN-g) induced SOCS-1 and enhanced SOCS-3 expression, and was associated with decreased tumor necrosis factor-alpha (TNF) and increased leukemia inhibitory factor (LIF) in culture supernatants. |
| 364 | 15145618 | Treatment with conditioned medium from myelin basic protein-stimulated encephalitogenic lymphoid cells (MBP-CM) increased SOCS-3 and induced SOCS-1 expression. |
| 365 | 15507306 | Peripheral blood mononuclear cells (PBMC) isolated from these pigs responded to PRRSV exposure with a limited increase in their expression of the Th1 immune markers, IFNG, tumor necrosis factor-alpha and interleukin-15 (IL15), and a reduction in the quantity of mRNAs encoding the innate and inflammatory proteins, IL1B, IL8 and IFNA. |
| 366 | 15507306 | Efforts to enhance Th1 immunity, by utilizing an expression plasmid encoding porcine IFNA (pINA) as an adjuvant, resulted in a temporary increase in the frequency of PRRSV-specific IFNG SC but only minor changes overall in the expression of Th1 associated cytokine or innate immune marker mRNA by virus-stimulated PBMC. |
| 367 | 15507306 | Administration of pINA, however, did correlate with decreased IL1B secretion by cultured, unstimulated PBMC but had no effect on their ability to release IFNG. |
| 368 | 15597685 | The role of -immunomodulation in systemic anti-fungal therapy has been proposed and recombinant cytokine therapy (G-CSF, GM-CSF, IFN-g, IL-I, TNF-a) either alone or in combination with AmB have shown good results. |
| 369 | 15652446 | The aim of this study was to evaluate whether there was any correlation between Helicobacter pylori-associated diseases and (1) H. pylori virulence genes or (2) IL-1B, IL-1RN, IFN-G, TNF-A, IL-10 genetic polymorphisms. |
| 370 | 15652446 | IL-1RN intron 2 VNTR polymorphism (PCR), IL-1B -31 C/T (RFLP), the SNPs of IFN-G (+874 A/T), TNF-A (-1031 C/T, -857 C/T, -376 A/G, -308 A/G, -238 A/G), IL-10 (-1082 A/G, -819 C/T, -592 A/C) (Taqman chemistry) were studied. cagA, s1 and m1 vacA, were PCR amplified. |
| 371 | 15652446 | Antral inflammation was associated with TNF-A -1031 TT, while corpus activity with IL-10 -819 CC. |
| 372 | 15652446 | H. pylori infection was associated with TNF-A -308 AG genotype, while IFN-G +874 AA genotype was associated with cagA. |
| 373 | 15652446 | In conclusion, among host genetic factors contributing to H. pylori disease outcome, IFN-G +874 AA genotype favors cagA positive infections, TNF-A -857 TT duodenal ulcer while IL-10 -819 TT intestinal metaplasia and NCGC. |
| 374 | 15652446 | The aim of this study was to evaluate whether there was any correlation between Helicobacter pylori-associated diseases and (1) H. pylori virulence genes or (2) IL-1B, IL-1RN, IFN-G, TNF-A, IL-10 genetic polymorphisms. |
| 375 | 15652446 | IL-1RN intron 2 VNTR polymorphism (PCR), IL-1B -31 C/T (RFLP), the SNPs of IFN-G (+874 A/T), TNF-A (-1031 C/T, -857 C/T, -376 A/G, -308 A/G, -238 A/G), IL-10 (-1082 A/G, -819 C/T, -592 A/C) (Taqman chemistry) were studied. cagA, s1 and m1 vacA, were PCR amplified. |
| 376 | 15652446 | Antral inflammation was associated with TNF-A -1031 TT, while corpus activity with IL-10 -819 CC. |
| 377 | 15652446 | H. pylori infection was associated with TNF-A -308 AG genotype, while IFN-G +874 AA genotype was associated with cagA. |
| 378 | 15652446 | In conclusion, among host genetic factors contributing to H. pylori disease outcome, IFN-G +874 AA genotype favors cagA positive infections, TNF-A -857 TT duodenal ulcer while IL-10 -819 TT intestinal metaplasia and NCGC. |
| 379 | 15652446 | The aim of this study was to evaluate whether there was any correlation between Helicobacter pylori-associated diseases and (1) H. pylori virulence genes or (2) IL-1B, IL-1RN, IFN-G, TNF-A, IL-10 genetic polymorphisms. |
| 380 | 15652446 | IL-1RN intron 2 VNTR polymorphism (PCR), IL-1B -31 C/T (RFLP), the SNPs of IFN-G (+874 A/T), TNF-A (-1031 C/T, -857 C/T, -376 A/G, -308 A/G, -238 A/G), IL-10 (-1082 A/G, -819 C/T, -592 A/C) (Taqman chemistry) were studied. cagA, s1 and m1 vacA, were PCR amplified. |
| 381 | 15652446 | Antral inflammation was associated with TNF-A -1031 TT, while corpus activity with IL-10 -819 CC. |
| 382 | 15652446 | H. pylori infection was associated with TNF-A -308 AG genotype, while IFN-G +874 AA genotype was associated with cagA. |
| 383 | 15652446 | In conclusion, among host genetic factors contributing to H. pylori disease outcome, IFN-G +874 AA genotype favors cagA positive infections, TNF-A -857 TT duodenal ulcer while IL-10 -819 TT intestinal metaplasia and NCGC. |
| 384 | 15652446 | The aim of this study was to evaluate whether there was any correlation between Helicobacter pylori-associated diseases and (1) H. pylori virulence genes or (2) IL-1B, IL-1RN, IFN-G, TNF-A, IL-10 genetic polymorphisms. |
| 385 | 15652446 | IL-1RN intron 2 VNTR polymorphism (PCR), IL-1B -31 C/T (RFLP), the SNPs of IFN-G (+874 A/T), TNF-A (-1031 C/T, -857 C/T, -376 A/G, -308 A/G, -238 A/G), IL-10 (-1082 A/G, -819 C/T, -592 A/C) (Taqman chemistry) were studied. cagA, s1 and m1 vacA, were PCR amplified. |
| 386 | 15652446 | Antral inflammation was associated with TNF-A -1031 TT, while corpus activity with IL-10 -819 CC. |
| 387 | 15652446 | H. pylori infection was associated with TNF-A -308 AG genotype, while IFN-G +874 AA genotype was associated with cagA. |
| 388 | 15652446 | In conclusion, among host genetic factors contributing to H. pylori disease outcome, IFN-G +874 AA genotype favors cagA positive infections, TNF-A -857 TT duodenal ulcer while IL-10 -819 TT intestinal metaplasia and NCGC. |
| 389 | 15652446 | The aim of this study was to evaluate whether there was any correlation between Helicobacter pylori-associated diseases and (1) H. pylori virulence genes or (2) IL-1B, IL-1RN, IFN-G, TNF-A, IL-10 genetic polymorphisms. |
| 390 | 15652446 | IL-1RN intron 2 VNTR polymorphism (PCR), IL-1B -31 C/T (RFLP), the SNPs of IFN-G (+874 A/T), TNF-A (-1031 C/T, -857 C/T, -376 A/G, -308 A/G, -238 A/G), IL-10 (-1082 A/G, -819 C/T, -592 A/C) (Taqman chemistry) were studied. cagA, s1 and m1 vacA, were PCR amplified. |
| 391 | 15652446 | Antral inflammation was associated with TNF-A -1031 TT, while corpus activity with IL-10 -819 CC. |
| 392 | 15652446 | H. pylori infection was associated with TNF-A -308 AG genotype, while IFN-G +874 AA genotype was associated with cagA. |
| 393 | 15652446 | In conclusion, among host genetic factors contributing to H. pylori disease outcome, IFN-G +874 AA genotype favors cagA positive infections, TNF-A -857 TT duodenal ulcer while IL-10 -819 TT intestinal metaplasia and NCGC. |
| 394 | 15661146 | The most noteworthy changes in gene expression mainly affected the transcriptional network regulated by interferons (IFNs), including both IFN-alpha/beta-inducible genes (STAT1, STAT2, ISGF3G/IRF9, IFI27, G1P3, G1P2, OAS2, MX1) and IFN-gamma-inducible genes (CXCL9, CXCL10, CXCL11). |
| 395 | 15661146 | Interesting, upregulation of IFN-alpha/beta-inducible genes (but not IFN-gamma-inducible genes) was independent of histological scores (grade and stage of fibrosis) and HCV characteristics (hepatic HCV mRNA levels and the HCV genotype), and was specific to HCV (as compared to hepatitis B virus (HBV)). |
| 396 | 15661146 | Other genes dysregulated in F1-CH-C, albeit less markedly than IFN-alpha/beta- and IFN-gamma-inducible genes, were mainly involved in the activation of lymphocytes infiltrating the liver (IFNG, TNF, CXCL6, IL6, CCL8, CXCR3, CXCR4, CCR2), cell proliferation (p16/CDKN2A, MKI67, p14/ARF), extracellular matrix remodeling (MMP9, ITGA2), lymphangiogenesis (XLKD1/LYVE), oxidative stress (CYP2E1), and cytoskeleton microtubule organization (STMN2/SCG10). |
| 397 | 15733644 | Forty-eight patients were analyzed for mutations in the IL1A, IL1B, IL6 and TNFA genes, and 16 polymorphisms in 10 candidate cytokine genes (IL1A, IL1B, IL1RN, TNFA, IL2, IL4, IL4R, IL6, IL10, IFNG) were genotyped from all subjects. |
| 398 | 15733644 | No disease-causing mutations were identified in IL1A, IL1B, IL6 or TNFA. |
| 399 | 15733644 | Forty-eight patients were analyzed for mutations in the IL1A, IL1B, IL6 and TNFA genes, and 16 polymorphisms in 10 candidate cytokine genes (IL1A, IL1B, IL1RN, TNFA, IL2, IL4, IL4R, IL6, IL10, IFNG) were genotyped from all subjects. |
| 400 | 15733644 | No disease-causing mutations were identified in IL1A, IL1B, IL6 or TNFA. |
| 401 | 15741670 | Candidate gene and genome wide studies have localized genetic regions involved in the disease, such as the A1AR and CLCA1 genes (chromosome 1), IL-1RN and DPP10 (2q14), HLA-G and TNF-a (6p21), GPRA (7p14), FceRI and GSTP1 (11q13), NOS1, IFNG, STAT6, VDR, and other genes (12q13-26), PHF11 and flanking genes (13q14), AACT and PTGDR (14q), and ADAM33 (20p13). |
| 402 | 15799696 | The changes in mRNA expression level of interleukin 2 (Il2), Il4, tumor necrosis factor alpha (Tnf), interferon gamma (Ifng), and transforming growth factor beta (Tgfb) were examined. |
| 403 | 15799696 | The mRNA expression of Il2 and Il4 decreased from day 5 to day 14 after irradiation. |
| 404 | 15799696 | Thereafter, the expression level of Il2 mRNA recovered to normal control levels; however, the expression of Il4 mRNA tended toward significantly low levels. |
| 405 | 16223768 | NK-cell activation by LIGHT triggers tumor-specific CD8+ T-cell immunity to reject established tumors. |
| 406 | 16223768 | We now demonstrate that the TNF superfamily member, LIGHT, known as TNFSF14 and a T-cell costimulatory molecule, is a critical ligand for the activation of NK cells. |
| 407 | 16223768 | Herpesvirus entry mediator (HVEM) is expressed on NK cells, and its engagement with LIGHT mediates NK-cell activation. |
| 408 | 16223768 | Interestingly, activated NK cells do not kill tumors directly but can facilitate the priming of tumor-specific CD8+ T cells in an IFN-gamma-dependent manner. |
| 409 | 16223768 | Conversely, intratumor depletion of either NK cells or IFN-gamma during tumor progression disrupts CD8+ cell-mediated tumor rejection, suggesting that the tumor is the essential site for the crosstalk between NK and CD8+ cells. |
| 410 | 16223768 | Furthermore, IFNG-deficient NK cells fail to effectively activate CD8+ T cells, suggesting IFN-gamma plays an important role in NK-mediated activation of cytotoxic T lymphocytes (CTLs). |
| 411 | 16223768 | Our findings establish a direct role for LIGHT in NK activation/expansion and a critical helper role of activated NK cells in priming CD8+ T cells and breaking T-cell tolerance at the tumor site. |
| 412 | 16724074 | Previous studies identified mucosa-specific CD2 cis-elements within the -204 to -108 bp IFNG promoter. |
| 413 | 16724074 | Within this region, a single-site nucleotide polymorphism, -179G/T, imparts tumor necrosis factor-alpha stimulation of IFNG in peripheral blood lymphocytes, and is linked with accelerated AIDS progression. |
| 414 | 16750565 | The clone secreted GM-CSF, TNFa, and IFNg when stimulated with AML blasts from 3 of 11 patients or cell lines tested, but not with K562 or autologous B-LCL. |
| 415 | 16835788 | The polymorphic positions studied were: TNFA -1031, -863, -857, -851, -574, -376, -308, -238, +488; TGFB1 -988, -800, -509, +869, +915, +652, +673, +713, +788; IL10 -1082, -819, -592; IL6 -174; IFNG -333, +874. |
| 416 | 16835788 | It was found that TNFA -238 GA, TGFB1 -509 CT, -800 GG, IFNG +874 AT, IL6 -174 GG, IL10 -1082 GA genotypes were significantly decreased, while TNFA -238 AA, -857 CC, TGFB1 -509 TT, IFNG +874 AA, IL6 -174 CC, IL10 -1082 AA, -819 TT, -592 AA genotypes were significantly increased, in MM. |
| 417 | 16835788 | This suggests that genotypes provisionally associated with low expression of pro-inflammatory and immunomodulatory TNF-alpha, IFN-gamma and IL-6 and anti-inflammatory IL-10 and TGF-beta1 could be involved in the mechanisms of cancer progression and escape from immunosurveillance. |
| 418 | 16835788 | The polymorphic positions studied were: TNFA -1031, -863, -857, -851, -574, -376, -308, -238, +488; TGFB1 -988, -800, -509, +869, +915, +652, +673, +713, +788; IL10 -1082, -819, -592; IL6 -174; IFNG -333, +874. |
| 419 | 16835788 | It was found that TNFA -238 GA, TGFB1 -509 CT, -800 GG, IFNG +874 AT, IL6 -174 GG, IL10 -1082 GA genotypes were significantly decreased, while TNFA -238 AA, -857 CC, TGFB1 -509 TT, IFNG +874 AA, IL6 -174 CC, IL10 -1082 AA, -819 TT, -592 AA genotypes were significantly increased, in MM. |
| 420 | 16835788 | This suggests that genotypes provisionally associated with low expression of pro-inflammatory and immunomodulatory TNF-alpha, IFN-gamma and IL-6 and anti-inflammatory IL-10 and TGF-beta1 could be involved in the mechanisms of cancer progression and escape from immunosurveillance. |
| 421 | 16835788 | The polymorphic positions studied were: TNFA -1031, -863, -857, -851, -574, -376, -308, -238, +488; TGFB1 -988, -800, -509, +869, +915, +652, +673, +713, +788; IL10 -1082, -819, -592; IL6 -174; IFNG -333, +874. |
| 422 | 16835788 | It was found that TNFA -238 GA, TGFB1 -509 CT, -800 GG, IFNG +874 AT, IL6 -174 GG, IL10 -1082 GA genotypes were significantly decreased, while TNFA -238 AA, -857 CC, TGFB1 -509 TT, IFNG +874 AA, IL6 -174 CC, IL10 -1082 AA, -819 TT, -592 AA genotypes were significantly increased, in MM. |
| 423 | 16835788 | This suggests that genotypes provisionally associated with low expression of pro-inflammatory and immunomodulatory TNF-alpha, IFN-gamma and IL-6 and anti-inflammatory IL-10 and TGF-beta1 could be involved in the mechanisms of cancer progression and escape from immunosurveillance. |
| 424 | 16930709 | Network analysis indicates that TNF and NFKB1 are key regulators of gene expression at this early time point. |
| 425 | 16930709 | At 4h, IL1B in addition to TNF and NFKB1 play dominant roles in the up-regulation of immune gene expression, whereas by 8h this function is mediated by TNF, IFNG, and MYC. |
| 426 | 16930709 | Network analysis indicates that TNF and NFKB1 are key regulators of gene expression at this early time point. |
| 427 | 16930709 | At 4h, IL1B in addition to TNF and NFKB1 play dominant roles in the up-regulation of immune gene expression, whereas by 8h this function is mediated by TNF, IFNG, and MYC. |
| 428 | 16985010 | Messenger RNA (mRNA) transcript levels for the IL2, IL8, and IL1RN genes were significantly downregulated across the time course of infection in both breeds. |
| 429 | 16985010 | There was an early increase in transcripts for genes encoding proinflammatory mediators (IFNG, IL1A, TNF, and IL12) in N'Dama by 14 days postinfection (dpi) compared with preinfection levels that was not detected in the susceptible Boran breed. |
| 430 | 17215490 | After LPS administration, inflammatory cytokines tumor necrosis factor-alpha (TNFA) and IL6 were markedly increased in serum, uterine, and conceptus tissues in Il10(-/-) mice compared with Il10(+/+) mice, with elevated local synthesis of Tnfa and Il6 mRNAs in the gestational tissues. |
| 431 | 17215490 | IL1A and IL12p40 were similarly elevated in serum and gestational tissues, whereas interferon gamma (IFNG) and soluble TNFRII content were unchanged in the absence of IL10. |
| 432 | 17215490 | IL10 genotype also influenced the responsiveness of mice to a TNFA antagonist, etanercept. |
| 433 | 17215490 | Fetal loss in Il10(-/-) mice was partly alleviated by moderate or high doses of etanercept, whereas Il10(+/+) mice were refractory to high-dose etanercept, consistent with attenuation by IL10 status of TNFA bioavailability after etanercept treatment. |
| 434 | 17215490 | These data show that IL10 modulates resistance to inflammatory stimuli by downregulating expression of proinflammatory cytokines TNFA, IL6, IL1A, and IL12, acting to protect against inflammation-induced pathology in the implantation site. |
| 435 | 17215490 | After LPS administration, inflammatory cytokines tumor necrosis factor-alpha (TNFA) and IL6 were markedly increased in serum, uterine, and conceptus tissues in Il10(-/-) mice compared with Il10(+/+) mice, with elevated local synthesis of Tnfa and Il6 mRNAs in the gestational tissues. |
| 436 | 17215490 | IL1A and IL12p40 were similarly elevated in serum and gestational tissues, whereas interferon gamma (IFNG) and soluble TNFRII content were unchanged in the absence of IL10. |
| 437 | 17215490 | IL10 genotype also influenced the responsiveness of mice to a TNFA antagonist, etanercept. |
| 438 | 17215490 | Fetal loss in Il10(-/-) mice was partly alleviated by moderate or high doses of etanercept, whereas Il10(+/+) mice were refractory to high-dose etanercept, consistent with attenuation by IL10 status of TNFA bioavailability after etanercept treatment. |
| 439 | 17215490 | These data show that IL10 modulates resistance to inflammatory stimuli by downregulating expression of proinflammatory cytokines TNFA, IL6, IL1A, and IL12, acting to protect against inflammation-induced pathology in the implantation site. |
| 440 | 17215490 | After LPS administration, inflammatory cytokines tumor necrosis factor-alpha (TNFA) and IL6 were markedly increased in serum, uterine, and conceptus tissues in Il10(-/-) mice compared with Il10(+/+) mice, with elevated local synthesis of Tnfa and Il6 mRNAs in the gestational tissues. |
| 441 | 17215490 | IL1A and IL12p40 were similarly elevated in serum and gestational tissues, whereas interferon gamma (IFNG) and soluble TNFRII content were unchanged in the absence of IL10. |
| 442 | 17215490 | IL10 genotype also influenced the responsiveness of mice to a TNFA antagonist, etanercept. |
| 443 | 17215490 | Fetal loss in Il10(-/-) mice was partly alleviated by moderate or high doses of etanercept, whereas Il10(+/+) mice were refractory to high-dose etanercept, consistent with attenuation by IL10 status of TNFA bioavailability after etanercept treatment. |
| 444 | 17215490 | These data show that IL10 modulates resistance to inflammatory stimuli by downregulating expression of proinflammatory cytokines TNFA, IL6, IL1A, and IL12, acting to protect against inflammation-induced pathology in the implantation site. |
| 445 | 17215490 | After LPS administration, inflammatory cytokines tumor necrosis factor-alpha (TNFA) and IL6 were markedly increased in serum, uterine, and conceptus tissues in Il10(-/-) mice compared with Il10(+/+) mice, with elevated local synthesis of Tnfa and Il6 mRNAs in the gestational tissues. |
| 446 | 17215490 | IL1A and IL12p40 were similarly elevated in serum and gestational tissues, whereas interferon gamma (IFNG) and soluble TNFRII content were unchanged in the absence of IL10. |
| 447 | 17215490 | IL10 genotype also influenced the responsiveness of mice to a TNFA antagonist, etanercept. |
| 448 | 17215490 | Fetal loss in Il10(-/-) mice was partly alleviated by moderate or high doses of etanercept, whereas Il10(+/+) mice were refractory to high-dose etanercept, consistent with attenuation by IL10 status of TNFA bioavailability after etanercept treatment. |
| 449 | 17215490 | These data show that IL10 modulates resistance to inflammatory stimuli by downregulating expression of proinflammatory cytokines TNFA, IL6, IL1A, and IL12, acting to protect against inflammation-induced pathology in the implantation site. |
| 450 | 17334537 | Bosentan failed to affect the infection-associated increase in the cardiac levels of the cytokines IFN-g and TNF-a and the chemokines CCL2/MCP-1, CCL3/MIP-1a and CCL5/RANTES. |
| 451 | 17611223 | The IL-4/IL-13/Stat6 signalling pathway promotes luminal mammary epithelial cell development. |
| 452 | 17611223 | The Th1/Th2 cytokine milieu is a key paradigm in lineage commitment, and IL-4 (Il4), IL-13 (Il13) and Stat6 are important mediators of Th2 development. |
| 453 | 17611223 | Thus, the Th1 cytokines IL-12 (Il12), interferon gamma (INFgamma; also known as Ifng) and Tnfalpha are downregulated concomitantly with the upregulation of the Th2 cytokines IL-4, IL-13 and IL-5 (Il5) as epithelial cells commit to the luminal lineage. |
| 454 | 17611223 | Moreover, we show that Th2 cytokines play a crucial role in mammary gland development in vivo, because differentiation and alveolar morphogenesis are reduced in both Stat6 and IL-4/IL-13 doubly deficient mice during pregnancy. |
| 455 | 17612762 | The genotyping for TNF (-308), TGFB1 (+869, +915), IL-10 (1082, -819, and -592), IL-6 (-174), and IFNG (+874) was accomplished by the PCR-SSP (polymerase chain reaction with sequence specific primers technique using the One Lambda kit. |
| 456 | 18026101 | The LPS hypersensitivity phenotype is not suppressed by mutations in Myd88, Trif, Tnf, Tnfrsf1a, Ifnb, Ifng or Stat1, genes contributing to LPS responses, and results from an abnormality extrinsic to hematopoietic cells. |
| 457 | 18056971 | We identified four genetic risk sets for acute myocardial infarction (AMI) from information on functional gene variants that favor inflammation or modulate cholesterol metabolism: IL6 -174 G/C, TNF -308 G/A, IL10 -1082 G/A, SERPINA3 -51 G/T, IFNG +874 T/A, HMGCR -911 C/A, and APOE epsilon2/3/4; 316 patients and 461 healthy subjects, all Italian. |
| 458 | 18056971 | The 'low intrinsic risk' set had alleles that downregulate inflammation and cholesterol synthesis (IL6, TNF, ILl0, HMGCR). |
| 459 | 18056971 | 'AMI across a broad age range' carried multiple proinflammatory alleles (IL6, TNF, IL10, SERPINA3): All 72 persons like this set were affected yet had relatively low plasma cholesterol levels. |
| 460 | 18056971 | 'A subset of AMI in middle age' had numerous proinflammatory alleles (IL6, TNF, SERPINA3, IFNG, HMGCR). |
| 461 | 18056971 | 'AMI after age 80' had a reduced risk set (IL6, IL10, IFNG). |
| 462 | 18056971 | We identified four genetic risk sets for acute myocardial infarction (AMI) from information on functional gene variants that favor inflammation or modulate cholesterol metabolism: IL6 -174 G/C, TNF -308 G/A, IL10 -1082 G/A, SERPINA3 -51 G/T, IFNG +874 T/A, HMGCR -911 C/A, and APOE epsilon2/3/4; 316 patients and 461 healthy subjects, all Italian. |
| 463 | 18056971 | The 'low intrinsic risk' set had alleles that downregulate inflammation and cholesterol synthesis (IL6, TNF, ILl0, HMGCR). |
| 464 | 18056971 | 'AMI across a broad age range' carried multiple proinflammatory alleles (IL6, TNF, IL10, SERPINA3): All 72 persons like this set were affected yet had relatively low plasma cholesterol levels. |
| 465 | 18056971 | 'A subset of AMI in middle age' had numerous proinflammatory alleles (IL6, TNF, SERPINA3, IFNG, HMGCR). |
| 466 | 18056971 | 'AMI after age 80' had a reduced risk set (IL6, IL10, IFNG). |
| 467 | 18056971 | We identified four genetic risk sets for acute myocardial infarction (AMI) from information on functional gene variants that favor inflammation or modulate cholesterol metabolism: IL6 -174 G/C, TNF -308 G/A, IL10 -1082 G/A, SERPINA3 -51 G/T, IFNG +874 T/A, HMGCR -911 C/A, and APOE epsilon2/3/4; 316 patients and 461 healthy subjects, all Italian. |
| 468 | 18056971 | The 'low intrinsic risk' set had alleles that downregulate inflammation and cholesterol synthesis (IL6, TNF, ILl0, HMGCR). |
| 469 | 18056971 | 'AMI across a broad age range' carried multiple proinflammatory alleles (IL6, TNF, IL10, SERPINA3): All 72 persons like this set were affected yet had relatively low plasma cholesterol levels. |
| 470 | 18056971 | 'A subset of AMI in middle age' had numerous proinflammatory alleles (IL6, TNF, SERPINA3, IFNG, HMGCR). |
| 471 | 18056971 | 'AMI after age 80' had a reduced risk set (IL6, IL10, IFNG). |
| 472 | 18056971 | We identified four genetic risk sets for acute myocardial infarction (AMI) from information on functional gene variants that favor inflammation or modulate cholesterol metabolism: IL6 -174 G/C, TNF -308 G/A, IL10 -1082 G/A, SERPINA3 -51 G/T, IFNG +874 T/A, HMGCR -911 C/A, and APOE epsilon2/3/4; 316 patients and 461 healthy subjects, all Italian. |
| 473 | 18056971 | The 'low intrinsic risk' set had alleles that downregulate inflammation and cholesterol synthesis (IL6, TNF, ILl0, HMGCR). |
| 474 | 18056971 | 'AMI across a broad age range' carried multiple proinflammatory alleles (IL6, TNF, IL10, SERPINA3): All 72 persons like this set were affected yet had relatively low plasma cholesterol levels. |
| 475 | 18056971 | 'A subset of AMI in middle age' had numerous proinflammatory alleles (IL6, TNF, SERPINA3, IFNG, HMGCR). |
| 476 | 18056971 | 'AMI after age 80' had a reduced risk set (IL6, IL10, IFNG). |
| 477 | 18158121 | Cytokine gene polymorphism in kidney transplantation--impact of TGF-beta 1, TNF-alpha and IL-6 on graft outcome. |
| 478 | 18158121 | Eight single nucleotide polymorphisms (SNPs) including TNFA (-308), TGFB1 (cdns10, 25), IL-10 (-1082, -819, -592), IL-6 (-174) and IFNG (+874) were analyzed in 56 patients with stable graft function (SGF), 10 with CAN and 28 kidney donors by PCR-SSP method. |
| 479 | 18158121 | No statistically significant differences in distribution of IL-10, IL-6 and IFNG genotypes between recipients with SGF and CAN were found. |
| 480 | 18158121 | In conclusion our data suggest that the high producer genotype of profibrogenetic TGF-beta1, pro-inflammatory TNF-alpha and genetically determined low production of immunoregulatory IL-6 cytokine might be risk factors for CAN development. |
| 481 | 18158121 | Cytokine gene polymorphism in kidney transplantation--impact of TGF-beta 1, TNF-alpha and IL-6 on graft outcome. |
| 482 | 18158121 | Eight single nucleotide polymorphisms (SNPs) including TNFA (-308), TGFB1 (cdns10, 25), IL-10 (-1082, -819, -592), IL-6 (-174) and IFNG (+874) were analyzed in 56 patients with stable graft function (SGF), 10 with CAN and 28 kidney donors by PCR-SSP method. |
| 483 | 18158121 | No statistically significant differences in distribution of IL-10, IL-6 and IFNG genotypes between recipients with SGF and CAN were found. |
| 484 | 18158121 | In conclusion our data suggest that the high producer genotype of profibrogenetic TGF-beta1, pro-inflammatory TNF-alpha and genetically determined low production of immunoregulatory IL-6 cytokine might be risk factors for CAN development. |
| 485 | 18158121 | Cytokine gene polymorphism in kidney transplantation--impact of TGF-beta 1, TNF-alpha and IL-6 on graft outcome. |
| 486 | 18158121 | Eight single nucleotide polymorphisms (SNPs) including TNFA (-308), TGFB1 (cdns10, 25), IL-10 (-1082, -819, -592), IL-6 (-174) and IFNG (+874) were analyzed in 56 patients with stable graft function (SGF), 10 with CAN and 28 kidney donors by PCR-SSP method. |
| 487 | 18158121 | No statistically significant differences in distribution of IL-10, IL-6 and IFNG genotypes between recipients with SGF and CAN were found. |
| 488 | 18158121 | In conclusion our data suggest that the high producer genotype of profibrogenetic TGF-beta1, pro-inflammatory TNF-alpha and genetically determined low production of immunoregulatory IL-6 cytokine might be risk factors for CAN development. |
| 489 | 18199828 | We used high-throughput SYBR-green-based genotyping of single nucleotide polymorphisms (SNPs) to characterize 59 transfused trauma patients, with MC (n=30) and without MC (n=29), for 4 functionally significant SNPs: TNF (-308), IL 10 (-1082), IFNG (+874), and TGFB1 (+915). |
| 490 | 18216180 | In this study, we compare the intensity of lipid peroxidation (estimated as malondialdehyde (MDA) serum levels), the antioxidant status, (measured as glutathione peroxidase (GPX) and superoxide dismutase (SOD) activities in red blood cells), and levels of cytokines derived from Th1 cells (such as interferon gamma (IFNG)), Th2 cells (such as interleukin (IL)-4), Th3 cells (such as transforming growth factor beta (TGF-beta)), and IL-6, IL-8, and tumor necrosis factor (TNF)-alpha in patients affected by chronic hepatitis C virus infection, 26 drinkers of alcohol and 40 nondrinkers of alcohol. |
| 491 | 18216180 | Patients showed significantly higher TNF-alpha (Z = 4.92, P < 0.001), IL-8 (Z = 4.95, P < 0.001), IFNG (Z = 2.81, P = 0.005), TGF-beta (t = 2.12, P = 0.037), MDA (Z = 5, P < 0.001), but lower IL-6 (Z = 3.61, P < 0.001) and GPX (F = 4.30, P < 0.05) than controls, whereas no differences were observed regarding IL-4 (Z = 0.35, P = 0.72), GPX and SOD activities. |
| 492 | 18216180 | Alcoholics showed significantly higher TNF-alpha, but lower IL-4, MDA, and GPX, than nonalcoholics. |
| 493 | 18216180 | TNF-alpha was significantly related to albumin and prothrombin activity, whereas TGF-beta was significantly related to MDA levels. |
| 494 | 18216180 | In this study, we compare the intensity of lipid peroxidation (estimated as malondialdehyde (MDA) serum levels), the antioxidant status, (measured as glutathione peroxidase (GPX) and superoxide dismutase (SOD) activities in red blood cells), and levels of cytokines derived from Th1 cells (such as interferon gamma (IFNG)), Th2 cells (such as interleukin (IL)-4), Th3 cells (such as transforming growth factor beta (TGF-beta)), and IL-6, IL-8, and tumor necrosis factor (TNF)-alpha in patients affected by chronic hepatitis C virus infection, 26 drinkers of alcohol and 40 nondrinkers of alcohol. |
| 495 | 18216180 | Patients showed significantly higher TNF-alpha (Z = 4.92, P < 0.001), IL-8 (Z = 4.95, P < 0.001), IFNG (Z = 2.81, P = 0.005), TGF-beta (t = 2.12, P = 0.037), MDA (Z = 5, P < 0.001), but lower IL-6 (Z = 3.61, P < 0.001) and GPX (F = 4.30, P < 0.05) than controls, whereas no differences were observed regarding IL-4 (Z = 0.35, P = 0.72), GPX and SOD activities. |
| 496 | 18216180 | Alcoholics showed significantly higher TNF-alpha, but lower IL-4, MDA, and GPX, than nonalcoholics. |
| 497 | 18216180 | TNF-alpha was significantly related to albumin and prothrombin activity, whereas TGF-beta was significantly related to MDA levels. |
| 498 | 18216180 | In this study, we compare the intensity of lipid peroxidation (estimated as malondialdehyde (MDA) serum levels), the antioxidant status, (measured as glutathione peroxidase (GPX) and superoxide dismutase (SOD) activities in red blood cells), and levels of cytokines derived from Th1 cells (such as interferon gamma (IFNG)), Th2 cells (such as interleukin (IL)-4), Th3 cells (such as transforming growth factor beta (TGF-beta)), and IL-6, IL-8, and tumor necrosis factor (TNF)-alpha in patients affected by chronic hepatitis C virus infection, 26 drinkers of alcohol and 40 nondrinkers of alcohol. |
| 499 | 18216180 | Patients showed significantly higher TNF-alpha (Z = 4.92, P < 0.001), IL-8 (Z = 4.95, P < 0.001), IFNG (Z = 2.81, P = 0.005), TGF-beta (t = 2.12, P = 0.037), MDA (Z = 5, P < 0.001), but lower IL-6 (Z = 3.61, P < 0.001) and GPX (F = 4.30, P < 0.05) than controls, whereas no differences were observed regarding IL-4 (Z = 0.35, P = 0.72), GPX and SOD activities. |
| 500 | 18216180 | Alcoholics showed significantly higher TNF-alpha, but lower IL-4, MDA, and GPX, than nonalcoholics. |
| 501 | 18216180 | TNF-alpha was significantly related to albumin and prothrombin activity, whereas TGF-beta was significantly related to MDA levels. |
| 502 | 18216180 | In this study, we compare the intensity of lipid peroxidation (estimated as malondialdehyde (MDA) serum levels), the antioxidant status, (measured as glutathione peroxidase (GPX) and superoxide dismutase (SOD) activities in red blood cells), and levels of cytokines derived from Th1 cells (such as interferon gamma (IFNG)), Th2 cells (such as interleukin (IL)-4), Th3 cells (such as transforming growth factor beta (TGF-beta)), and IL-6, IL-8, and tumor necrosis factor (TNF)-alpha in patients affected by chronic hepatitis C virus infection, 26 drinkers of alcohol and 40 nondrinkers of alcohol. |
| 503 | 18216180 | Patients showed significantly higher TNF-alpha (Z = 4.92, P < 0.001), IL-8 (Z = 4.95, P < 0.001), IFNG (Z = 2.81, P = 0.005), TGF-beta (t = 2.12, P = 0.037), MDA (Z = 5, P < 0.001), but lower IL-6 (Z = 3.61, P < 0.001) and GPX (F = 4.30, P < 0.05) than controls, whereas no differences were observed regarding IL-4 (Z = 0.35, P = 0.72), GPX and SOD activities. |
| 504 | 18216180 | Alcoholics showed significantly higher TNF-alpha, but lower IL-4, MDA, and GPX, than nonalcoholics. |
| 505 | 18216180 | TNF-alpha was significantly related to albumin and prothrombin activity, whereas TGF-beta was significantly related to MDA levels. |
| 506 | 18218610 | Cortisol (an active GC) reduced the mRNA expression of caspase 8 (CASP8) and caspase 3 (CASP3) and reduced the enzymatic activity of CASP3 and cell death induced by tumor necrosis factor (TNF) and interferon gamma (IFNG) in cultured bovine luteal cells. mRNAs and proteins of GC receptor (NR3C1), 11beta-hydroxysteroid dehydrogenase type 1 (HSD11B1), and HSD11B2 were expressed in CL throughout the estrous cycle. |
| 507 | 18218610 | These results suggest that cortisol suppresses TNF-IFNG-induced apoptosis in vitro by reducing apoptosis signals via CASP8 and CASP3 in bovine CL and that the local increase in cortisol production resulting from increased HSD11B1 at the early and midluteal stages helps to maintain CL function by suppressing apoptosis of luteal cells. |
| 508 | 18296866 | The CLENDOs were also exposed to cytokines to assess differences in activation of nuclear factor kappa B signaling (NF-kappaB), induction of the transcription factor interferon regulatory factor 1 (IRF1), cytokine production, and cytokine-induced cell death. |
| 509 | 18296866 | In response to TNF, for instance, both types of CLENDOs exhibited a rapid, 5-fold decrease in NF-kappaB inhibitor alpha (NFKBIA) protein expression (P<0.05), and a 4-fold increase in IRF1 expression (P<0.05), that did not differ with phenotype (P>0.05). |
| 510 | 18296866 | Similarly, both types of CLENDOs produced tumor necrosis factor alpha and chemokine ligand 2 in response to IFNG stimulation (P<0.05) that did not differ with phenotype (P>0.05). |
| 511 | 18296866 | The CLENDOs were also exposed to cytokines to assess differences in activation of nuclear factor kappa B signaling (NF-kappaB), induction of the transcription factor interferon regulatory factor 1 (IRF1), cytokine production, and cytokine-induced cell death. |
| 512 | 18296866 | In response to TNF, for instance, both types of CLENDOs exhibited a rapid, 5-fold decrease in NF-kappaB inhibitor alpha (NFKBIA) protein expression (P<0.05), and a 4-fold increase in IRF1 expression (P<0.05), that did not differ with phenotype (P>0.05). |
| 513 | 18296866 | Similarly, both types of CLENDOs produced tumor necrosis factor alpha and chemokine ligand 2 in response to IFNG stimulation (P<0.05) that did not differ with phenotype (P>0.05). |
| 514 | 18337305 | New approach reveals CD28 and IFNG gene interaction in the susceptibility to cervical cancer. |
| 515 | 18337305 | A total of 14 single nucleotide polymorphisms (SNPs) distributed in CD28, CTLA4, ICOS, PDCD1, FAS, TNFA, IL6, IFNG, TGFB1 and IL10 genes were determined in patients and healthy individuals from three independent case/control sets. |
| 516 | 18337305 | The multi-locus analysis revealed higher frequencies in cancer patients of three three-genotype combinations [CD28+17(TT)/IFNG+874(AA)/TNFA-308(GG), CD28+17(TT)/IFN+847(AA)/PDCD1+7785(CT), and CD28 +17(TT)/IFNG+874(AA)/ICOS+1564(TT)] (P < 0.01, Monte Carlo simulation). |
| 517 | 18337305 | We hypothesized that this two-genotype [CD28(TT) and IFNG(AA)] combination could have a major contribution to the observed association. |
| 518 | 18337305 | To address this question, we analyzed the frequency of the CD28(TT), IFNG(AA) genotype combination in the three groups combined, and observed its increase in patients (P = 0.0011 by Fisher's exact test). |
| 519 | 18337305 | Further analysis suggested that gene-gene interaction between CD28 and IFNG might contribute to susceptibility to cervical cancer. |
| 520 | 18337305 | Our results showed an epistatic effect between CD28 and IFNG genes in susceptibility to cervical cancer, a finding that might be relevant for a better understanding of the disease pathogenesis. |
| 521 | 18345012 | Fibrous tissue formation is regulated by the balance between plasminogen activator inhibitor type 1 (PAI-1) and tissue-type plasminogen activator (tPA), which reciprocally regulate fibrin deposition. |
| 522 | 18345012 | Adhesion development depended upon the interferon-gamma (IFN-gamma) and signal transducer and activator of transcription-1 (STAT1) system. |
| 523 | 18345012 | This response does not depend on STAT4, STAT6, interleukin-12 (IL-12), IL-18, tumor necrosis factor-alpha, Toll-like receptor 4 or myeloid differentiation factor-88-mediated signals. |
| 524 | 18345012 | Wild-type mice increased the ratio of PAI-1 to tPA after cecal cauterization, whereas Ifng(-/-) or Stat1(-/-) mice did not, suggesting that IFN-gamma has a crucial role in the differential regulation of PAI-1 and tPA. |
| 525 | 18345012 | Additionally, hepatocyte growth factor, a potent mitogenic factor for hepatocytes, strongly inhibited intestinal adhesion by diminishing IFN-gamma production, providing a potential new way to prevent postoperative adhesions. |
| 526 | 18414898 | IFNG +874T/A, IL10 -1082G/A and TNF -308G/A polymorphisms in association with tuberculosis susceptibility: a meta-analysis study. |
| 527 | 18414898 | In tuberculosis (TB), interferon-gamma (IFNgamma) is crucial to control intracellular growth of Mycobacterium tuberculosis while interleukin-10 (IL-10) has an antagonistic role. |
| 528 | 18414898 | Tumor necrosis factor (TNF) is a central mediator of granuloma formation and control of bacilli spread synergizing with IFNgamma to hamper M. tuberculosis infection. |
| 529 | 18414898 | The aim of this study was to determine the association of the interferon-gamma gene (IFNG) +874T/A, interleukin-10 gene (IL10) -1082G/A and tumor necrosis factor gene (TNF) -308G/A SNPs with TB in several populations using meta-analysis. |
| 530 | 18414898 | Eleven studies were included in the IFNG +874T/A meta-analysis, while eight were used for the IL10 -1082G/A, and 10 were employed for TNF -308G/A. |
| 531 | 18414898 | IFNG +874T/A, IL10 -1082G/A and TNF -308G/A polymorphisms in association with tuberculosis susceptibility: a meta-analysis study. |
| 532 | 18414898 | In tuberculosis (TB), interferon-gamma (IFNgamma) is crucial to control intracellular growth of Mycobacterium tuberculosis while interleukin-10 (IL-10) has an antagonistic role. |
| 533 | 18414898 | Tumor necrosis factor (TNF) is a central mediator of granuloma formation and control of bacilli spread synergizing with IFNgamma to hamper M. tuberculosis infection. |
| 534 | 18414898 | The aim of this study was to determine the association of the interferon-gamma gene (IFNG) +874T/A, interleukin-10 gene (IL10) -1082G/A and tumor necrosis factor gene (TNF) -308G/A SNPs with TB in several populations using meta-analysis. |
| 535 | 18414898 | Eleven studies were included in the IFNG +874T/A meta-analysis, while eight were used for the IL10 -1082G/A, and 10 were employed for TNF -308G/A. |
| 536 | 18414898 | IFNG +874T/A, IL10 -1082G/A and TNF -308G/A polymorphisms in association with tuberculosis susceptibility: a meta-analysis study. |
| 537 | 18414898 | In tuberculosis (TB), interferon-gamma (IFNgamma) is crucial to control intracellular growth of Mycobacterium tuberculosis while interleukin-10 (IL-10) has an antagonistic role. |
| 538 | 18414898 | Tumor necrosis factor (TNF) is a central mediator of granuloma formation and control of bacilli spread synergizing with IFNgamma to hamper M. tuberculosis infection. |
| 539 | 18414898 | The aim of this study was to determine the association of the interferon-gamma gene (IFNG) +874T/A, interleukin-10 gene (IL10) -1082G/A and tumor necrosis factor gene (TNF) -308G/A SNPs with TB in several populations using meta-analysis. |
| 540 | 18414898 | Eleven studies were included in the IFNG +874T/A meta-analysis, while eight were used for the IL10 -1082G/A, and 10 were employed for TNF -308G/A. |
| 541 | 18414898 | IFNG +874T/A, IL10 -1082G/A and TNF -308G/A polymorphisms in association with tuberculosis susceptibility: a meta-analysis study. |
| 542 | 18414898 | In tuberculosis (TB), interferon-gamma (IFNgamma) is crucial to control intracellular growth of Mycobacterium tuberculosis while interleukin-10 (IL-10) has an antagonistic role. |
| 543 | 18414898 | Tumor necrosis factor (TNF) is a central mediator of granuloma formation and control of bacilli spread synergizing with IFNgamma to hamper M. tuberculosis infection. |
| 544 | 18414898 | The aim of this study was to determine the association of the interferon-gamma gene (IFNG) +874T/A, interleukin-10 gene (IL10) -1082G/A and tumor necrosis factor gene (TNF) -308G/A SNPs with TB in several populations using meta-analysis. |
| 545 | 18414898 | Eleven studies were included in the IFNG +874T/A meta-analysis, while eight were used for the IL10 -1082G/A, and 10 were employed for TNF -308G/A. |
| 546 | 18463360 | Prostaglandin E2 (1 microM) and PGF2alpha (1 microM) significantly stimulated progesterone (P4) production and reduced the levels of cell death in the cells cultured with or without tumor necrosis factor alpha (TNF)/interferon gamma (IFNG), in the presence and absence of FAS ligand (P < 0.05). |
| 547 | 18463360 | Furthermore, DNA fragmentation induced by TNF/IFNG was observed to be suppressed by PGE2 and PGF2alpha. |
| 548 | 18463360 | Prostaglandin E2 and PGF2alpha also attenuated mRNA expression of caspase 3 and caspase 8, as well as caspase 3 activity (P < 0.05) in TNF/IFNG-treated cells. |
| 549 | 18463360 | A specific P4 receptor antagonist (onapristone) attenuated the apoptosis-inhibitory effects of PGE2 and PGF2alpha in the absence of TNF/IFNG (P < 0.05). |
| 550 | 18463360 | Prostaglandin E2 (1 microM) and PGF2alpha (1 microM) significantly stimulated progesterone (P4) production and reduced the levels of cell death in the cells cultured with or without tumor necrosis factor alpha (TNF)/interferon gamma (IFNG), in the presence and absence of FAS ligand (P < 0.05). |
| 551 | 18463360 | Furthermore, DNA fragmentation induced by TNF/IFNG was observed to be suppressed by PGE2 and PGF2alpha. |
| 552 | 18463360 | Prostaglandin E2 and PGF2alpha also attenuated mRNA expression of caspase 3 and caspase 8, as well as caspase 3 activity (P < 0.05) in TNF/IFNG-treated cells. |
| 553 | 18463360 | A specific P4 receptor antagonist (onapristone) attenuated the apoptosis-inhibitory effects of PGE2 and PGF2alpha in the absence of TNF/IFNG (P < 0.05). |
| 554 | 18463360 | Prostaglandin E2 (1 microM) and PGF2alpha (1 microM) significantly stimulated progesterone (P4) production and reduced the levels of cell death in the cells cultured with or without tumor necrosis factor alpha (TNF)/interferon gamma (IFNG), in the presence and absence of FAS ligand (P < 0.05). |
| 555 | 18463360 | Furthermore, DNA fragmentation induced by TNF/IFNG was observed to be suppressed by PGE2 and PGF2alpha. |
| 556 | 18463360 | Prostaglandin E2 and PGF2alpha also attenuated mRNA expression of caspase 3 and caspase 8, as well as caspase 3 activity (P < 0.05) in TNF/IFNG-treated cells. |
| 557 | 18463360 | A specific P4 receptor antagonist (onapristone) attenuated the apoptosis-inhibitory effects of PGE2 and PGF2alpha in the absence of TNF/IFNG (P < 0.05). |
| 558 | 18463360 | Prostaglandin E2 (1 microM) and PGF2alpha (1 microM) significantly stimulated progesterone (P4) production and reduced the levels of cell death in the cells cultured with or without tumor necrosis factor alpha (TNF)/interferon gamma (IFNG), in the presence and absence of FAS ligand (P < 0.05). |
| 559 | 18463360 | Furthermore, DNA fragmentation induced by TNF/IFNG was observed to be suppressed by PGE2 and PGF2alpha. |
| 560 | 18463360 | Prostaglandin E2 and PGF2alpha also attenuated mRNA expression of caspase 3 and caspase 8, as well as caspase 3 activity (P < 0.05) in TNF/IFNG-treated cells. |
| 561 | 18463360 | A specific P4 receptor antagonist (onapristone) attenuated the apoptosis-inhibitory effects of PGE2 and PGF2alpha in the absence of TNF/IFNG (P < 0.05). |
| 562 | 18632870 | Interestingly, in SARS-CoV-infected aged mice, a subset of genes, including Tnfa, Il6, Ccl2, Ccl3, Cxcl10, and Ifng, was induced in a biphasic pattern that correlated with peak viral replication and a subsequent influx of lymphocytes and severe histopathologic changes in the lungs. |
| 563 | 19017962 | Self-antigen prevents CD8 T cell effector differentiation by CD134 and CD137 dual costimulation. |
| 564 | 19017962 | Enforced dual costimulation through OX40 and 4-1BB redirected CD8 cells encountering soluble exogenous peptide to expand and differentiate into IFN-gamma and TNF-alpha double-producing effectors rather than becoming tolerant. |
| 565 | 19017962 | Thus, the ability of enforced OX40 plus 4-1BB dual costimulation to redirect CD8 cells to undergo effector differentiation was unexpectedly influenced by the source of tolerizing Ag and help was selectively required to facilitate CD8 cell effector differentiation when the tolerizing Ag derived from self. |
| 566 | 19058987 | Influence of TNF and IL10 gene polymorphisms in the immunopathogenesis of leprosy in the south of Brazil. |
| 567 | 19075734 | Three major cytokines, namely, tumor necrosis factor (TNF-alpha), interleukin (IL)-1, and IL-6 are produced by cultured brain cells after various stimuli such as ischemia. |
| 568 | 19075734 | TNF-alpha expression after stroke stimulates expression of tissue factor and adhesion molecules for leukocytes, release of interleukin-1 (IL-1), nitric oxide, factor VIII/von Willebrand factor, platelet-activating factor and endothelin, suppression of the thrombomodulin-protein C-protein S system, reduction of tissue-plasminogen activator and release of plasminogen activator inhibitor-1. |
| 569 | 19075734 | IL-6 can be induced by a variety of molecules including IL-1, TNF-alpha, transforming growth factor-beta and prostaglandins (PGs), and many other mediators such as b-amyloid, interferon-g (IFNg) and IL-4 can potentiate these primary inducers, highlighting the complex nature of IL-6 modulation. |
| 570 | 19075734 | Several studies reported that plasma levels of TNF-alpha and IL-6 are associated with prognosis after ischemic stroke and our group showed that plasma levels of cytokines such as TNF-alpha, IL-1beta are different in every diagnostic subtype of ischemic stroke, and how plasma levels of some immunoinflammatory markers and thrombotic-phybrinolitic markers are predictive of acute ischemic stroke diagnosis in the acute setting. |
| 571 | 19075734 | Three major cytokines, namely, tumor necrosis factor (TNF-alpha), interleukin (IL)-1, and IL-6 are produced by cultured brain cells after various stimuli such as ischemia. |
| 572 | 19075734 | TNF-alpha expression after stroke stimulates expression of tissue factor and adhesion molecules for leukocytes, release of interleukin-1 (IL-1), nitric oxide, factor VIII/von Willebrand factor, platelet-activating factor and endothelin, suppression of the thrombomodulin-protein C-protein S system, reduction of tissue-plasminogen activator and release of plasminogen activator inhibitor-1. |
| 573 | 19075734 | IL-6 can be induced by a variety of molecules including IL-1, TNF-alpha, transforming growth factor-beta and prostaglandins (PGs), and many other mediators such as b-amyloid, interferon-g (IFNg) and IL-4 can potentiate these primary inducers, highlighting the complex nature of IL-6 modulation. |
| 574 | 19075734 | Several studies reported that plasma levels of TNF-alpha and IL-6 are associated with prognosis after ischemic stroke and our group showed that plasma levels of cytokines such as TNF-alpha, IL-1beta are different in every diagnostic subtype of ischemic stroke, and how plasma levels of some immunoinflammatory markers and thrombotic-phybrinolitic markers are predictive of acute ischemic stroke diagnosis in the acute setting. |
| 575 | 19075734 | Three major cytokines, namely, tumor necrosis factor (TNF-alpha), interleukin (IL)-1, and IL-6 are produced by cultured brain cells after various stimuli such as ischemia. |
| 576 | 19075734 | TNF-alpha expression after stroke stimulates expression of tissue factor and adhesion molecules for leukocytes, release of interleukin-1 (IL-1), nitric oxide, factor VIII/von Willebrand factor, platelet-activating factor and endothelin, suppression of the thrombomodulin-protein C-protein S system, reduction of tissue-plasminogen activator and release of plasminogen activator inhibitor-1. |
| 577 | 19075734 | IL-6 can be induced by a variety of molecules including IL-1, TNF-alpha, transforming growth factor-beta and prostaglandins (PGs), and many other mediators such as b-amyloid, interferon-g (IFNg) and IL-4 can potentiate these primary inducers, highlighting the complex nature of IL-6 modulation. |
| 578 | 19075734 | Several studies reported that plasma levels of TNF-alpha and IL-6 are associated with prognosis after ischemic stroke and our group showed that plasma levels of cytokines such as TNF-alpha, IL-1beta are different in every diagnostic subtype of ischemic stroke, and how plasma levels of some immunoinflammatory markers and thrombotic-phybrinolitic markers are predictive of acute ischemic stroke diagnosis in the acute setting. |
| 579 | 19075734 | Three major cytokines, namely, tumor necrosis factor (TNF-alpha), interleukin (IL)-1, and IL-6 are produced by cultured brain cells after various stimuli such as ischemia. |
| 580 | 19075734 | TNF-alpha expression after stroke stimulates expression of tissue factor and adhesion molecules for leukocytes, release of interleukin-1 (IL-1), nitric oxide, factor VIII/von Willebrand factor, platelet-activating factor and endothelin, suppression of the thrombomodulin-protein C-protein S system, reduction of tissue-plasminogen activator and release of plasminogen activator inhibitor-1. |
| 581 | 19075734 | IL-6 can be induced by a variety of molecules including IL-1, TNF-alpha, transforming growth factor-beta and prostaglandins (PGs), and many other mediators such as b-amyloid, interferon-g (IFNg) and IL-4 can potentiate these primary inducers, highlighting the complex nature of IL-6 modulation. |
| 582 | 19075734 | Several studies reported that plasma levels of TNF-alpha and IL-6 are associated with prognosis after ischemic stroke and our group showed that plasma levels of cytokines such as TNF-alpha, IL-1beta are different in every diagnostic subtype of ischemic stroke, and how plasma levels of some immunoinflammatory markers and thrombotic-phybrinolitic markers are predictive of acute ischemic stroke diagnosis in the acute setting. |
| 583 | 19129516 | The present study was conducted to explore the source of acetylcholine (ACH) in the corpus luteum (CL) and to test our hypothesis of an antiapoptotic role of ACH in the bovine CL and, further, to investigate whether nerve growth factor (NGF), insulin-like growth factor 1 (IGF1), and transforming growth factor beta1 (TGFB1) influence the expression of choline acetyltransferase (CHAT), the biosynthetic enzyme of ACH, in cultured bovine luteal cells. |
| 584 | 19129516 | Cell viability and TUNEL assays were performed on cultured midluteal cells treated with or without tumor necrosis factor alpha (TNF)/interferon gamma (IFNG) in the presence of ACH and its muscarinic (atropine) and nicotinic (mecamylamine) receptor antagonists. |
| 585 | 19129516 | ACH increased cell viability and prevented cell death induced by TNF/IFNG. |
| 586 | 19129516 | TNF/IFNG treatment downregulated CHAT expression, whereas NGF, IGF1, and TGFB1 upregulated CHAT expression, in cultured luteal cells. |
| 587 | 19129516 | Locally produced ACH appears to be regulated by NGF, IGF1, and TGFB1. |
| 588 | 19129516 | The present study was conducted to explore the source of acetylcholine (ACH) in the corpus luteum (CL) and to test our hypothesis of an antiapoptotic role of ACH in the bovine CL and, further, to investigate whether nerve growth factor (NGF), insulin-like growth factor 1 (IGF1), and transforming growth factor beta1 (TGFB1) influence the expression of choline acetyltransferase (CHAT), the biosynthetic enzyme of ACH, in cultured bovine luteal cells. |
| 589 | 19129516 | Cell viability and TUNEL assays were performed on cultured midluteal cells treated with or without tumor necrosis factor alpha (TNF)/interferon gamma (IFNG) in the presence of ACH and its muscarinic (atropine) and nicotinic (mecamylamine) receptor antagonists. |
| 590 | 19129516 | ACH increased cell viability and prevented cell death induced by TNF/IFNG. |
| 591 | 19129516 | TNF/IFNG treatment downregulated CHAT expression, whereas NGF, IGF1, and TGFB1 upregulated CHAT expression, in cultured luteal cells. |
| 592 | 19129516 | Locally produced ACH appears to be regulated by NGF, IGF1, and TGFB1. |
| 593 | 19129516 | The present study was conducted to explore the source of acetylcholine (ACH) in the corpus luteum (CL) and to test our hypothesis of an antiapoptotic role of ACH in the bovine CL and, further, to investigate whether nerve growth factor (NGF), insulin-like growth factor 1 (IGF1), and transforming growth factor beta1 (TGFB1) influence the expression of choline acetyltransferase (CHAT), the biosynthetic enzyme of ACH, in cultured bovine luteal cells. |
| 594 | 19129516 | Cell viability and TUNEL assays were performed on cultured midluteal cells treated with or without tumor necrosis factor alpha (TNF)/interferon gamma (IFNG) in the presence of ACH and its muscarinic (atropine) and nicotinic (mecamylamine) receptor antagonists. |
| 595 | 19129516 | ACH increased cell viability and prevented cell death induced by TNF/IFNG. |
| 596 | 19129516 | TNF/IFNG treatment downregulated CHAT expression, whereas NGF, IGF1, and TGFB1 upregulated CHAT expression, in cultured luteal cells. |
| 597 | 19129516 | Locally produced ACH appears to be regulated by NGF, IGF1, and TGFB1. |
| 598 | 19269042 | The Decoy Receptor 3 (DcR3) is known to compete with the signalling receptors of the Fas ligand (FasL), LIGHT and the TNF-like molecule 1A (TL1A). |
| 599 | 19269042 | Treatment of PLP-specific lymph node cells with DcR3.Fc protein resulted in a suppression of IFN-g and IL-17, in a reduced proportion of Th17 cells and in a decrease of encephalitogenicity. |
| 600 | 19269042 | The Th17 response promoting cytokines IL-6 and IL-23 were suppressed by DcR3.Fc as well. |
| 601 | 19269042 | DcR3.Fc-treatment of CD4+ T cells with a defective FasL did not influence the production of IL-17 indicating that DcR3 suppresses IL-17 production by disruption of Fas-FasL interactions. |
| 602 | 19283894 | In vitro, it inhibited the binding of both human and murine CD154 (CD40L) to their receptor (CD40) even in the presence of protein-containing media and prevented the CD154-induced proliferation of human B cells as well as the corresponding increase in surface expression of CD86, CD80, CD40, and MHC class II in a concentration-dependent manner. |
| 603 | 19283894 | Furthermore, in isolated human islets, it also decreased the CD154-induced release of inflammatory cytokines such as IFN-g, interleukin-6 (IL-6), and IL-8. |
| 604 | 19283894 | Suramin was selected for investigation because it has been reported to be an inhibitor of the interaction of TNF-a with its receptor and CD154 is a member of the TNF-family. |
| 605 | 19375805 | The objective was to search for an association between spontaneous preterm birth (sPTB) and single and/or combined polymorphisms in genes TNFA -308 G>A, IL10 -1082 G>A, IL10 -819 C>T, IL10 -592 C>A, IL6 -174 G>C, and IFNG +874 A>T. |
| 606 | 19375805 | The multi-locus analysis revealed a significant association between sPTB and the TNFA(GG)/IL6(GG)/IFNG(AA) genotype combination (p=0.002), confirmed by logistic regression. |
| 607 | 19375805 | Our data suggest that the combination of TNF-alpha, IFN-gamma, and IL-6 maternal gene polymorphisms might contribute to susceptibility to sPTB. |
| 608 | 19375805 | The objective was to search for an association between spontaneous preterm birth (sPTB) and single and/or combined polymorphisms in genes TNFA -308 G>A, IL10 -1082 G>A, IL10 -819 C>T, IL10 -592 C>A, IL6 -174 G>C, and IFNG +874 A>T. |
| 609 | 19375805 | The multi-locus analysis revealed a significant association between sPTB and the TNFA(GG)/IL6(GG)/IFNG(AA) genotype combination (p=0.002), confirmed by logistic regression. |
| 610 | 19375805 | Our data suggest that the combination of TNF-alpha, IFN-gamma, and IL-6 maternal gene polymorphisms might contribute to susceptibility to sPTB. |
| 611 | 19375805 | The objective was to search for an association between spontaneous preterm birth (sPTB) and single and/or combined polymorphisms in genes TNFA -308 G>A, IL10 -1082 G>A, IL10 -819 C>T, IL10 -592 C>A, IL6 -174 G>C, and IFNG +874 A>T. |
| 612 | 19375805 | The multi-locus analysis revealed a significant association between sPTB and the TNFA(GG)/IL6(GG)/IFNG(AA) genotype combination (p=0.002), confirmed by logistic regression. |
| 613 | 19375805 | Our data suggest that the combination of TNF-alpha, IFN-gamma, and IL-6 maternal gene polymorphisms might contribute to susceptibility to sPTB. |
| 614 | 19384924 | The well characterized human-mouse chimeric G250 (cG250) antibody has been shown in human studies to specifically enrich in CA-IX positive tumors and was chosen as a carrier for site specific delivery of TNF in form of our IgG-TNF-fusion protein (cG250-TNF) to RCC xenografts. |
| 615 | 19541593 | We found decreasing IL-2 expression, increasing IFN-gamma and TNF-alpha production and stable IL-4, Ki67 and TGFb levels with advancing age. |
| 616 | 19541593 | Apart from age, there was a differential expression in boys and girls: boys (< 6 years) produce significantly more IL-2 (p < 0,04), while girls > 12 years produce more IFNg than boys of the same age (p < 0.05). |
| 617 | 19879772 | TNFalpha and TGF-beta1 influence IL-18-induced IFNgamma production through regulation of IL-18 receptor and T-bet expression. |
| 618 | 19879772 | IL-18 is a pro-inflammatory cytokine that drives dendritic cell maturation and mediates IFNgamma production. |
| 619 | 19879772 | In this study, we demonstrate that in the dendritic precursor-like cell line KG-1, IFNgamma production induced by IL-18 is potentiated (>5-fold) by TNFalpha and completely suppressed by TGF-beta1. |
| 620 | 19879772 | IL-18 stimulation rapidly activates different MAPK signalling pathways but only blocking of p38 activation alleviates IFNgamma production. |
| 621 | 19879772 | The mechanism through which TNFalpha enhances IL-18 induced IFNgamma production is by promoting IL-18 receptor alpha-chain expression which results in higher levels of p38 activation and induces expression of T-bet, a transcriptional regulator of the IFNG gene. |
| 622 | 19879772 | In contrast, TGF-beta1 rapidly suppresses IFNgamma production by limiting IL-18 receptor numbers at the cell surface and preventing induction of T-bet expression. |
| 623 | 19879772 | TGF-beta1 experience by cells leads to sustained long-term inactivation of TNFalpha/IL-18-mediated cell activation but not IL-18 induced p38 activation suggesting transcriptional silencing of the T-BET and/or IFNG promoter independent of MAPK signalling. |
| 624 | 19879772 | TNFalpha and TGF-beta1 influence IL-18-induced IFNgamma production through regulation of IL-18 receptor and T-bet expression. |
| 625 | 19879772 | IL-18 is a pro-inflammatory cytokine that drives dendritic cell maturation and mediates IFNgamma production. |
| 626 | 19879772 | In this study, we demonstrate that in the dendritic precursor-like cell line KG-1, IFNgamma production induced by IL-18 is potentiated (>5-fold) by TNFalpha and completely suppressed by TGF-beta1. |
| 627 | 19879772 | IL-18 stimulation rapidly activates different MAPK signalling pathways but only blocking of p38 activation alleviates IFNgamma production. |
| 628 | 19879772 | The mechanism through which TNFalpha enhances IL-18 induced IFNgamma production is by promoting IL-18 receptor alpha-chain expression which results in higher levels of p38 activation and induces expression of T-bet, a transcriptional regulator of the IFNG gene. |
| 629 | 19879772 | In contrast, TGF-beta1 rapidly suppresses IFNgamma production by limiting IL-18 receptor numbers at the cell surface and preventing induction of T-bet expression. |
| 630 | 19879772 | TGF-beta1 experience by cells leads to sustained long-term inactivation of TNFalpha/IL-18-mediated cell activation but not IL-18 induced p38 activation suggesting transcriptional silencing of the T-BET and/or IFNG promoter independent of MAPK signalling. |
| 631 | 19879772 | TNFalpha and TGF-beta1 influence IL-18-induced IFNgamma production through regulation of IL-18 receptor and T-bet expression. |
| 632 | 19879772 | IL-18 is a pro-inflammatory cytokine that drives dendritic cell maturation and mediates IFNgamma production. |
| 633 | 19879772 | In this study, we demonstrate that in the dendritic precursor-like cell line KG-1, IFNgamma production induced by IL-18 is potentiated (>5-fold) by TNFalpha and completely suppressed by TGF-beta1. |
| 634 | 19879772 | IL-18 stimulation rapidly activates different MAPK signalling pathways but only blocking of p38 activation alleviates IFNgamma production. |
| 635 | 19879772 | The mechanism through which TNFalpha enhances IL-18 induced IFNgamma production is by promoting IL-18 receptor alpha-chain expression which results in higher levels of p38 activation and induces expression of T-bet, a transcriptional regulator of the IFNG gene. |
| 636 | 19879772 | In contrast, TGF-beta1 rapidly suppresses IFNgamma production by limiting IL-18 receptor numbers at the cell surface and preventing induction of T-bet expression. |
| 637 | 19879772 | TGF-beta1 experience by cells leads to sustained long-term inactivation of TNFalpha/IL-18-mediated cell activation but not IL-18 induced p38 activation suggesting transcriptional silencing of the T-BET and/or IFNG promoter independent of MAPK signalling. |
| 638 | 19879772 | TNFalpha and TGF-beta1 influence IL-18-induced IFNgamma production through regulation of IL-18 receptor and T-bet expression. |
| 639 | 19879772 | IL-18 is a pro-inflammatory cytokine that drives dendritic cell maturation and mediates IFNgamma production. |
| 640 | 19879772 | In this study, we demonstrate that in the dendritic precursor-like cell line KG-1, IFNgamma production induced by IL-18 is potentiated (>5-fold) by TNFalpha and completely suppressed by TGF-beta1. |
| 641 | 19879772 | IL-18 stimulation rapidly activates different MAPK signalling pathways but only blocking of p38 activation alleviates IFNgamma production. |
| 642 | 19879772 | The mechanism through which TNFalpha enhances IL-18 induced IFNgamma production is by promoting IL-18 receptor alpha-chain expression which results in higher levels of p38 activation and induces expression of T-bet, a transcriptional regulator of the IFNG gene. |
| 643 | 19879772 | In contrast, TGF-beta1 rapidly suppresses IFNgamma production by limiting IL-18 receptor numbers at the cell surface and preventing induction of T-bet expression. |
| 644 | 19879772 | TGF-beta1 experience by cells leads to sustained long-term inactivation of TNFalpha/IL-18-mediated cell activation but not IL-18 induced p38 activation suggesting transcriptional silencing of the T-BET and/or IFNG promoter independent of MAPK signalling. |
| 645 | 19904525 | Also, immunohistochemistry (IHC) was used to probe dectin-1 as well as anti-mouse Ccl3, Il1-alpha, and TNF-alpha expression to evaluate dose and time-course (4 and 12 h) postexposure (PE) response patterns in the lungs of intratracheally instilled mice exposed to a single 50 mul dose of curdlan at 10(-7), 10(-8), 10(-9), and 10(-10) M/animal (=4 mug to 4 ng curdlan/kg lung wt). |
| 646 | 19904525 | Nine gene mRNA transcripts (Ccl3, Ccl11, Ccl17, Ifng, Il1alpha, Il-20, TNF-alpha, Tnfrsf1b, and CD40lg) were significantly expressed at all doses suggesting they may have a central role in immunomodulating curdlan exposures. |
| 647 | 19904525 | IHC revealed Ccl3, Il1-alpha, and TNF-alpha expression in bronchiolar epithelium, AMs and ATIIs illustrate the important immunomodulatory role that these cells have in the recognition of, and response to glucan. |
| 648 | 19904525 | Also, immunohistochemistry (IHC) was used to probe dectin-1 as well as anti-mouse Ccl3, Il1-alpha, and TNF-alpha expression to evaluate dose and time-course (4 and 12 h) postexposure (PE) response patterns in the lungs of intratracheally instilled mice exposed to a single 50 mul dose of curdlan at 10(-7), 10(-8), 10(-9), and 10(-10) M/animal (=4 mug to 4 ng curdlan/kg lung wt). |
| 649 | 19904525 | Nine gene mRNA transcripts (Ccl3, Ccl11, Ccl17, Ifng, Il1alpha, Il-20, TNF-alpha, Tnfrsf1b, and CD40lg) were significantly expressed at all doses suggesting they may have a central role in immunomodulating curdlan exposures. |
| 650 | 19904525 | IHC revealed Ccl3, Il1-alpha, and TNF-alpha expression in bronchiolar epithelium, AMs and ATIIs illustrate the important immunomodulatory role that these cells have in the recognition of, and response to glucan. |
| 651 | 19904525 | Also, immunohistochemistry (IHC) was used to probe dectin-1 as well as anti-mouse Ccl3, Il1-alpha, and TNF-alpha expression to evaluate dose and time-course (4 and 12 h) postexposure (PE) response patterns in the lungs of intratracheally instilled mice exposed to a single 50 mul dose of curdlan at 10(-7), 10(-8), 10(-9), and 10(-10) M/animal (=4 mug to 4 ng curdlan/kg lung wt). |
| 652 | 19904525 | Nine gene mRNA transcripts (Ccl3, Ccl11, Ccl17, Ifng, Il1alpha, Il-20, TNF-alpha, Tnfrsf1b, and CD40lg) were significantly expressed at all doses suggesting they may have a central role in immunomodulating curdlan exposures. |
| 653 | 19904525 | IHC revealed Ccl3, Il1-alpha, and TNF-alpha expression in bronchiolar epithelium, AMs and ATIIs illustrate the important immunomodulatory role that these cells have in the recognition of, and response to glucan. |
| 654 | 20035105 | However, cultured mid luteal cells had a higher percentage of cFLIP-positive cells and a lower percentage of TUNEL-positive cells than luteal cells treated with tumor necrosis factor alpha (TNF)/interferon gamma (IFNG; P<0.01). |
| 655 | 20097948 | Of the cytokine gene polymorphisms that determine the level of gene expression, TNF-a -08G/A, IFN-g +874T/A and microsatellite (CA)n, TGF-b1 +869T/C and +915G/C, IL-6 -174G/C, and IL-10 -592C/A, -819C/T, and -1082G/A seem to have the strongest impact on graft survival. |
| 656 | 20097948 | Increased risk of acute rejection (AR) was demonstrated for high-producing genotypes of pro-inflammatory cytokines such as TNF-a and IFN-g, while the association with polymorphisms of TGF-b1 and IL-10 remains unclear. |
| 657 | 20097948 | The risk of graft loss was greater among high TNF-a and low TGF-b1 or IL-6 producers. |
| 658 | 20097948 | Low donor transcriptional TGF-b1 gene activity predisposed the recipient to AR episodes and high IFN-g expression to IF/TA development. |
| 659 | 20097948 | Of the cytokine gene polymorphisms that determine the level of gene expression, TNF-a -08G/A, IFN-g +874T/A and microsatellite (CA)n, TGF-b1 +869T/C and +915G/C, IL-6 -174G/C, and IL-10 -592C/A, -819C/T, and -1082G/A seem to have the strongest impact on graft survival. |
| 660 | 20097948 | Increased risk of acute rejection (AR) was demonstrated for high-producing genotypes of pro-inflammatory cytokines such as TNF-a and IFN-g, while the association with polymorphisms of TGF-b1 and IL-10 remains unclear. |
| 661 | 20097948 | The risk of graft loss was greater among high TNF-a and low TGF-b1 or IL-6 producers. |
| 662 | 20097948 | Low donor transcriptional TGF-b1 gene activity predisposed the recipient to AR episodes and high IFN-g expression to IF/TA development. |
| 663 | 20097948 | Of the cytokine gene polymorphisms that determine the level of gene expression, TNF-a -08G/A, IFN-g +874T/A and microsatellite (CA)n, TGF-b1 +869T/C and +915G/C, IL-6 -174G/C, and IL-10 -592C/A, -819C/T, and -1082G/A seem to have the strongest impact on graft survival. |
| 664 | 20097948 | Increased risk of acute rejection (AR) was demonstrated for high-producing genotypes of pro-inflammatory cytokines such as TNF-a and IFN-g, while the association with polymorphisms of TGF-b1 and IL-10 remains unclear. |
| 665 | 20097948 | The risk of graft loss was greater among high TNF-a and low TGF-b1 or IL-6 producers. |
| 666 | 20097948 | Low donor transcriptional TGF-b1 gene activity predisposed the recipient to AR episodes and high IFN-g expression to IF/TA development. |
| 667 | 20164427 | Induction of genes implicated in diabetes, such as Il18, Tnfa, and Inos but not Il4, Il17 or Ifng, was repressed in splenocytes derived from protected mice. |
| 668 | 20213229 | Polymorphisms in the genes of IL-lA, IL-lB, IL-2, IL-4, IL-6, IL-10, IL-12, IFN-G, TGF-beta, TNF-alpha, and of the cytokine receptors IL-lR, IL-IRA, IL-4RA were investigated. |
| 669 | 20213229 | APO-E and ACE gene polymorphisms were carried out in the patient's group only to evaluate a possible association with known genetic risk factors for AD. |
| 670 | 20213229 | A highly significant presence of some alleles belonging to anti-inflammatory cytokine genes was found; particularly the C allele for the -590 promoter and T allele for the -1098 promoter of IL-4 appeared in a significantly higher percentage as compared with controls (P < 0.0006 and P < 0.0005, respectively), while a lesser significance was observed for the allele C of the -819 promoter of IL-10 (P < 0.03). |
| 671 | 20213229 | Finally, in the group of demented patients for the APO-E gene we found a statistically significant presence of the E4 allele, whereas no difference was found for the polymorphisms of the ACE gene. |
| 672 | 20404426 | Association of interleukin-10, interferon-gamma, transforming growth factor-beta, and tumor necrosis factor-alpha gene polymorphisms with long-term kidney allograft survival. |
| 673 | 20419805 | The genotyping for TNF (-308), TGFB1 (+869, +915), IL-10 (-1082, -819, -592), IL-6 (-174), and IFNG (+874) was accomplished by the PCR-SSP technique. |
| 674 | 20562522 | Cell death of LSCs and LECs is essential for structural luteolysis. |
| 675 | 20562522 | We previously reported that a treatment combining tumor necrosis factor α (TNF) and interferon γ (IFNG) induced cell death in LSCs and that LECs express TNF receptor type I (TNFRI). |
| 676 | 20562522 | To induce cell death in LECs, LECs were treated with TNF or IFNG (0, 0.05, 0.5, 1.0, 2.5 nM) and a combination of TNF (0.5 nM) and IFNG (0.5 nM) for 24 h. |
| 677 | 20562522 | The viability of LECs was reduced by a single treatment with TNF or IFNG dose-dependently (P<0.05). |
| 678 | 20562522 | Cell viability was further decreased by treatment with a combination of TNF and IFNG (P<0.05). |
| 679 | 20562522 | Cells with DNA fragmentation (TUNEL-positive cells) were observed after the treatment with TNF and IFNG. |
| 680 | 20562522 | Semi-quantitative RT-PCR analysis revealed that treatment with IFNG alone or in combination with TNF increased the expression of TNFRI mRNA compared with the control (P<0.05). |
| 681 | 20562522 | In summary, TNF and IFNG increased cell death in cultured bovine LECs. |
| 682 | 20562522 | The upregulation of TNFRI mRNA expression by IFNG suggests that TNF and IFNG synergistically affect the death of LECs resulting in acute luteolysis. |
| 683 | 20562522 | Cell death of LSCs and LECs is essential for structural luteolysis. |
| 684 | 20562522 | We previously reported that a treatment combining tumor necrosis factor α (TNF) and interferon γ (IFNG) induced cell death in LSCs and that LECs express TNF receptor type I (TNFRI). |
| 685 | 20562522 | To induce cell death in LECs, LECs were treated with TNF or IFNG (0, 0.05, 0.5, 1.0, 2.5 nM) and a combination of TNF (0.5 nM) and IFNG (0.5 nM) for 24 h. |
| 686 | 20562522 | The viability of LECs was reduced by a single treatment with TNF or IFNG dose-dependently (P<0.05). |
| 687 | 20562522 | Cell viability was further decreased by treatment with a combination of TNF and IFNG (P<0.05). |
| 688 | 20562522 | Cells with DNA fragmentation (TUNEL-positive cells) were observed after the treatment with TNF and IFNG. |
| 689 | 20562522 | Semi-quantitative RT-PCR analysis revealed that treatment with IFNG alone or in combination with TNF increased the expression of TNFRI mRNA compared with the control (P<0.05). |
| 690 | 20562522 | In summary, TNF and IFNG increased cell death in cultured bovine LECs. |
| 691 | 20562522 | The upregulation of TNFRI mRNA expression by IFNG suggests that TNF and IFNG synergistically affect the death of LECs resulting in acute luteolysis. |
| 692 | 20562522 | Cell death of LSCs and LECs is essential for structural luteolysis. |
| 693 | 20562522 | We previously reported that a treatment combining tumor necrosis factor α (TNF) and interferon γ (IFNG) induced cell death in LSCs and that LECs express TNF receptor type I (TNFRI). |
| 694 | 20562522 | To induce cell death in LECs, LECs were treated with TNF or IFNG (0, 0.05, 0.5, 1.0, 2.5 nM) and a combination of TNF (0.5 nM) and IFNG (0.5 nM) for 24 h. |
| 695 | 20562522 | The viability of LECs was reduced by a single treatment with TNF or IFNG dose-dependently (P<0.05). |
| 696 | 20562522 | Cell viability was further decreased by treatment with a combination of TNF and IFNG (P<0.05). |
| 697 | 20562522 | Cells with DNA fragmentation (TUNEL-positive cells) were observed after the treatment with TNF and IFNG. |
| 698 | 20562522 | Semi-quantitative RT-PCR analysis revealed that treatment with IFNG alone or in combination with TNF increased the expression of TNFRI mRNA compared with the control (P<0.05). |
| 699 | 20562522 | In summary, TNF and IFNG increased cell death in cultured bovine LECs. |
| 700 | 20562522 | The upregulation of TNFRI mRNA expression by IFNG suggests that TNF and IFNG synergistically affect the death of LECs resulting in acute luteolysis. |
| 701 | 20562522 | Cell death of LSCs and LECs is essential for structural luteolysis. |
| 702 | 20562522 | We previously reported that a treatment combining tumor necrosis factor α (TNF) and interferon γ (IFNG) induced cell death in LSCs and that LECs express TNF receptor type I (TNFRI). |
| 703 | 20562522 | To induce cell death in LECs, LECs were treated with TNF or IFNG (0, 0.05, 0.5, 1.0, 2.5 nM) and a combination of TNF (0.5 nM) and IFNG (0.5 nM) for 24 h. |
| 704 | 20562522 | The viability of LECs was reduced by a single treatment with TNF or IFNG dose-dependently (P<0.05). |
| 705 | 20562522 | Cell viability was further decreased by treatment with a combination of TNF and IFNG (P<0.05). |
| 706 | 20562522 | Cells with DNA fragmentation (TUNEL-positive cells) were observed after the treatment with TNF and IFNG. |
| 707 | 20562522 | Semi-quantitative RT-PCR analysis revealed that treatment with IFNG alone or in combination with TNF increased the expression of TNFRI mRNA compared with the control (P<0.05). |
| 708 | 20562522 | In summary, TNF and IFNG increased cell death in cultured bovine LECs. |
| 709 | 20562522 | The upregulation of TNFRI mRNA expression by IFNG suggests that TNF and IFNG synergistically affect the death of LECs resulting in acute luteolysis. |
| 710 | 20562522 | Cell death of LSCs and LECs is essential for structural luteolysis. |
| 711 | 20562522 | We previously reported that a treatment combining tumor necrosis factor α (TNF) and interferon γ (IFNG) induced cell death in LSCs and that LECs express TNF receptor type I (TNFRI). |
| 712 | 20562522 | To induce cell death in LECs, LECs were treated with TNF or IFNG (0, 0.05, 0.5, 1.0, 2.5 nM) and a combination of TNF (0.5 nM) and IFNG (0.5 nM) for 24 h. |
| 713 | 20562522 | The viability of LECs was reduced by a single treatment with TNF or IFNG dose-dependently (P<0.05). |
| 714 | 20562522 | Cell viability was further decreased by treatment with a combination of TNF and IFNG (P<0.05). |
| 715 | 20562522 | Cells with DNA fragmentation (TUNEL-positive cells) were observed after the treatment with TNF and IFNG. |
| 716 | 20562522 | Semi-quantitative RT-PCR analysis revealed that treatment with IFNG alone or in combination with TNF increased the expression of TNFRI mRNA compared with the control (P<0.05). |
| 717 | 20562522 | In summary, TNF and IFNG increased cell death in cultured bovine LECs. |
| 718 | 20562522 | The upregulation of TNFRI mRNA expression by IFNG suggests that TNF and IFNG synergistically affect the death of LECs resulting in acute luteolysis. |
| 719 | 20562522 | Cell death of LSCs and LECs is essential for structural luteolysis. |
| 720 | 20562522 | We previously reported that a treatment combining tumor necrosis factor α (TNF) and interferon γ (IFNG) induced cell death in LSCs and that LECs express TNF receptor type I (TNFRI). |
| 721 | 20562522 | To induce cell death in LECs, LECs were treated with TNF or IFNG (0, 0.05, 0.5, 1.0, 2.5 nM) and a combination of TNF (0.5 nM) and IFNG (0.5 nM) for 24 h. |
| 722 | 20562522 | The viability of LECs was reduced by a single treatment with TNF or IFNG dose-dependently (P<0.05). |
| 723 | 20562522 | Cell viability was further decreased by treatment with a combination of TNF and IFNG (P<0.05). |
| 724 | 20562522 | Cells with DNA fragmentation (TUNEL-positive cells) were observed after the treatment with TNF and IFNG. |
| 725 | 20562522 | Semi-quantitative RT-PCR analysis revealed that treatment with IFNG alone or in combination with TNF increased the expression of TNFRI mRNA compared with the control (P<0.05). |
| 726 | 20562522 | In summary, TNF and IFNG increased cell death in cultured bovine LECs. |
| 727 | 20562522 | The upregulation of TNFRI mRNA expression by IFNG suggests that TNF and IFNG synergistically affect the death of LECs resulting in acute luteolysis. |
| 728 | 20562522 | Cell death of LSCs and LECs is essential for structural luteolysis. |
| 729 | 20562522 | We previously reported that a treatment combining tumor necrosis factor α (TNF) and interferon γ (IFNG) induced cell death in LSCs and that LECs express TNF receptor type I (TNFRI). |
| 730 | 20562522 | To induce cell death in LECs, LECs were treated with TNF or IFNG (0, 0.05, 0.5, 1.0, 2.5 nM) and a combination of TNF (0.5 nM) and IFNG (0.5 nM) for 24 h. |
| 731 | 20562522 | The viability of LECs was reduced by a single treatment with TNF or IFNG dose-dependently (P<0.05). |
| 732 | 20562522 | Cell viability was further decreased by treatment with a combination of TNF and IFNG (P<0.05). |
| 733 | 20562522 | Cells with DNA fragmentation (TUNEL-positive cells) were observed after the treatment with TNF and IFNG. |
| 734 | 20562522 | Semi-quantitative RT-PCR analysis revealed that treatment with IFNG alone or in combination with TNF increased the expression of TNFRI mRNA compared with the control (P<0.05). |
| 735 | 20562522 | In summary, TNF and IFNG increased cell death in cultured bovine LECs. |
| 736 | 20562522 | The upregulation of TNFRI mRNA expression by IFNG suggests that TNF and IFNG synergistically affect the death of LECs resulting in acute luteolysis. |
| 737 | 20562522 | Cell death of LSCs and LECs is essential for structural luteolysis. |
| 738 | 20562522 | We previously reported that a treatment combining tumor necrosis factor α (TNF) and interferon γ (IFNG) induced cell death in LSCs and that LECs express TNF receptor type I (TNFRI). |
| 739 | 20562522 | To induce cell death in LECs, LECs were treated with TNF or IFNG (0, 0.05, 0.5, 1.0, 2.5 nM) and a combination of TNF (0.5 nM) and IFNG (0.5 nM) for 24 h. |
| 740 | 20562522 | The viability of LECs was reduced by a single treatment with TNF or IFNG dose-dependently (P<0.05). |
| 741 | 20562522 | Cell viability was further decreased by treatment with a combination of TNF and IFNG (P<0.05). |
| 742 | 20562522 | Cells with DNA fragmentation (TUNEL-positive cells) were observed after the treatment with TNF and IFNG. |
| 743 | 20562522 | Semi-quantitative RT-PCR analysis revealed that treatment with IFNG alone or in combination with TNF increased the expression of TNFRI mRNA compared with the control (P<0.05). |
| 744 | 20562522 | In summary, TNF and IFNG increased cell death in cultured bovine LECs. |
| 745 | 20562522 | The upregulation of TNFRI mRNA expression by IFNG suggests that TNF and IFNG synergistically affect the death of LECs resulting in acute luteolysis. |
| 746 | 20625487 | Fifty six genes such as TNF, NFKB1, IL2, IL6, and MAPK8 were ranked among the top 25 by at least one of the centrality methods in one or both networks. |
| 747 | 20720169 | Is FAS/Fas ligand system involved in equine corpus luteum functional regression? |
| 748 | 20720169 | Proapoptotic factor Fas ligand (FASL) and its cell surface receptor FAS are tumor necrosis factor superfamily members that trigger apoptosis in different cell types. |
| 749 | 20720169 | The aim of the present work was to determine (i) the presence of the cytokine FASL and its receptor FAS in the mare's corpus luteum (CL) throughout the luteal phase, as well as (ii) the influence of FASL alone, or together with the cytokines tumor necrosis factor alpha (TNF) and interferon gamma (IFNG), on equine luteal cell production of luteotrophic and luteolytic factors, cell viability, and apoptosis. |
| 750 | 20720169 | FASL and FAS protein expression and mRNA transcription were evaluated in different luteal stages of the equine CL by Western blotting and real-time PCR assays, respectively. |
| 751 | 20720169 | Also, FAS and FASL proteins were present in large steroidogenic and endothelial CL cells throughout the luteal phase, as demonstrated by immunohistochemistry. |
| 752 | 20720169 | Equine luteal cells isolated from midluteal phase CL were stimulated without (control) or with exogenous cytokines: FASL (10 ng/ml); TNF+IFNG (10 ng/ml each; positive control) or FASL+TNF+IFNG (10 ng/ml each). |
| 753 | 20720169 | Furthermore, FASL effect on equine luteal cell viability depended on the presence of cytokines TNF and IFNG. |
| 754 | 20720169 | In conclusion, this study shows the presence of FASL and FAS in the equine CL and suggests their importance in functional luteolysis. |
| 755 | 20720169 | Is FAS/Fas ligand system involved in equine corpus luteum functional regression? |
| 756 | 20720169 | Proapoptotic factor Fas ligand (FASL) and its cell surface receptor FAS are tumor necrosis factor superfamily members that trigger apoptosis in different cell types. |
| 757 | 20720169 | The aim of the present work was to determine (i) the presence of the cytokine FASL and its receptor FAS in the mare's corpus luteum (CL) throughout the luteal phase, as well as (ii) the influence of FASL alone, or together with the cytokines tumor necrosis factor alpha (TNF) and interferon gamma (IFNG), on equine luteal cell production of luteotrophic and luteolytic factors, cell viability, and apoptosis. |
| 758 | 20720169 | FASL and FAS protein expression and mRNA transcription were evaluated in different luteal stages of the equine CL by Western blotting and real-time PCR assays, respectively. |
| 759 | 20720169 | Also, FAS and FASL proteins were present in large steroidogenic and endothelial CL cells throughout the luteal phase, as demonstrated by immunohistochemistry. |
| 760 | 20720169 | Equine luteal cells isolated from midluteal phase CL were stimulated without (control) or with exogenous cytokines: FASL (10 ng/ml); TNF+IFNG (10 ng/ml each; positive control) or FASL+TNF+IFNG (10 ng/ml each). |
| 761 | 20720169 | Furthermore, FASL effect on equine luteal cell viability depended on the presence of cytokines TNF and IFNG. |
| 762 | 20720169 | In conclusion, this study shows the presence of FASL and FAS in the equine CL and suggests their importance in functional luteolysis. |
| 763 | 20720169 | Is FAS/Fas ligand system involved in equine corpus luteum functional regression? |
| 764 | 20720169 | Proapoptotic factor Fas ligand (FASL) and its cell surface receptor FAS are tumor necrosis factor superfamily members that trigger apoptosis in different cell types. |
| 765 | 20720169 | The aim of the present work was to determine (i) the presence of the cytokine FASL and its receptor FAS in the mare's corpus luteum (CL) throughout the luteal phase, as well as (ii) the influence of FASL alone, or together with the cytokines tumor necrosis factor alpha (TNF) and interferon gamma (IFNG), on equine luteal cell production of luteotrophic and luteolytic factors, cell viability, and apoptosis. |
| 766 | 20720169 | FASL and FAS protein expression and mRNA transcription were evaluated in different luteal stages of the equine CL by Western blotting and real-time PCR assays, respectively. |
| 767 | 20720169 | Also, FAS and FASL proteins were present in large steroidogenic and endothelial CL cells throughout the luteal phase, as demonstrated by immunohistochemistry. |
| 768 | 20720169 | Equine luteal cells isolated from midluteal phase CL were stimulated without (control) or with exogenous cytokines: FASL (10 ng/ml); TNF+IFNG (10 ng/ml each; positive control) or FASL+TNF+IFNG (10 ng/ml each). |
| 769 | 20720169 | Furthermore, FASL effect on equine luteal cell viability depended on the presence of cytokines TNF and IFNG. |
| 770 | 20720169 | In conclusion, this study shows the presence of FASL and FAS in the equine CL and suggests their importance in functional luteolysis. |
| 771 | 20722470 | Cystic fibrosis conductance regulator, tumor necrosis factor, interferon alpha-10, interferon alpha-17, and interferon gamma genotyping as potential risk markers in pulmonary sarcoidosis pathogenesis in Greek patients. |
| 772 | 20722470 | We have screened for mutations in the cystic fibrosis conductance regulator (CFTR) gene and genotyped single-nucleotide polymorphisms in the tumor necrosis factor (TNF), interferon alpha-10 (IFNA10), IFNA17, and interferon gamma (IFNG) genes in 89 Greek patients with sarcoidosis and 212 control subjects to detect possible association between them and the risk for developing sarcoidosis. |
| 773 | 20722470 | Our study did not reproduce the associations previously noted with the TNF, IFNA10, IFNA17, and IFNG genes, which highlights the genetic complexity of the disorder and is in agreement with previous studies showing that CFTR might be an important factor in the clinical course of the disease. |
| 774 | 20722470 | Cystic fibrosis conductance regulator, tumor necrosis factor, interferon alpha-10, interferon alpha-17, and interferon gamma genotyping as potential risk markers in pulmonary sarcoidosis pathogenesis in Greek patients. |
| 775 | 20722470 | We have screened for mutations in the cystic fibrosis conductance regulator (CFTR) gene and genotyped single-nucleotide polymorphisms in the tumor necrosis factor (TNF), interferon alpha-10 (IFNA10), IFNA17, and interferon gamma (IFNG) genes in 89 Greek patients with sarcoidosis and 212 control subjects to detect possible association between them and the risk for developing sarcoidosis. |
| 776 | 20722470 | Our study did not reproduce the associations previously noted with the TNF, IFNA10, IFNA17, and IFNG genes, which highlights the genetic complexity of the disorder and is in agreement with previous studies showing that CFTR might be an important factor in the clinical course of the disease. |
| 777 | 20722470 | Cystic fibrosis conductance regulator, tumor necrosis factor, interferon alpha-10, interferon alpha-17, and interferon gamma genotyping as potential risk markers in pulmonary sarcoidosis pathogenesis in Greek patients. |
| 778 | 20722470 | We have screened for mutations in the cystic fibrosis conductance regulator (CFTR) gene and genotyped single-nucleotide polymorphisms in the tumor necrosis factor (TNF), interferon alpha-10 (IFNA10), IFNA17, and interferon gamma (IFNG) genes in 89 Greek patients with sarcoidosis and 212 control subjects to detect possible association between them and the risk for developing sarcoidosis. |
| 779 | 20722470 | Our study did not reproduce the associations previously noted with the TNF, IFNA10, IFNA17, and IFNG genes, which highlights the genetic complexity of the disorder and is in agreement with previous studies showing that CFTR might be an important factor in the clinical course of the disease. |
| 780 | 20944005 | PRDM1 response elements are defined at the IFNG and TNF loci. |
| 781 | 20953611 | We genotyped ten polymorphisms in three cytokine genes (IFNG, TNF, and TGFB1) and FAS gene. |
| 782 | 20953611 | In addition, it was found that polymorphisms in IFNG and TGFB1 are associated with response to IST. |
| 783 | 21090238 | [Analysis of linkage and association of alleles of proinflammatory cytokines genes IL-6, IFNg and TNF with multiple sclerosis using transmission disequilibrium test (TDT)]. |
| 784 | 21090238 | Proinflammatory cytokines Interleukin-6 (IL-6), Interferon-gamma (IFNg) and Tumor necrosis factor (TNF) are known as participants of inflammation and play an important role in pathogenesis of multiple sclerosis (MS). |
| 785 | 21090238 | Based on literature data about influence of SNPs G(-308)A of TNF gene, A(+874)T of IFNG gene and G(-174)C of IL-6 gene on production of these cytokines, we investigated association of these polymorphic sites with MS. |
| 786 | 21090238 | Linkage/association of IFNG and IL-6 alleles with MS was not revealed. |
| 787 | 21090238 | [Analysis of linkage and association of alleles of proinflammatory cytokines genes IL-6, IFNg and TNF with multiple sclerosis using transmission disequilibrium test (TDT)]. |
| 788 | 21090238 | Proinflammatory cytokines Interleukin-6 (IL-6), Interferon-gamma (IFNg) and Tumor necrosis factor (TNF) are known as participants of inflammation and play an important role in pathogenesis of multiple sclerosis (MS). |
| 789 | 21090238 | Based on literature data about influence of SNPs G(-308)A of TNF gene, A(+874)T of IFNG gene and G(-174)C of IL-6 gene on production of these cytokines, we investigated association of these polymorphic sites with MS. |
| 790 | 21090238 | Linkage/association of IFNG and IL-6 alleles with MS was not revealed. |
| 791 | 21090238 | [Analysis of linkage and association of alleles of proinflammatory cytokines genes IL-6, IFNg and TNF with multiple sclerosis using transmission disequilibrium test (TDT)]. |
| 792 | 21090238 | Proinflammatory cytokines Interleukin-6 (IL-6), Interferon-gamma (IFNg) and Tumor necrosis factor (TNF) are known as participants of inflammation and play an important role in pathogenesis of multiple sclerosis (MS). |
| 793 | 21090238 | Based on literature data about influence of SNPs G(-308)A of TNF gene, A(+874)T of IFNG gene and G(-174)C of IL-6 gene on production of these cytokines, we investigated association of these polymorphic sites with MS. |
| 794 | 21090238 | Linkage/association of IFNG and IL-6 alleles with MS was not revealed. |
| 795 | 21098980 | We investigated a panel of relevant polymorphisms to distinguish genetic backgrounds for AMI and AD: IL10 -1082G/A, IL6 -174G/C, TNF -308G/A, IFNG +874T/A, SERPINA3 -51G/T, HMGCR -911C/A, APOE ε2/3/4 (280 AMI cases, 257 AD cases, and 1307 population controls, all Italian (presumed risk alleles are shown in bold). |
| 796 | 21098980 | Set V 'AMI over a broad range of age' included risk alleles for TNF+IL6. |
| 797 | 21098980 | We investigated a panel of relevant polymorphisms to distinguish genetic backgrounds for AMI and AD: IL10 -1082G/A, IL6 -174G/C, TNF -308G/A, IFNG +874T/A, SERPINA3 -51G/T, HMGCR -911C/A, APOE ε2/3/4 (280 AMI cases, 257 AD cases, and 1307 population controls, all Italian (presumed risk alleles are shown in bold). |
| 798 | 21098980 | Set V 'AMI over a broad range of age' included risk alleles for TNF+IL6. |
| 799 | 21215285 | Chlamydia trachomatis-induced fallopian tube damage leading to tubal factor infertility (TFI) is linked with TNF, IL-10, and probably IFNG gene polymorphisms. |
| 800 | 21215285 | Cytokine polymorphisms (IL-10 -1082A/G, -819T/C, and -592A/C, IFNG +874T/A, and TNF -308G/A) were genotyped by polymerase chain reaction in 139 women. |
| 801 | 21215285 | IL-10 -1082/-819/-592 and IFNG +874 SNPs were associated with the intensity of LP responses to C trachomatis antigens. |
| 802 | 21215285 | These cytokines also interact with each other and a cumulative effect of IL-10 -1082 and IFNG +874 genotypes was seen in LP responses to C trachomatis antigens. |
| 803 | 21215285 | Chlamydia trachomatis-induced fallopian tube damage leading to tubal factor infertility (TFI) is linked with TNF, IL-10, and probably IFNG gene polymorphisms. |
| 804 | 21215285 | Cytokine polymorphisms (IL-10 -1082A/G, -819T/C, and -592A/C, IFNG +874T/A, and TNF -308G/A) were genotyped by polymerase chain reaction in 139 women. |
| 805 | 21215285 | IL-10 -1082/-819/-592 and IFNG +874 SNPs were associated with the intensity of LP responses to C trachomatis antigens. |
| 806 | 21215285 | These cytokines also interact with each other and a cumulative effect of IL-10 -1082 and IFNG +874 genotypes was seen in LP responses to C trachomatis antigens. |
| 807 | 21321581 | Protection against diabetes was accompanied by histone hyperacetylation in pancreas and spleen, enhanced frequency of CD4(+) CD62L(+) cells in the spleen, reduction in cellular infiltration of islets, restoration of normoglycemia and glucose-induced insulin release by beta cells. |
| 808 | 21321581 | Activation of splenic T lymphocytes derived from protected mice in vitro with pharmacological agents that bypass the antigen receptor or immobilized anti-CD3 antibody resulted in enhanced expression of Ifng mRNA and protein without altering the expression of Il4, Il17, Il18, Inos and Tnfa genes nor the secretion of IL-2, IL-4, IL-17 and TNF-α proteins. |
| 809 | 21321581 | Consistently, expression of the transcription factor involved in Ifng transcription, Tbet/Tbx21 but not Gata3 and Rorgt, respectively, required for the transcription of Il4 and Il17, was upregulated in activated splenocytes of protected mice. |
| 810 | 21393251 | Expression of proinflammatory cytokines, including Tnfa, Il17a, and Ifng, was up-regulated, whereas expression of antimicrobial peptides was down-regulated in the colon of Traf2(-/-) mice. |
| 811 | 21393251 | Moreover, a number of IL-17-producing helper T cells were increased in the colonic lamina propria of Traf2(-/-) mice. |
| 812 | 21393251 | Finally, deletion of Tnfr1, but not Il17a, dramatically ameliorated colitis in Traf2(-/-) mice by preventing apoptosis of colonic epithelial cells, down-regulation of proinflammatory cytokines, and restoration of wild-type commensal bacteria. |
| 813 | 21463712 | In the current study we investigated genotype variants pertaining to five cytokine genes namely IFNG, TNFA, IL4, IL10 and IL12 in the north Indian population with active pulmonary tuberculosis (APTB) and correlated the serum cytokine levels with the corresponding genotypes. |
| 814 | 21463712 | Compared to HC mean serum IFN-γ, IL-12, IL-4, and IL-10 levels were higher in APTB (p = 0.3661, p = 0.0186, p = 0.003, p = 0.7, respectively). |
| 815 | 21463712 | In contrast the genotypes of the selected rsIDs in the TNFA, IL12 and IL10 genes showed significant association with the varying serum levels of corresponding cytokines. |
| 816 | 21463712 | The variant of the TNFA gene at rs3093662, the IL12 gene at rs3213094 and rs3212220 and the IL10 gene at rs3024498 did show a strong indication to be of relevance to the immunity to tuberculosis. |
| 817 | 21463712 | In the current study we investigated genotype variants pertaining to five cytokine genes namely IFNG, TNFA, IL4, IL10 and IL12 in the north Indian population with active pulmonary tuberculosis (APTB) and correlated the serum cytokine levels with the corresponding genotypes. |
| 818 | 21463712 | Compared to HC mean serum IFN-γ, IL-12, IL-4, and IL-10 levels were higher in APTB (p = 0.3661, p = 0.0186, p = 0.003, p = 0.7, respectively). |
| 819 | 21463712 | In contrast the genotypes of the selected rsIDs in the TNFA, IL12 and IL10 genes showed significant association with the varying serum levels of corresponding cytokines. |
| 820 | 21463712 | The variant of the TNFA gene at rs3093662, the IL12 gene at rs3213094 and rs3212220 and the IL10 gene at rs3024498 did show a strong indication to be of relevance to the immunity to tuberculosis. |
| 821 | 21463712 | In the current study we investigated genotype variants pertaining to five cytokine genes namely IFNG, TNFA, IL4, IL10 and IL12 in the north Indian population with active pulmonary tuberculosis (APTB) and correlated the serum cytokine levels with the corresponding genotypes. |
| 822 | 21463712 | Compared to HC mean serum IFN-γ, IL-12, IL-4, and IL-10 levels were higher in APTB (p = 0.3661, p = 0.0186, p = 0.003, p = 0.7, respectively). |
| 823 | 21463712 | In contrast the genotypes of the selected rsIDs in the TNFA, IL12 and IL10 genes showed significant association with the varying serum levels of corresponding cytokines. |
| 824 | 21463712 | The variant of the TNFA gene at rs3093662, the IL12 gene at rs3213094 and rs3212220 and the IL10 gene at rs3024498 did show a strong indication to be of relevance to the immunity to tuberculosis. |
| 825 | 21585261 | During the early events of host-pathogen interaction identified genes are involved in pattern recognition receptors, and mycobacterial uptake (TLRs, NOD2 and MRC1), which modulate autophagy. |
| 826 | 21585261 | Together, the activation of these pathways regulates cellular metabolism upon infection, activating cytokine production through NF-κB and vitamin D-vitamin D receptor pathways, while PARK2 and LRRK2 participate in the regulation of host-cell apoptosis. |
| 827 | 21585261 | Concomitantly, genes triggered to form and maintain granulomas (TNF, LTA and IFNG) and genes involved in activating and differentiating T-helper cells (HLA, IL10, as well as the TNF/LTA axis and the IFNG/IL12 axis) bridge immunological regulation towards adaptive immunity. |
| 828 | 21685942 | Comparative analysis of inflammation-related genes showed that Ifng, Il1b and Nos2 had expression concordant with methylation induction whereas Il2, Il6, Il10, Tnf did not. |
| 829 | 21744329 | Assessment of the levels of nitric oxide (NO) and cytokines (IL-5, IL-6, IL-13, TNF, IFN-gamma) in giardiosis. |
| 830 | 21744329 | The serum concentrations of IL-5, IL-6, IL-13, TNF, IFN-g were assayed using a set of Quantikine human. |
| 831 | 21744329 | Patients infected with G. intestinalis showed a statistically significant increase in the levels of NO, IFN-g and IL-13. |
| 832 | 21744329 | Assessment of the levels of nitric oxide (NO) and cytokines (IL-5, IL-6, IL-13, TNF, IFN-gamma) in giardiosis. |
| 833 | 21744329 | The serum concentrations of IL-5, IL-6, IL-13, TNF, IFN-g were assayed using a set of Quantikine human. |
| 834 | 21744329 | Patients infected with G. intestinalis showed a statistically significant increase in the levels of NO, IFN-g and IL-13. |
| 835 | 21876173 | The experiments show that, although the majority of naive CD8(+) T-cell precursors are preprogrammed to produce TNF-α soon after stimulation and a proportion make both TNF-α and IL-2, the progressive acquisition of IFN-γ expression depends on continued lymphocyte proliferation. |
| 836 | 21876173 | Such proliferation-dependent variation in cytokine production appears tied to the epigenetic signatures within the ifnG and tnfA proximal promoters. |
| 837 | 21966102 | No association was observed with risk of BPH for IFN-G +874, IL-1 RN VNTR, IL-6 -174, IL-10 -819 and TGF-B +28. |
| 838 | 21966102 | Our findings of IL-1B -511, TNF-A -1031 and IL-10 -1082 suggested that these variants play important role in susceptibility to BPH. |
| 839 | 21976969 | Microarray and qRT-PCR data analyses showed significant upregulation of some cytotoxicity-related genes, including those from the granzyme family, tumor necrosis factor, Fas Ligand, and chemokines, in the spleen cells of IFNg KO mice. |
| 840 | 21976969 | Furthermore, CD8+ cells instead of NK cells of IFNg KO mice exhibited increased transcription of cytotoxic genes compared with WT mice. |
| 841 | 21976969 | Additionally, Schistosoma japonicum-specific egg antigen immunization also could activate CD8+ T cells to upregulate the expression of cytotoxic genes in IFNg KO mice. |
| 842 | 22019771 | We used a gene panel of regulatory/inflammatory molecules (FOXP3, GATA3, IL10, TGFB1, TGFBR1/ TBX21, TNF and IFNG) to investigate the gene expression profile in peripheral blood mononuclear cells of renal-transplanted individuals experiencing OT compared to transplanted individuals not displaying OT and healthy individuals (HI). |
| 843 | 22019771 | OT subjects showed a predominant regulatory (REG) profile with higher gene expression of GATA3, FOXP3, TGFB1 and TGFB receptor 1 compared to the other groups. |
| 844 | 22121102 | JAK/STAT/SOCS-signaling pathway and colon and rectal cancer. |
| 845 | 22121102 | We evaluated the association between genetic variation in JAK1 (10 SNPs), JAK2 (9 SNPs), TYK2 (5 SNPs), suppressors of cytokine signaling (SOCS)1 (2 SNPs), SOCS2 (2 SNPs), STAT1 (16 SNPs), STAT2 (2 SNPs), STAT3 (6 SNPs), STAT4 (21 SNPs), STAT5A (2 SNPs), STAT5B (3 SNPs), STAT6 (4 SNPs) with risk of colorectal cancer. |
| 846 | 22121102 | JAK2, SOCS2, STAT1, STAT3, STAT5A, STAT5B, and STAT6 were associated with colon cancer; STAT3, STAT4, STAT6, and TYK2 were associated with rectal cancer. |
| 847 | 22121102 | Given the biological role of the JAK/STAT-signaling pathway and cytokines, we evaluated interaction with IFNG, TNF, and IL6; numerous statistically significant associations after adjustment for multiple comparisons were observed. |
| 848 | 22121102 | The following statistically significant interactions were observed: TYK2 with aspirin/NSAID use; STAT1, STAT4, and TYK2 with estrogen status; and JAK2, STAT2, STAT4, STAT5A, STAT5B, and STAT6 with smoking status and colon cancer risk; JAK2, STAT6, and TYK2 with aspirin/NSAID use; JAK1 with estrogen status; STAT2 with cigarette smoking and rectal cancer. |
| 849 | 22121102 | JAK2, SOCS1, STAT3, STAT5, and TYK2 were associated with colon cancer survival (hazard rate ratio (HRR) of 3.3 95% CI 2.01,5.42 for high mutational load). |
| 850 | 22121102 | JAK2, SOCS1, STAT1, STAT4, and TYK2 were associated with rectal cancer survival (HRR 2.80 95% CI 1.63,4.80). |
| 851 | 22186103 | In this study, the presence of cytokines tumor necrosis factor alpha (TNF) and interferon gamma (IFNG), and their receptors (TNFRI, TNFRII and IFNRI), was investigated in equine CL throughout the luteal phase. |
| 852 | 22186103 | The effects of TNF and IFNG on secretory function and viability of luteal cells were defined in vitro. |
| 853 | 22186103 | In the mid luteal phase, TNF increased PGF(2α) secretion and TNF+IFNG decreased PGE(2) secretion. |
| 854 | 22186103 | In the regressing luteal phase, TNF, IFNG and TNF+IFNG decreased P(4) and PGE(2) secretion, but TNF and TNF+IFNG increased PGF(2α) secretion by luteal cells. |
| 855 | 22186103 | Cell viability was reduced by TNF+IFNG in regressing CL. |
| 856 | 22186103 | These data show the presence of cytokines TNF and IFNG, and their receptors, in the equine CL and indicate their potential involvement in regulation of luteal function. |
| 857 | 22186103 | In this study, the presence of cytokines tumor necrosis factor alpha (TNF) and interferon gamma (IFNG), and their receptors (TNFRI, TNFRII and IFNRI), was investigated in equine CL throughout the luteal phase. |
| 858 | 22186103 | The effects of TNF and IFNG on secretory function and viability of luteal cells were defined in vitro. |
| 859 | 22186103 | In the mid luteal phase, TNF increased PGF(2α) secretion and TNF+IFNG decreased PGE(2) secretion. |
| 860 | 22186103 | In the regressing luteal phase, TNF, IFNG and TNF+IFNG decreased P(4) and PGE(2) secretion, but TNF and TNF+IFNG increased PGF(2α) secretion by luteal cells. |
| 861 | 22186103 | Cell viability was reduced by TNF+IFNG in regressing CL. |
| 862 | 22186103 | These data show the presence of cytokines TNF and IFNG, and their receptors, in the equine CL and indicate their potential involvement in regulation of luteal function. |
| 863 | 22186103 | In this study, the presence of cytokines tumor necrosis factor alpha (TNF) and interferon gamma (IFNG), and their receptors (TNFRI, TNFRII and IFNRI), was investigated in equine CL throughout the luteal phase. |
| 864 | 22186103 | The effects of TNF and IFNG on secretory function and viability of luteal cells were defined in vitro. |
| 865 | 22186103 | In the mid luteal phase, TNF increased PGF(2α) secretion and TNF+IFNG decreased PGE(2) secretion. |
| 866 | 22186103 | In the regressing luteal phase, TNF, IFNG and TNF+IFNG decreased P(4) and PGE(2) secretion, but TNF and TNF+IFNG increased PGF(2α) secretion by luteal cells. |
| 867 | 22186103 | Cell viability was reduced by TNF+IFNG in regressing CL. |
| 868 | 22186103 | These data show the presence of cytokines TNF and IFNG, and their receptors, in the equine CL and indicate their potential involvement in regulation of luteal function. |
| 869 | 22186103 | In this study, the presence of cytokines tumor necrosis factor alpha (TNF) and interferon gamma (IFNG), and their receptors (TNFRI, TNFRII and IFNRI), was investigated in equine CL throughout the luteal phase. |
| 870 | 22186103 | The effects of TNF and IFNG on secretory function and viability of luteal cells were defined in vitro. |
| 871 | 22186103 | In the mid luteal phase, TNF increased PGF(2α) secretion and TNF+IFNG decreased PGE(2) secretion. |
| 872 | 22186103 | In the regressing luteal phase, TNF, IFNG and TNF+IFNG decreased P(4) and PGE(2) secretion, but TNF and TNF+IFNG increased PGF(2α) secretion by luteal cells. |
| 873 | 22186103 | Cell viability was reduced by TNF+IFNG in regressing CL. |
| 874 | 22186103 | These data show the presence of cytokines TNF and IFNG, and their receptors, in the equine CL and indicate their potential involvement in regulation of luteal function. |
| 875 | 22186103 | In this study, the presence of cytokines tumor necrosis factor alpha (TNF) and interferon gamma (IFNG), and their receptors (TNFRI, TNFRII and IFNRI), was investigated in equine CL throughout the luteal phase. |
| 876 | 22186103 | The effects of TNF and IFNG on secretory function and viability of luteal cells were defined in vitro. |
| 877 | 22186103 | In the mid luteal phase, TNF increased PGF(2α) secretion and TNF+IFNG decreased PGE(2) secretion. |
| 878 | 22186103 | In the regressing luteal phase, TNF, IFNG and TNF+IFNG decreased P(4) and PGE(2) secretion, but TNF and TNF+IFNG increased PGF(2α) secretion by luteal cells. |
| 879 | 22186103 | Cell viability was reduced by TNF+IFNG in regressing CL. |
| 880 | 22186103 | These data show the presence of cytokines TNF and IFNG, and their receptors, in the equine CL and indicate their potential involvement in regulation of luteal function. |
| 881 | 22186103 | In this study, the presence of cytokines tumor necrosis factor alpha (TNF) and interferon gamma (IFNG), and their receptors (TNFRI, TNFRII and IFNRI), was investigated in equine CL throughout the luteal phase. |
| 882 | 22186103 | The effects of TNF and IFNG on secretory function and viability of luteal cells were defined in vitro. |
| 883 | 22186103 | In the mid luteal phase, TNF increased PGF(2α) secretion and TNF+IFNG decreased PGE(2) secretion. |
| 884 | 22186103 | In the regressing luteal phase, TNF, IFNG and TNF+IFNG decreased P(4) and PGE(2) secretion, but TNF and TNF+IFNG increased PGF(2α) secretion by luteal cells. |
| 885 | 22186103 | Cell viability was reduced by TNF+IFNG in regressing CL. |
| 886 | 22186103 | These data show the presence of cytokines TNF and IFNG, and their receptors, in the equine CL and indicate their potential involvement in regulation of luteal function. |
| 887 | 22295566 | Complex association analysis of copaxone (glatiramer acetate) immunotherapy efficacy with allelic polymorphism in the number of immune response genes, which encode interferone beta (IFNB1), transforming growth factor beta1 (TGFB1), interferone gamma (IFNG), tumor necrosis factor (TNF), interferon alpha/beta receptor 1 (IFNAR1), CC chemokine receptor 5 (CCR5), interleukin 7 receptor alpha subunit (IL7RA), cytotoxic T-lymphocyte antigen 4 (CTLA4) and HLA class II histocompatibility antigen beta chain (DRB1) was performed with APSampler algorithm for 285 multiple sclerosis patients of Russian ethnicity. |
| 888 | 22295566 | The results show evidence for the contribution of polymorphic variants in CCRS, DRB1, IFNG, TGFB1, IFNAR1, IL7RA and, probably, TNF and CTLA4 genes to copaxone treatment response. |
| 889 | 22295566 | Single alleles of CCR5 and DRB1 genes are reliably associated with treatment efficacy. |
| 890 | 22295566 | Complex association analysis of copaxone (glatiramer acetate) immunotherapy efficacy with allelic polymorphism in the number of immune response genes, which encode interferone beta (IFNB1), transforming growth factor beta1 (TGFB1), interferone gamma (IFNG), tumor necrosis factor (TNF), interferon alpha/beta receptor 1 (IFNAR1), CC chemokine receptor 5 (CCR5), interleukin 7 receptor alpha subunit (IL7RA), cytotoxic T-lymphocyte antigen 4 (CTLA4) and HLA class II histocompatibility antigen beta chain (DRB1) was performed with APSampler algorithm for 285 multiple sclerosis patients of Russian ethnicity. |
| 891 | 22295566 | The results show evidence for the contribution of polymorphic variants in CCRS, DRB1, IFNG, TGFB1, IFNAR1, IL7RA and, probably, TNF and CTLA4 genes to copaxone treatment response. |
| 892 | 22295566 | Single alleles of CCR5 and DRB1 genes are reliably associated with treatment efficacy. |
| 893 | 22307794 | The SNP c.611 T>A showed significant association with the transcription levels of IFNG, TNFA, and IL-6 (P < 0.05); the SNP c.962 G>A showed significant association with the transcription of IFNG, IL-2, and IL-4 (P < 0.05); the SNP c.1,027 C>A showed significant association with the transcription of IFNG and IL-6 (P < 0.05); the haplotypes showed significant association with the transcription of IFNG, IL-2, IL-4, IL-6, and TNFA (P < 0.05). |
| 894 | 22378921 | β (CCL2) and α (CXCL10) chemokine modulations by cytokines and peroxisome proliferator-activated receptor-α agonists in Graves' ophthalmopathy. |
| 895 | 22378921 | No data are present in the literature about the effect of cytokines on the prototype β chemokine (C-C motif) ligand 2 (CCL2) or of peroxisome proliferator-activated receptor α (PPARα (PPARA)) activation on CCL2 and CXCL10 chemokines secretion in fibroblasts or preadipocytes in Graves' ophthalmopathy (GO). |
| 896 | 22378921 | We have tested the effect of interferon γ (IFNγ (IFNG)) and tumor necrosis factor α (TNFα) on CCL2, and for comparison on the prototype α chemokine (C-X-C motif) ligand 10 (CXCL10), and the possible modulatory role of PPARα activation on secretion of these chemokines in normal and GO fibroblasts or preadipocytes in primary cell cultures. |
| 897 | 22378921 | PPARα activators were able to inhibit the secretion of CXCL10 and CCL2, while PPARγ activators were confirmed to be able to inhibit CXCL10 but had no effect on CCL2. |
| 898 | 22378921 | In conclusion, CCL2 and CXCL10 are modulated by IFNγ and TNFα in GO. |
| 899 | 22378921 | PPARα activators inhibit the secretion of the main prototype α (CXCL10) and β (CCL2) chemokines in GO fibroblasts or preadipocytes, suggesting that PPARα may be involved in the modulation of the immune response in GO. |
| 900 | 22492973 | Therefore, the purpose of this study was to evaluate the role of cytokines--tumor necrosis factor alpha (TNF), interferon gamma (IFNG) and Fas ligand (FASL)--on in vitro modulation of angiogenic activity and mRNA level of vascular endothelial growth factor A (VEGF), its receptor VEGFR2, thrombospondin 1 (TSP1), and its receptor CD36 in equine corpus luteum (CL) throughout the luteal phase. |
| 901 | 22492973 | The role of VEGF on regulation of luteal secretory capacity was assessed by progesterone (P(4)) and prostaglandin E(2) (PGE(2)) production and by mRNA levels for steroidogenic enzymes 3-beta-hydroxysteroid dehydrogenase (3betaHSD) and PGE synthase (PGES). |
| 902 | 22492973 | In early CL cells, TNF increased angiogenic activity (bovine aortic endothelial cell viability) and VEGF and VEGFR2 mRNA levels and decreased CD36 (real-time PCR relative quantification). |
| 903 | 22492973 | In mid-CL cells, TNF increased VEGF mRNA and protein expression (Western blot analysis) and reduced CD36 mRNA levels, while FASL and TNF+IFNG+FASL decreased VEGF protein expression. |
| 904 | 22492973 | In late CL cells, TNF and TNF+IFNG+FASL reduced VEGFR2 mRNA, but TNF+IFNG+FASL increased TSP1 and CD36 mRNA. |
| 905 | 22492973 | VEGF treatment increased mRNA levels of 3betaHSD and PGES and secretion of P(4) and PGE(2). |
| 906 | 22492973 | In conclusion, these findings suggest a novel auto/paracrine action of cytokines, specifically TNF, on the up-regulation of VEGF for angiogenesis stimulation in equine early CL, while at luteolysis, cytokines down-regulated angiogenesis. |
| 907 | 22492973 | Therefore, the purpose of this study was to evaluate the role of cytokines--tumor necrosis factor alpha (TNF), interferon gamma (IFNG) and Fas ligand (FASL)--on in vitro modulation of angiogenic activity and mRNA level of vascular endothelial growth factor A (VEGF), its receptor VEGFR2, thrombospondin 1 (TSP1), and its receptor CD36 in equine corpus luteum (CL) throughout the luteal phase. |
| 908 | 22492973 | The role of VEGF on regulation of luteal secretory capacity was assessed by progesterone (P(4)) and prostaglandin E(2) (PGE(2)) production and by mRNA levels for steroidogenic enzymes 3-beta-hydroxysteroid dehydrogenase (3betaHSD) and PGE synthase (PGES). |
| 909 | 22492973 | In early CL cells, TNF increased angiogenic activity (bovine aortic endothelial cell viability) and VEGF and VEGFR2 mRNA levels and decreased CD36 (real-time PCR relative quantification). |
| 910 | 22492973 | In mid-CL cells, TNF increased VEGF mRNA and protein expression (Western blot analysis) and reduced CD36 mRNA levels, while FASL and TNF+IFNG+FASL decreased VEGF protein expression. |
| 911 | 22492973 | In late CL cells, TNF and TNF+IFNG+FASL reduced VEGFR2 mRNA, but TNF+IFNG+FASL increased TSP1 and CD36 mRNA. |
| 912 | 22492973 | VEGF treatment increased mRNA levels of 3betaHSD and PGES and secretion of P(4) and PGE(2). |
| 913 | 22492973 | In conclusion, these findings suggest a novel auto/paracrine action of cytokines, specifically TNF, on the up-regulation of VEGF for angiogenesis stimulation in equine early CL, while at luteolysis, cytokines down-regulated angiogenesis. |
| 914 | 22492973 | Therefore, the purpose of this study was to evaluate the role of cytokines--tumor necrosis factor alpha (TNF), interferon gamma (IFNG) and Fas ligand (FASL)--on in vitro modulation of angiogenic activity and mRNA level of vascular endothelial growth factor A (VEGF), its receptor VEGFR2, thrombospondin 1 (TSP1), and its receptor CD36 in equine corpus luteum (CL) throughout the luteal phase. |
| 915 | 22492973 | The role of VEGF on regulation of luteal secretory capacity was assessed by progesterone (P(4)) and prostaglandin E(2) (PGE(2)) production and by mRNA levels for steroidogenic enzymes 3-beta-hydroxysteroid dehydrogenase (3betaHSD) and PGE synthase (PGES). |
| 916 | 22492973 | In early CL cells, TNF increased angiogenic activity (bovine aortic endothelial cell viability) and VEGF and VEGFR2 mRNA levels and decreased CD36 (real-time PCR relative quantification). |
| 917 | 22492973 | In mid-CL cells, TNF increased VEGF mRNA and protein expression (Western blot analysis) and reduced CD36 mRNA levels, while FASL and TNF+IFNG+FASL decreased VEGF protein expression. |
| 918 | 22492973 | In late CL cells, TNF and TNF+IFNG+FASL reduced VEGFR2 mRNA, but TNF+IFNG+FASL increased TSP1 and CD36 mRNA. |
| 919 | 22492973 | VEGF treatment increased mRNA levels of 3betaHSD and PGES and secretion of P(4) and PGE(2). |
| 920 | 22492973 | In conclusion, these findings suggest a novel auto/paracrine action of cytokines, specifically TNF, on the up-regulation of VEGF for angiogenesis stimulation in equine early CL, while at luteolysis, cytokines down-regulated angiogenesis. |
| 921 | 22492973 | Therefore, the purpose of this study was to evaluate the role of cytokines--tumor necrosis factor alpha (TNF), interferon gamma (IFNG) and Fas ligand (FASL)--on in vitro modulation of angiogenic activity and mRNA level of vascular endothelial growth factor A (VEGF), its receptor VEGFR2, thrombospondin 1 (TSP1), and its receptor CD36 in equine corpus luteum (CL) throughout the luteal phase. |
| 922 | 22492973 | The role of VEGF on regulation of luteal secretory capacity was assessed by progesterone (P(4)) and prostaglandin E(2) (PGE(2)) production and by mRNA levels for steroidogenic enzymes 3-beta-hydroxysteroid dehydrogenase (3betaHSD) and PGE synthase (PGES). |
| 923 | 22492973 | In early CL cells, TNF increased angiogenic activity (bovine aortic endothelial cell viability) and VEGF and VEGFR2 mRNA levels and decreased CD36 (real-time PCR relative quantification). |
| 924 | 22492973 | In mid-CL cells, TNF increased VEGF mRNA and protein expression (Western blot analysis) and reduced CD36 mRNA levels, while FASL and TNF+IFNG+FASL decreased VEGF protein expression. |
| 925 | 22492973 | In late CL cells, TNF and TNF+IFNG+FASL reduced VEGFR2 mRNA, but TNF+IFNG+FASL increased TSP1 and CD36 mRNA. |
| 926 | 22492973 | VEGF treatment increased mRNA levels of 3betaHSD and PGES and secretion of P(4) and PGE(2). |
| 927 | 22492973 | In conclusion, these findings suggest a novel auto/paracrine action of cytokines, specifically TNF, on the up-regulation of VEGF for angiogenesis stimulation in equine early CL, while at luteolysis, cytokines down-regulated angiogenesis. |
| 928 | 22492973 | Therefore, the purpose of this study was to evaluate the role of cytokines--tumor necrosis factor alpha (TNF), interferon gamma (IFNG) and Fas ligand (FASL)--on in vitro modulation of angiogenic activity and mRNA level of vascular endothelial growth factor A (VEGF), its receptor VEGFR2, thrombospondin 1 (TSP1), and its receptor CD36 in equine corpus luteum (CL) throughout the luteal phase. |
| 929 | 22492973 | The role of VEGF on regulation of luteal secretory capacity was assessed by progesterone (P(4)) and prostaglandin E(2) (PGE(2)) production and by mRNA levels for steroidogenic enzymes 3-beta-hydroxysteroid dehydrogenase (3betaHSD) and PGE synthase (PGES). |
| 930 | 22492973 | In early CL cells, TNF increased angiogenic activity (bovine aortic endothelial cell viability) and VEGF and VEGFR2 mRNA levels and decreased CD36 (real-time PCR relative quantification). |
| 931 | 22492973 | In mid-CL cells, TNF increased VEGF mRNA and protein expression (Western blot analysis) and reduced CD36 mRNA levels, while FASL and TNF+IFNG+FASL decreased VEGF protein expression. |
| 932 | 22492973 | In late CL cells, TNF and TNF+IFNG+FASL reduced VEGFR2 mRNA, but TNF+IFNG+FASL increased TSP1 and CD36 mRNA. |
| 933 | 22492973 | VEGF treatment increased mRNA levels of 3betaHSD and PGES and secretion of P(4) and PGE(2). |
| 934 | 22492973 | In conclusion, these findings suggest a novel auto/paracrine action of cytokines, specifically TNF, on the up-regulation of VEGF for angiogenesis stimulation in equine early CL, while at luteolysis, cytokines down-regulated angiogenesis. |
| 935 | 22584669 | Cytokines induce tight junction disassembly in airway cells via an EGFR-dependent MAPK/ERK1/2-pathway. |
| 936 | 22584669 | To evaluate in vitro whether pro-inflammatory cytokines involved in the pathogenesis of respiratory disorders could alter TJ organization and epithelial barrier integrity, and to characterize the signal transduction pathway involved Calu-3 airway epithelial cells were exposed to TNF-a, IL-4 and IFN-g to assess changes in: (a) TJ assembly, that is, occludin and zonula occludens (ZO)-1 expression and localization, evaluated by confocal microscopy; (b) apoptotic activity, quantified using terminal transferase deoxyuridine triphosphate nick-end labeling staining; (c) epithelial barrier integrity, detected as transmembrane electrical resistance and expressed as G(T) values; (d) epidermal growth factor receptor (EGFR)-dependent mitogenactivated protein (MAP) kinase (MAPK)/extracellular signal-regulated kinases (ERK)1/2 phosphorylation, assessed by western blotting. |
| 937 | 22584669 | The degree ZO-1 and occludin colocalization was 62±2% in control cultures and significantly decreased in the presence of TNF-a (47±3%), IL-4 (43±1%) and INF-g (35±3%). |
| 938 | 22584669 | G(T) values were, respectively, 1.030±0.0, 1.300±0.04, 1.260±0.020 and 2.220±0.015 (mS/cm²)1000 in control cultures and in those exposed to TNF-a, IFN-g and IL-4. |
| 939 | 22584669 | The involvement of EGFR-dependent MAPK/ERK1/2 signaling pathway in cytokine-induced damage was demonstrated by a significant increase in threonine/tyrosine phosphorylation of ERK1/2, already detectable after 5 min incubation. |
| 940 | 22584669 | All these cytokine-induced changes were markedly prevented when Calu-3 cells were cultured in the presence of an EGFR inhibitor (AG1478, 1 μM) or a MAP kinase inhibitor (U0126, 25 μM). |
| 941 | 22584669 | In conclusion, cytokine-induced epithelial injury includes TJ disassembly and epithelial barrier permeability alteration and involves the EGFR-dependent MAPK/ERK1/2 signaling pathway. |
| 942 | 22584669 | Cytokines induce tight junction disassembly in airway cells via an EGFR-dependent MAPK/ERK1/2-pathway. |
| 943 | 22584669 | To evaluate in vitro whether pro-inflammatory cytokines involved in the pathogenesis of respiratory disorders could alter TJ organization and epithelial barrier integrity, and to characterize the signal transduction pathway involved Calu-3 airway epithelial cells were exposed to TNF-a, IL-4 and IFN-g to assess changes in: (a) TJ assembly, that is, occludin and zonula occludens (ZO)-1 expression and localization, evaluated by confocal microscopy; (b) apoptotic activity, quantified using terminal transferase deoxyuridine triphosphate nick-end labeling staining; (c) epithelial barrier integrity, detected as transmembrane electrical resistance and expressed as G(T) values; (d) epidermal growth factor receptor (EGFR)-dependent mitogenactivated protein (MAP) kinase (MAPK)/extracellular signal-regulated kinases (ERK)1/2 phosphorylation, assessed by western blotting. |
| 944 | 22584669 | The degree ZO-1 and occludin colocalization was 62±2% in control cultures and significantly decreased in the presence of TNF-a (47±3%), IL-4 (43±1%) and INF-g (35±3%). |
| 945 | 22584669 | G(T) values were, respectively, 1.030±0.0, 1.300±0.04, 1.260±0.020 and 2.220±0.015 (mS/cm²)1000 in control cultures and in those exposed to TNF-a, IFN-g and IL-4. |
| 946 | 22584669 | The involvement of EGFR-dependent MAPK/ERK1/2 signaling pathway in cytokine-induced damage was demonstrated by a significant increase in threonine/tyrosine phosphorylation of ERK1/2, already detectable after 5 min incubation. |
| 947 | 22584669 | All these cytokine-induced changes were markedly prevented when Calu-3 cells were cultured in the presence of an EGFR inhibitor (AG1478, 1 μM) or a MAP kinase inhibitor (U0126, 25 μM). |
| 948 | 22584669 | In conclusion, cytokine-induced epithelial injury includes TJ disassembly and epithelial barrier permeability alteration and involves the EGFR-dependent MAPK/ERK1/2 signaling pathway. |
| 949 | 22584669 | Cytokines induce tight junction disassembly in airway cells via an EGFR-dependent MAPK/ERK1/2-pathway. |
| 950 | 22584669 | To evaluate in vitro whether pro-inflammatory cytokines involved in the pathogenesis of respiratory disorders could alter TJ organization and epithelial barrier integrity, and to characterize the signal transduction pathway involved Calu-3 airway epithelial cells were exposed to TNF-a, IL-4 and IFN-g to assess changes in: (a) TJ assembly, that is, occludin and zonula occludens (ZO)-1 expression and localization, evaluated by confocal microscopy; (b) apoptotic activity, quantified using terminal transferase deoxyuridine triphosphate nick-end labeling staining; (c) epithelial barrier integrity, detected as transmembrane electrical resistance and expressed as G(T) values; (d) epidermal growth factor receptor (EGFR)-dependent mitogenactivated protein (MAP) kinase (MAPK)/extracellular signal-regulated kinases (ERK)1/2 phosphorylation, assessed by western blotting. |
| 951 | 22584669 | The degree ZO-1 and occludin colocalization was 62±2% in control cultures and significantly decreased in the presence of TNF-a (47±3%), IL-4 (43±1%) and INF-g (35±3%). |
| 952 | 22584669 | G(T) values were, respectively, 1.030±0.0, 1.300±0.04, 1.260±0.020 and 2.220±0.015 (mS/cm²)1000 in control cultures and in those exposed to TNF-a, IFN-g and IL-4. |
| 953 | 22584669 | The involvement of EGFR-dependent MAPK/ERK1/2 signaling pathway in cytokine-induced damage was demonstrated by a significant increase in threonine/tyrosine phosphorylation of ERK1/2, already detectable after 5 min incubation. |
| 954 | 22584669 | All these cytokine-induced changes were markedly prevented when Calu-3 cells were cultured in the presence of an EGFR inhibitor (AG1478, 1 μM) or a MAP kinase inhibitor (U0126, 25 μM). |
| 955 | 22584669 | In conclusion, cytokine-induced epithelial injury includes TJ disassembly and epithelial barrier permeability alteration and involves the EGFR-dependent MAPK/ERK1/2 signaling pathway. |
| 956 | 22847916 | The purpose of the present study was to elucidate if tumor necrosis factor-α (TNF), interferon γ (IFNG), and/or progesterone (P4) play roles in regulating NO generating system in LECs. |
| 957 | 22847916 | Cultured bovine LECs obtained from the CL at the mid-luteal stage (Days 8-12 of the cycle) were treated for 24 hr with TNF (2.9 nM), IFNG (2.5 nM), or P4 (0.032-32 µM). |
| 958 | 22847916 | NO production was increased by TNF and IFNG, but decreased by P4 (P < 0.05). |
| 959 | 22847916 | TNF and IFNG stimulated the relative steady-state amounts of inducible nitric oxide synthase (iNOS) mRNA and iNOS protein expression (P < 0.05), whereas P4 inhibited relative steady-state amounts of iNOS mRNA and iNOS protein expression (P < 0.05). |
| 960 | 22847916 | TNF and IFNG stimulated NOS activity (P < 0.05) and 1400W, a specific inhibitor of iNOS, reduced NO production stimulated by TNF and IFNG in LECs (P < 0.05). |
| 961 | 22847916 | The overall findings suggest that TNF and IFNG accelerate luteolysis by increasing NO production via stimulation of iNOS expression and NOS activity in bovine LECs. |
| 962 | 22847916 | P4, on the other hand, may act in maintaining CL function by suppressing iNOS expression in bovine LECs. |
| 963 | 22847916 | The purpose of the present study was to elucidate if tumor necrosis factor-α (TNF), interferon γ (IFNG), and/or progesterone (P4) play roles in regulating NO generating system in LECs. |
| 964 | 22847916 | Cultured bovine LECs obtained from the CL at the mid-luteal stage (Days 8-12 of the cycle) were treated for 24 hr with TNF (2.9 nM), IFNG (2.5 nM), or P4 (0.032-32 µM). |
| 965 | 22847916 | NO production was increased by TNF and IFNG, but decreased by P4 (P < 0.05). |
| 966 | 22847916 | TNF and IFNG stimulated the relative steady-state amounts of inducible nitric oxide synthase (iNOS) mRNA and iNOS protein expression (P < 0.05), whereas P4 inhibited relative steady-state amounts of iNOS mRNA and iNOS protein expression (P < 0.05). |
| 967 | 22847916 | TNF and IFNG stimulated NOS activity (P < 0.05) and 1400W, a specific inhibitor of iNOS, reduced NO production stimulated by TNF and IFNG in LECs (P < 0.05). |
| 968 | 22847916 | The overall findings suggest that TNF and IFNG accelerate luteolysis by increasing NO production via stimulation of iNOS expression and NOS activity in bovine LECs. |
| 969 | 22847916 | P4, on the other hand, may act in maintaining CL function by suppressing iNOS expression in bovine LECs. |
| 970 | 22847916 | The purpose of the present study was to elucidate if tumor necrosis factor-α (TNF), interferon γ (IFNG), and/or progesterone (P4) play roles in regulating NO generating system in LECs. |
| 971 | 22847916 | Cultured bovine LECs obtained from the CL at the mid-luteal stage (Days 8-12 of the cycle) were treated for 24 hr with TNF (2.9 nM), IFNG (2.5 nM), or P4 (0.032-32 µM). |
| 972 | 22847916 | NO production was increased by TNF and IFNG, but decreased by P4 (P < 0.05). |
| 973 | 22847916 | TNF and IFNG stimulated the relative steady-state amounts of inducible nitric oxide synthase (iNOS) mRNA and iNOS protein expression (P < 0.05), whereas P4 inhibited relative steady-state amounts of iNOS mRNA and iNOS protein expression (P < 0.05). |
| 974 | 22847916 | TNF and IFNG stimulated NOS activity (P < 0.05) and 1400W, a specific inhibitor of iNOS, reduced NO production stimulated by TNF and IFNG in LECs (P < 0.05). |
| 975 | 22847916 | The overall findings suggest that TNF and IFNG accelerate luteolysis by increasing NO production via stimulation of iNOS expression and NOS activity in bovine LECs. |
| 976 | 22847916 | P4, on the other hand, may act in maintaining CL function by suppressing iNOS expression in bovine LECs. |
| 977 | 22847916 | The purpose of the present study was to elucidate if tumor necrosis factor-α (TNF), interferon γ (IFNG), and/or progesterone (P4) play roles in regulating NO generating system in LECs. |
| 978 | 22847916 | Cultured bovine LECs obtained from the CL at the mid-luteal stage (Days 8-12 of the cycle) were treated for 24 hr with TNF (2.9 nM), IFNG (2.5 nM), or P4 (0.032-32 µM). |
| 979 | 22847916 | NO production was increased by TNF and IFNG, but decreased by P4 (P < 0.05). |
| 980 | 22847916 | TNF and IFNG stimulated the relative steady-state amounts of inducible nitric oxide synthase (iNOS) mRNA and iNOS protein expression (P < 0.05), whereas P4 inhibited relative steady-state amounts of iNOS mRNA and iNOS protein expression (P < 0.05). |
| 981 | 22847916 | TNF and IFNG stimulated NOS activity (P < 0.05) and 1400W, a specific inhibitor of iNOS, reduced NO production stimulated by TNF and IFNG in LECs (P < 0.05). |
| 982 | 22847916 | The overall findings suggest that TNF and IFNG accelerate luteolysis by increasing NO production via stimulation of iNOS expression and NOS activity in bovine LECs. |
| 983 | 22847916 | P4, on the other hand, may act in maintaining CL function by suppressing iNOS expression in bovine LECs. |
| 984 | 22847916 | The purpose of the present study was to elucidate if tumor necrosis factor-α (TNF), interferon γ (IFNG), and/or progesterone (P4) play roles in regulating NO generating system in LECs. |
| 985 | 22847916 | Cultured bovine LECs obtained from the CL at the mid-luteal stage (Days 8-12 of the cycle) were treated for 24 hr with TNF (2.9 nM), IFNG (2.5 nM), or P4 (0.032-32 µM). |
| 986 | 22847916 | NO production was increased by TNF and IFNG, but decreased by P4 (P < 0.05). |
| 987 | 22847916 | TNF and IFNG stimulated the relative steady-state amounts of inducible nitric oxide synthase (iNOS) mRNA and iNOS protein expression (P < 0.05), whereas P4 inhibited relative steady-state amounts of iNOS mRNA and iNOS protein expression (P < 0.05). |
| 988 | 22847916 | TNF and IFNG stimulated NOS activity (P < 0.05) and 1400W, a specific inhibitor of iNOS, reduced NO production stimulated by TNF and IFNG in LECs (P < 0.05). |
| 989 | 22847916 | The overall findings suggest that TNF and IFNG accelerate luteolysis by increasing NO production via stimulation of iNOS expression and NOS activity in bovine LECs. |
| 990 | 22847916 | P4, on the other hand, may act in maintaining CL function by suppressing iNOS expression in bovine LECs. |
| 991 | 22847916 | The purpose of the present study was to elucidate if tumor necrosis factor-α (TNF), interferon γ (IFNG), and/or progesterone (P4) play roles in regulating NO generating system in LECs. |
| 992 | 22847916 | Cultured bovine LECs obtained from the CL at the mid-luteal stage (Days 8-12 of the cycle) were treated for 24 hr with TNF (2.9 nM), IFNG (2.5 nM), or P4 (0.032-32 µM). |
| 993 | 22847916 | NO production was increased by TNF and IFNG, but decreased by P4 (P < 0.05). |
| 994 | 22847916 | TNF and IFNG stimulated the relative steady-state amounts of inducible nitric oxide synthase (iNOS) mRNA and iNOS protein expression (P < 0.05), whereas P4 inhibited relative steady-state amounts of iNOS mRNA and iNOS protein expression (P < 0.05). |
| 995 | 22847916 | TNF and IFNG stimulated NOS activity (P < 0.05) and 1400W, a specific inhibitor of iNOS, reduced NO production stimulated by TNF and IFNG in LECs (P < 0.05). |
| 996 | 22847916 | The overall findings suggest that TNF and IFNG accelerate luteolysis by increasing NO production via stimulation of iNOS expression and NOS activity in bovine LECs. |
| 997 | 22847916 | P4, on the other hand, may act in maintaining CL function by suppressing iNOS expression in bovine LECs. |
| 998 | 23060289 | The binding affinity and molecular basis of the structure-binding relationship between urinary Tamm-Horsfall glycoprotein and tumor necrosis factor-α. |
| 999 | 23060289 | In this study, we used lectin-binding ELISA to assess the carbohydrate compositions of THP, BSA, IgG, TNF-α, and IFN-g. |
| 1000 | 23060289 | We identified β(1,4)-N-acetylglucosamine oligomers (GlcNAc) and GlcNAc/branched mannose in BSA, IgG, TNF-α, and THP, but not in IFN-g. |
| 1001 | 23060289 | To elucidate the structure-binding relationship of THP-TNF-α, THP was digested with neuraminidase, β-galactosidase, O-sialoglycoprotein endopeptidase, carboxypeptidase Y, or proteinase K. β-galactosidase increased binding capacity of THP for TNF-α. |
| 1002 | 23071669 | These included five that were common to both ages (TNF, HNF4A, IL15, Progesterone, and YWHAZ), and others that were unique to 2 weeks (e.g. |
| 1003 | 23071669 | MYC/MYCN, TGFB1, and IL2) and to 4 weeks (e.g. |
| 1004 | 23071669 | IFNG, beta-estradiol, p53, NFKB, AKT, PRKCA, IL12, and HLA-C). |
| 1005 | 23071669 | Based on the literature, genes that may play a role in regulating metabolic pathways at 2 weeks include Myc and HNF4A, and at 4 weeks, beta-estradiol, p53, Akt, HNF4A and AR. |
| 1006 | 23179933 | The cytokines tumor necrosis factor α (TNFα), macrophage migration inhibitory factor (MIF) and interferon γ (INFγ) are proinflammatory cytokines of the innate immune response. |
| 1007 | 23179933 | We investigated the association between functional allelic variants of MIF (rs35688089), IFNG (rs2234688) and TNFA (rs1800629) in patients with MD. |
| 1008 | 23179933 | Moreover, no genetic associations for variants in either the TNFA or IFNG genes and MD were found. |
| 1009 | 23179933 | The cytokines tumor necrosis factor α (TNFα), macrophage migration inhibitory factor (MIF) and interferon γ (INFγ) are proinflammatory cytokines of the innate immune response. |
| 1010 | 23179933 | We investigated the association between functional allelic variants of MIF (rs35688089), IFNG (rs2234688) and TNFA (rs1800629) in patients with MD. |
| 1011 | 23179933 | Moreover, no genetic associations for variants in either the TNFA or IFNG genes and MD were found. |
| 1012 | 23179933 | The cytokines tumor necrosis factor α (TNFα), macrophage migration inhibitory factor (MIF) and interferon γ (INFγ) are proinflammatory cytokines of the innate immune response. |
| 1013 | 23179933 | We investigated the association between functional allelic variants of MIF (rs35688089), IFNG (rs2234688) and TNFA (rs1800629) in patients with MD. |
| 1014 | 23179933 | Moreover, no genetic associations for variants in either the TNFA or IFNG genes and MD were found. |
| 1015 | 23333334 | It down-regulates pro-inflammatory cytokines: TNF, IFNG and ICAM-1, resulting in decreased adherence of Plasmodium falciparum parasitized RBC to capillary wall, entry into the brain and delayed onset of death. |
| 1016 | 23580950 | Mares were inseminated over five estrous cycles and endometrial biopsies were collected at one time point per cycle before (0) and 2, 6, 12, and 24 h after insemination. qPCR analysis for IL1B, IL6, IL8, IFNG, TNF (TNFA), IL10, and IL1RN was performed, and endometrial inflammatory cells were counted for each sample. |
| 1017 | 23580950 | Cytokine mRNA increased at 2 h, peaked between 2 and 12 h, and then decreased.Differences were detected between groups of mares 6 h after challenge; resistant mares had higher mRNA expression of IL6, IL1RN,and IL10 than susceptible mares. |
| 1018 | 23634300 | Therefore, the aim of this study was to verify if IFNG, IL12B, TNF, IL17A, IL10, and TGFB1 gene polymorphisms influence the immune response of Brazilian patients with pulmonary tuberculosis (PTB) at different time points of antituberculosis treatment (T1, T2, and T3). |
| 1019 | 23634300 | Our results showed the following associations: IFNG +874 T allele and IFNG +2109 A allele with higher IFN- γ levels; IL12B +1188 C allele with higher IL-12 levels; TNF -308 A allele with higher TNF- α plasma levels in controls and mRNA levels in PTB patients at T1; IL17A A allele at rs7747909 with higher IL-17 levels; IL10 -819 T allele with higher IL-10 levels; and TGFB1 +29 CC genotype higher TGF- β plasma levels in PTB patients at T2. |
| 1020 | 23634300 | The present study suggests that IFNG +874T/A, IFNG +2109A/G, IL12B +1188A/C, IL10 -819C/T, and TGFB1 +21C/T are associated with differential cytokine levels in pulmonary tuberculosis patients and may play a role in the initiation and maintenance of acquired cellular immunity to tuberculosis and in the outcome of the active disease while on antituberculosis treatment. |
| 1021 | 23634300 | Therefore, the aim of this study was to verify if IFNG, IL12B, TNF, IL17A, IL10, and TGFB1 gene polymorphisms influence the immune response of Brazilian patients with pulmonary tuberculosis (PTB) at different time points of antituberculosis treatment (T1, T2, and T3). |
| 1022 | 23634300 | Our results showed the following associations: IFNG +874 T allele and IFNG +2109 A allele with higher IFN- γ levels; IL12B +1188 C allele with higher IL-12 levels; TNF -308 A allele with higher TNF- α plasma levels in controls and mRNA levels in PTB patients at T1; IL17A A allele at rs7747909 with higher IL-17 levels; IL10 -819 T allele with higher IL-10 levels; and TGFB1 +29 CC genotype higher TGF- β plasma levels in PTB patients at T2. |
| 1023 | 23634300 | The present study suggests that IFNG +874T/A, IFNG +2109A/G, IL12B +1188A/C, IL10 -819C/T, and TGFB1 +21C/T are associated with differential cytokine levels in pulmonary tuberculosis patients and may play a role in the initiation and maintenance of acquired cellular immunity to tuberculosis and in the outcome of the active disease while on antituberculosis treatment. |
| 1024 | 23764468 | Firstly, epigenetic enzyme gene expression (histone deacetylase (HDAC) and DNA methyltransferase (DNMT)) was measured after LPS stimulation. |
| 1025 | 23764468 | Results showed differential expression of HDAC6, HDAC7 and DNMT3A genes in response to LPS in cells from all animals, while TSA significantly inhibited pro-inflammatory cytokine (TNF, IL2 and IFNG) expression (P<0.05), presumably by histone acetylation. |
| 1026 | 23793505 | The role of tumor necrosis factor-α and interferon-γ in regulating angiomotin-like protein 1 expression in lung microvascular endothelial cells. |
| 1027 | 23819002 | We previously reported that foetuses congenitally infected with Trypanosoma cruzi, the agent of Chagas disease, mount an adult-like parasite-specific CD8(+) T-cell response, producing IFN-g, and present an altered NK cell phenotype, possibly reflecting a post-activation state supported by the ability of the parasite to trigger IFN-g synthesis by NK cells in vitro. |
| 1028 | 23819002 | Twenty-four hours co-culture of cord blood mononuclear cells with T. cruzi trypomastigotes and IL-15 induced high accumulation of IFN-g transcripts and IFN-g release. |
| 1029 | 23819002 | TNF-a, but not IL-10, was also produced. |
| 1030 | 23819002 | This was associated with up-regulation of CD69 and CD54, and down-regulation of CD62L on NK cells. |
| 1031 | 23819002 | The CD56(bright) NK cell subset was the major IFN-g responding subset (up to 70% IFN-g-positive cells), while CD56(dim) NK cells produced IFN-g to a lesser extent. |
| 1032 | 23819002 | This work highlights the ability of T. cruzi to trigger a robust IFN-g response by IL-15-sensitized human neonatal NK cells and the important role of monocytes in it, which might perhaps partially compensate for the neonatal defects of DCs. |
| 1033 | 23819002 | It suggests that monocyte- and IL-12- dependent IFN-g release by NK cells is a potentially important innate immune response pathway allowing T. cruzi to favour a type 1 immune response in neonates. |
| 1034 | 23831616 | Arg1 deficiency did not affect the allergic response in lungs and large-airway resistance, but it improved peripheral lung function (tissue elastance and resistance) and attenuated adaptive increases in mRNA expression of arginine-catabolizing enzymes Arg2 and Nos2, arginine transporters Slc7a1 and Slc7a7, chemokines Ccl2 and Ccl11, cytokines Tnfa and Ifng, mucus-associated epithelial markers Clca3 and Muc5ac, and lung content of IL-13 and CCL11. |
| 1035 | 23831616 | However, expression of Il4, Il5, Il10, and Il13 mRNA; lung content of IL-4, IL-5, IL-10, TNF-α, and IFN-γ protein; and lung pathology were not affected. |
| 1036 | 23840095 | Using the mare CL as a model, reports on locally produced cytokines, such as tumor necrosis factor α (TNF), interferon gamma (IFNG), or Fas ligand (FASL), pointed out their role on angiogenic activity modulation throughout the luteal phase. |
| 1037 | 23874546 | Of these transcripts, six (TNFAIP6, FCN1, CXCL10, GBP1, CXCL5 and PID1) were differentially expressed in septic patients' blood compared to healthy blood upon ex vivo LPS stimulation and were restored by IFN-γ. |
| 1038 | 23874546 | Along with the previously identified markers TNFa, IL10 and HLA-DRA, the potential value of these markers should now be evaluated in a larger cohort of patients. |
| 1039 | 23936772 | The aim of this study was to investigate the association of polymorphic immune response genes, namely KIR, HLA class I and II, and single-nucleotide polymorphisms (SNPs) of cytokines with HPV-related cervical disease. |
| 1040 | 23936772 | SNPs of TNF -308G>A, IL6 -174G>C, IFNG +874T>A, TGFB1 +869T>C +915G>C, and IL10 -592C>A -819C>T -1082G>A were evaluated using PCR-SSP. |
| 1041 | 23941776 | Role of tumor necrosis factor-α, interferon-γ and Fas-ligand on in vitro nitric oxide activity in the corpus luteum. |
| 1042 | 23941776 | Moreover, TNF, IFNG and FASL were shown to regulate equine CL establishment and regression. |
| 1043 | 23941776 | TNF increased eNOS mRNA level and NO metabolite (nitrite) production during CL growth. |
| 1044 | 23941776 | Cytokines combined action (TNF+IFNG+FASL) promoted eNOS protein upregulation in mid-CL and nitrite production in mid and late-CL. |
| 1045 | 23941776 | These results indicate that in equine CL, cytokines TNF, IFNG and FASL regulate NO activity, via eNOS expression modulation. |
| 1046 | 23941776 | Role of tumor necrosis factor-α, interferon-γ and Fas-ligand on in vitro nitric oxide activity in the corpus luteum. |
| 1047 | 23941776 | Moreover, TNF, IFNG and FASL were shown to regulate equine CL establishment and regression. |
| 1048 | 23941776 | TNF increased eNOS mRNA level and NO metabolite (nitrite) production during CL growth. |
| 1049 | 23941776 | Cytokines combined action (TNF+IFNG+FASL) promoted eNOS protein upregulation in mid-CL and nitrite production in mid and late-CL. |
| 1050 | 23941776 | These results indicate that in equine CL, cytokines TNF, IFNG and FASL regulate NO activity, via eNOS expression modulation. |
| 1051 | 23941776 | Role of tumor necrosis factor-α, interferon-γ and Fas-ligand on in vitro nitric oxide activity in the corpus luteum. |
| 1052 | 23941776 | Moreover, TNF, IFNG and FASL were shown to regulate equine CL establishment and regression. |
| 1053 | 23941776 | TNF increased eNOS mRNA level and NO metabolite (nitrite) production during CL growth. |
| 1054 | 23941776 | Cytokines combined action (TNF+IFNG+FASL) promoted eNOS protein upregulation in mid-CL and nitrite production in mid and late-CL. |
| 1055 | 23941776 | These results indicate that in equine CL, cytokines TNF, IFNG and FASL regulate NO activity, via eNOS expression modulation. |
| 1056 | 23941776 | Role of tumor necrosis factor-α, interferon-γ and Fas-ligand on in vitro nitric oxide activity in the corpus luteum. |
| 1057 | 23941776 | Moreover, TNF, IFNG and FASL were shown to regulate equine CL establishment and regression. |
| 1058 | 23941776 | TNF increased eNOS mRNA level and NO metabolite (nitrite) production during CL growth. |
| 1059 | 23941776 | Cytokines combined action (TNF+IFNG+FASL) promoted eNOS protein upregulation in mid-CL and nitrite production in mid and late-CL. |
| 1060 | 23941776 | These results indicate that in equine CL, cytokines TNF, IFNG and FASL regulate NO activity, via eNOS expression modulation. |
| 1061 | 23941776 | Role of tumor necrosis factor-α, interferon-γ and Fas-ligand on in vitro nitric oxide activity in the corpus luteum. |
| 1062 | 23941776 | Moreover, TNF, IFNG and FASL were shown to regulate equine CL establishment and regression. |
| 1063 | 23941776 | TNF increased eNOS mRNA level and NO metabolite (nitrite) production during CL growth. |
| 1064 | 23941776 | Cytokines combined action (TNF+IFNG+FASL) promoted eNOS protein upregulation in mid-CL and nitrite production in mid and late-CL. |
| 1065 | 23941776 | These results indicate that in equine CL, cytokines TNF, IFNG and FASL regulate NO activity, via eNOS expression modulation. |
| 1066 | 23982206 | Activation of the transcriptional function of the NF-κB protein c-Rel by O-GlcNAc glycosylation. |
| 1067 | 23982206 | Blocking the O-GlcNAcylation of this residue abrogated c-Rel-mediated expression of the cytokine-encoding genes IL2, IFNG, and CSF2 in response to T cell receptor (TCR) activation, whereas increasing the extent of O-GlcNAcylation of cellular proteins enhanced the expression of these genes. |
| 1068 | 23982206 | TCR- or tumor necrosis factor (TNF)-induced expression of other NF-κB target genes, such as NFKBIA (which encodes IκBα) and TNFAIP3 (which encodes A20), occurred independently of the O-GlcNAcylation of c-Rel. |
| 1069 | 24084096 | The gene expression of cytokines/chemokines in skin biopsies from the CL group showed higher transcript levels of modulatory (IL10 and TGFB1), anti-inflammatory (IL4), and pro-inflammatory (TNF, IFNG, IL12B, CCL2, CCL3, CCL5, CXCL10) biomarkers in recent lesions than in late lesions. |
| 1070 | 24096714 | The BiPN grade was associated with phytohemagglutinin-induced IL2, IFNG and TNFSF2, as well as with lipopolysaccharide-induced IL6 levels. |
| 1071 | 24273896 | Cytokine gene polymorphisms of TNFα, IL-6, IL-10, TGFβ and IFNγ in the Saudi population. |
| 1072 | 24273896 | In the present work the authors examine polymorphisms in the genes encoding interleukin-6 (IL-6), IL-10, interferon-gamma (IFNgamma), tumour necrosis factor-alpha (TNFalpha) and transforming growth factor-beta (TGFbeta1) using the polymerase chain reaction sequence-specific primer (PCR-SSP) method in 150 healthy unrelated Saudis, and results compared with those from other studied populations. |
| 1073 | 24313359 | Peripheral and site-specific CD4(+) CD28(null) T cells from rheumatoid arthritis patients show distinct characteristics. |
| 1074 | 24313359 | Proinflammatory CD4(+) CD28(null) T cells are frequently found in the circulation of patients with rheumatoid arthritis (RA), but are less common in the rheumatic joint. |
| 1075 | 24313359 | In the present study, we sought to identify functional differences between CD4(+) CD28(null) T cells from blood and synovial fluid in comparison with conventional CD28-expressing CD4(+) T cells. |
| 1076 | 24313359 | Forty-four patients with RA, displaying a distinct CD4(+) CD28(null) T cell population in blood, were recruited for this study; the methylation status of the IFNG locus was examined in isolated T cell subsets, and intracellular cytokine production (IFN-γ, TNF, IL-17) and chemokine receptor expression (CXCR3, CCR6 and CCR7) were assessed by flow cytometry on T cells from the two compartments. |
| 1077 | 24313359 | Circulating CD4(+) CD28(null) T cells were significantly more hypomethylated in the CNS-1 region of the IFNG locus than conventional CD4(+) CD28(+) T cells and produced higher levels of both IFN-γ and TNF after TCR cross-linking. |
| 1078 | 24313359 | CD4(+) CD28(null) T cells from the site of inflammation expressed significantly more CXCR3 and CCR6 compared to their counterparts in blood. |
| 1079 | 24313359 | While IL-17A production could hardly be detected in CD4(+) CD28(null) cells from the blood, a significant production was observed in CD4(+) CD28(null) T cells from synovial fluid. |
| 1080 | 24313359 | CD4(+) CD28(null) T cells were not only found to differ from conventional CD4(+) CD28(+) T cells in the circulation, but we could also demonstrate that synovial CD4(+) CD28(null) T cells showed additional effector functions (IL-17 coproduction) as compared to the same subset in peripheral blood, suggesting an active role for these cells in the perpetuation of inflammation in the subset of patients having a CD28(null) population. |
| 1081 | 24313359 | Peripheral and site-specific CD4(+) CD28(null) T cells from rheumatoid arthritis patients show distinct characteristics. |
| 1082 | 24313359 | Proinflammatory CD4(+) CD28(null) T cells are frequently found in the circulation of patients with rheumatoid arthritis (RA), but are less common in the rheumatic joint. |
| 1083 | 24313359 | In the present study, we sought to identify functional differences between CD4(+) CD28(null) T cells from blood and synovial fluid in comparison with conventional CD28-expressing CD4(+) T cells. |
| 1084 | 24313359 | Forty-four patients with RA, displaying a distinct CD4(+) CD28(null) T cell population in blood, were recruited for this study; the methylation status of the IFNG locus was examined in isolated T cell subsets, and intracellular cytokine production (IFN-γ, TNF, IL-17) and chemokine receptor expression (CXCR3, CCR6 and CCR7) were assessed by flow cytometry on T cells from the two compartments. |
| 1085 | 24313359 | Circulating CD4(+) CD28(null) T cells were significantly more hypomethylated in the CNS-1 region of the IFNG locus than conventional CD4(+) CD28(+) T cells and produced higher levels of both IFN-γ and TNF after TCR cross-linking. |
| 1086 | 24313359 | CD4(+) CD28(null) T cells from the site of inflammation expressed significantly more CXCR3 and CCR6 compared to their counterparts in blood. |
| 1087 | 24313359 | While IL-17A production could hardly be detected in CD4(+) CD28(null) cells from the blood, a significant production was observed in CD4(+) CD28(null) T cells from synovial fluid. |
| 1088 | 24313359 | CD4(+) CD28(null) T cells were not only found to differ from conventional CD4(+) CD28(+) T cells in the circulation, but we could also demonstrate that synovial CD4(+) CD28(null) T cells showed additional effector functions (IL-17 coproduction) as compared to the same subset in peripheral blood, suggesting an active role for these cells in the perpetuation of inflammation in the subset of patients having a CD28(null) population. |