| # |
PMID |
Sentence |
| 1 |
1338891
|
Virus-specific T cells which proliferated in response to JHMV antigen and produced both IL-2 and IFN-g were present among mononuclear cells infiltrating the brain as early as day 5 post-infection.
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| 2 |
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.
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| 3 |
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.
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| 4 |
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.
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| 5 |
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.
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| 6 |
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.
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| 7 |
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.
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| 8 |
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.
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| 9 |
1404261
|
Production of IL-2 was suppressed by 14.1-31.9%, and IFN-G was reduced by 8.7-57.0%.
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| 10 |
1404261
|
Both IL-1 and TNF are endogenous pyrogens and activate polymorphonuclear leukocytes.
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| 11 |
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.
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| 12 |
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.
|
| 13 |
1404261
|
Production of IL-2 was suppressed by 14.1-31.9%, and IFN-G was reduced by 8.7-57.0%.
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| 14 |
1404261
|
Both IL-1 and TNF are endogenous pyrogens and activate polymorphonuclear leukocytes.
|
| 15 |
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.
|
| 16 |
1411093
|
Serum levels of interleukin (IL)-2, interferon gamma (IFNg) and soluble IL-2 receptors (sIL-2R) were determined in sera from 34 patients with poly- or pauciarticular juvenile chronic arthritis (JCA) by use of enzyme-linked immunosorbent assays (ELISAs).
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| 17 |
1733066
|
In addition, there were significantly fewer cellular infiltrates of total white blood cells, neutrophils, macrophages, T cells, IL-2 receptor-positive T cells, and mononuclear cells with positive staining for the activation cytokines IL-2 and IFN-g.
|
| 18 |
1903827
|
However, there was no significant correlation between the level of proliferative response and production of either interleukin 2 (IL-2) or interferon gamma (IFN-g).
|
| 19 |
1903827
|
In an effort to further explore the role of lymphokines in the decreased proliferative response of elderly subjects, various concentrations of exogenous IL-2 and/or IFN-gamma were added at the initiation of the mitogen stimulated cultures.
|
| 20 |
1903827
|
Similar increases in both the level of response and the number of subjects demonstrating an increase was observed for both young and elderly subjects upon addition of either IL-2 or IFN-gamma.
|
| 21 |
1903827
|
However, addition of a combination of IL-2 and IFN produced more pronounced effects in the elderly subjects.
|
| 22 |
1903827
|
The amounts of IL-2 and IFN-gamma required for this increase varied for each individual.
|
| 23 |
1903827
|
However, there was no significant correlation between the level of proliferative response and production of either interleukin 2 (IL-2) or interferon gamma (IFN-g).
|
| 24 |
1903827
|
In an effort to further explore the role of lymphokines in the decreased proliferative response of elderly subjects, various concentrations of exogenous IL-2 and/or IFN-gamma were added at the initiation of the mitogen stimulated cultures.
|
| 25 |
1903827
|
Similar increases in both the level of response and the number of subjects demonstrating an increase was observed for both young and elderly subjects upon addition of either IL-2 or IFN-gamma.
|
| 26 |
1903827
|
However, addition of a combination of IL-2 and IFN produced more pronounced effects in the elderly subjects.
|
| 27 |
1903827
|
The amounts of IL-2 and IFN-gamma required for this increase varied for each individual.
|
| 28 |
1903827
|
However, there was no significant correlation between the level of proliferative response and production of either interleukin 2 (IL-2) or interferon gamma (IFN-g).
|
| 29 |
1903827
|
In an effort to further explore the role of lymphokines in the decreased proliferative response of elderly subjects, various concentrations of exogenous IL-2 and/or IFN-gamma were added at the initiation of the mitogen stimulated cultures.
|
| 30 |
1903827
|
Similar increases in both the level of response and the number of subjects demonstrating an increase was observed for both young and elderly subjects upon addition of either IL-2 or IFN-gamma.
|
| 31 |
1903827
|
However, addition of a combination of IL-2 and IFN produced more pronounced effects in the elderly subjects.
|
| 32 |
1903827
|
The amounts of IL-2 and IFN-gamma required for this increase varied for each individual.
|
| 33 |
1903827
|
However, there was no significant correlation between the level of proliferative response and production of either interleukin 2 (IL-2) or interferon gamma (IFN-g).
|
| 34 |
1903827
|
In an effort to further explore the role of lymphokines in the decreased proliferative response of elderly subjects, various concentrations of exogenous IL-2 and/or IFN-gamma were added at the initiation of the mitogen stimulated cultures.
|
| 35 |
1903827
|
Similar increases in both the level of response and the number of subjects demonstrating an increase was observed for both young and elderly subjects upon addition of either IL-2 or IFN-gamma.
|
| 36 |
1903827
|
However, addition of a combination of IL-2 and IFN produced more pronounced effects in the elderly subjects.
|
| 37 |
1903827
|
The amounts of IL-2 and IFN-gamma required for this increase varied for each individual.
|
| 38 |
1903827
|
However, there was no significant correlation between the level of proliferative response and production of either interleukin 2 (IL-2) or interferon gamma (IFN-g).
|
| 39 |
1903827
|
In an effort to further explore the role of lymphokines in the decreased proliferative response of elderly subjects, various concentrations of exogenous IL-2 and/or IFN-gamma were added at the initiation of the mitogen stimulated cultures.
|
| 40 |
1903827
|
Similar increases in both the level of response and the number of subjects demonstrating an increase was observed for both young and elderly subjects upon addition of either IL-2 or IFN-gamma.
|
| 41 |
1903827
|
However, addition of a combination of IL-2 and IFN produced more pronounced effects in the elderly subjects.
|
| 42 |
1903827
|
The amounts of IL-2 and IFN-gamma required for this increase varied for each individual.
|
| 43 |
1909215
|
Interferon-gamma (IFN-g) production, interleukin 2 (IL-2) receptor, and HLA-DR antigen expression were investigated, representing typical T-cell activation parameters.
|
| 44 |
1909215
|
In PMNC cultures, He-PC dose-dependently enhanced the production of IFN-g, provided IL-2 had been added exogenously.
|
| 45 |
1909215
|
Interferon-gamma (IFN-g) production, interleukin 2 (IL-2) receptor, and HLA-DR antigen expression were investigated, representing typical T-cell activation parameters.
|
| 46 |
1909215
|
In PMNC cultures, He-PC dose-dependently enhanced the production of IFN-g, provided IL-2 had been added exogenously.
|
| 47 |
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).
|
| 48 |
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.
|
| 49 |
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.
|
| 50 |
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).
|
| 51 |
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.
|
| 52 |
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.
|
| 53 |
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).
|
| 54 |
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.
|
| 55 |
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.
|
| 56 |
2219270
|
In contrast, suppression in the recipient spleens was donor-specific; both CD4 and CD8 cells prolonged test graft survival.
|
| 57 |
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.
|
| 58 |
3083688
|
They determined the distribution of gamma interferon (IFN-g), interleukin-2 (IL-2), and corresponding IL-2 receptors (IL-2R), plus T cells and T cell subsets, B cells, and macrophages within thoracic lymph nodes and lung specimens of 9 patients with active pulmonary sarcoidosis.
|
| 59 |
3083688
|
Epithelioid and multinucleate giant cells within sarcoid granulomas of all specimens showed membrane labeling for IL-2R and IFN-g, in addition to IL-2, suggesting that these cells indeed express functional IL-2 receptors.
|
| 60 |
3083688
|
Infiltrating T cells, largely T4+, were also IL-2R+, and many showed IL-2 and IFN-g labeling.
|
| 61 |
3083688
|
By comparison, macrophages within sections of normal lung or lymph node failed to stain for IL-2, IL-2R, or IFN-g.
|
| 62 |
3083688
|
These immunohistologic studies extend recent in vitro observations by these authors and others that normal human blood monocytes and alveolar macrophages are induced by IFN-g or IL-2 to express functional membrane-bound IL-2 receptors.
|
| 63 |
3083688
|
They determined the distribution of gamma interferon (IFN-g), interleukin-2 (IL-2), and corresponding IL-2 receptors (IL-2R), plus T cells and T cell subsets, B cells, and macrophages within thoracic lymph nodes and lung specimens of 9 patients with active pulmonary sarcoidosis.
|
| 64 |
3083688
|
Epithelioid and multinucleate giant cells within sarcoid granulomas of all specimens showed membrane labeling for IL-2R and IFN-g, in addition to IL-2, suggesting that these cells indeed express functional IL-2 receptors.
|
| 65 |
3083688
|
Infiltrating T cells, largely T4+, were also IL-2R+, and many showed IL-2 and IFN-g labeling.
|
| 66 |
3083688
|
By comparison, macrophages within sections of normal lung or lymph node failed to stain for IL-2, IL-2R, or IFN-g.
|
| 67 |
3083688
|
These immunohistologic studies extend recent in vitro observations by these authors and others that normal human blood monocytes and alveolar macrophages are induced by IFN-g or IL-2 to express functional membrane-bound IL-2 receptors.
|
| 68 |
3083688
|
They determined the distribution of gamma interferon (IFN-g), interleukin-2 (IL-2), and corresponding IL-2 receptors (IL-2R), plus T cells and T cell subsets, B cells, and macrophages within thoracic lymph nodes and lung specimens of 9 patients with active pulmonary sarcoidosis.
|
| 69 |
3083688
|
Epithelioid and multinucleate giant cells within sarcoid granulomas of all specimens showed membrane labeling for IL-2R and IFN-g, in addition to IL-2, suggesting that these cells indeed express functional IL-2 receptors.
|
| 70 |
3083688
|
Infiltrating T cells, largely T4+, were also IL-2R+, and many showed IL-2 and IFN-g labeling.
|
| 71 |
3083688
|
By comparison, macrophages within sections of normal lung or lymph node failed to stain for IL-2, IL-2R, or IFN-g.
|
| 72 |
3083688
|
These immunohistologic studies extend recent in vitro observations by these authors and others that normal human blood monocytes and alveolar macrophages are induced by IFN-g or IL-2 to express functional membrane-bound IL-2 receptors.
|
| 73 |
3083688
|
They determined the distribution of gamma interferon (IFN-g), interleukin-2 (IL-2), and corresponding IL-2 receptors (IL-2R), plus T cells and T cell subsets, B cells, and macrophages within thoracic lymph nodes and lung specimens of 9 patients with active pulmonary sarcoidosis.
|
| 74 |
3083688
|
Epithelioid and multinucleate giant cells within sarcoid granulomas of all specimens showed membrane labeling for IL-2R and IFN-g, in addition to IL-2, suggesting that these cells indeed express functional IL-2 receptors.
|
| 75 |
3083688
|
Infiltrating T cells, largely T4+, were also IL-2R+, and many showed IL-2 and IFN-g labeling.
|
| 76 |
3083688
|
By comparison, macrophages within sections of normal lung or lymph node failed to stain for IL-2, IL-2R, or IFN-g.
|
| 77 |
3083688
|
These immunohistologic studies extend recent in vitro observations by these authors and others that normal human blood monocytes and alveolar macrophages are induced by IFN-g or IL-2 to express functional membrane-bound IL-2 receptors.
|
| 78 |
3083688
|
They determined the distribution of gamma interferon (IFN-g), interleukin-2 (IL-2), and corresponding IL-2 receptors (IL-2R), plus T cells and T cell subsets, B cells, and macrophages within thoracic lymph nodes and lung specimens of 9 patients with active pulmonary sarcoidosis.
|
| 79 |
3083688
|
Epithelioid and multinucleate giant cells within sarcoid granulomas of all specimens showed membrane labeling for IL-2R and IFN-g, in addition to IL-2, suggesting that these cells indeed express functional IL-2 receptors.
|
| 80 |
3083688
|
Infiltrating T cells, largely T4+, were also IL-2R+, and many showed IL-2 and IFN-g labeling.
|
| 81 |
3083688
|
By comparison, macrophages within sections of normal lung or lymph node failed to stain for IL-2, IL-2R, or IFN-g.
|
| 82 |
3083688
|
These immunohistologic studies extend recent in vitro observations by these authors and others that normal human blood monocytes and alveolar macrophages are induced by IFN-g or IL-2 to express functional membrane-bound IL-2 receptors.
|
| 83 |
3122387
|
Several studies have shown a decrease in interleukin 2 (IL-2) and interferon-Gamma (IFN-G) production of renal Tx recipients on CsA treatment and have suggested that increases in lymphokine production can be correlated with rejection episodes.
|
| 84 |
3122387
|
In this study we measured IL-2, IFN-G, and lymphotoxin (LT) production by mitogen-stimulated peripheral blood lymphocytes in eight renal Tx recipients before and at various times after Tx.
|
| 85 |
3122387
|
In only 3/5 patients did IL-2 production decrease with a return to stable graft function, while IFN-G production did not alter in these patients.
|
| 86 |
3122387
|
Several studies have shown a decrease in interleukin 2 (IL-2) and interferon-Gamma (IFN-G) production of renal Tx recipients on CsA treatment and have suggested that increases in lymphokine production can be correlated with rejection episodes.
|
| 87 |
3122387
|
In this study we measured IL-2, IFN-G, and lymphotoxin (LT) production by mitogen-stimulated peripheral blood lymphocytes in eight renal Tx recipients before and at various times after Tx.
|
| 88 |
3122387
|
In only 3/5 patients did IL-2 production decrease with a return to stable graft function, while IFN-G production did not alter in these patients.
|
| 89 |
3122387
|
Several studies have shown a decrease in interleukin 2 (IL-2) and interferon-Gamma (IFN-G) production of renal Tx recipients on CsA treatment and have suggested that increases in lymphokine production can be correlated with rejection episodes.
|
| 90 |
3122387
|
In this study we measured IL-2, IFN-G, and lymphotoxin (LT) production by mitogen-stimulated peripheral blood lymphocytes in eight renal Tx recipients before and at various times after Tx.
|
| 91 |
3122387
|
In only 3/5 patients did IL-2 production decrease with a return to stable graft function, while IFN-G production did not alter in these patients.
|
| 92 |
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).
|
| 93 |
7663570
|
Lymph nodes containing microscopic tumor and shed mucin exhibited approximately 40-fold expansion in short-term (< 21 days) cultures with either IL-2 or IL-1 plus IL-2; the combination of IL-2/anti-CD3 monoclonal antibody (mAb) resulted in significantly higher expansion.
|
| 94 |
7663570
|
Cultures generated with IL-2 alone favored the expansion of CD8+ and CD56+ cells, whereas addition of IL-1 or anti-CD3 mAb to IL-2 promoted outgrowth of CD4+ T-cells.
|
| 95 |
7663570
|
However, CD4+ cells expanded in IL-2/anti-CD3 retained the ability to proliferate in response to TAG-72 mucin-expressing autologous tumor as well as bovine submaxillary mucin (BSM) a soluble TAG-72+ mucin.
|
| 96 |
7663570
|
In addition, CD4+ cells expressed mRNA for IL-2, IL-4, tumor necrosis factor-beta and IFNg, and retained the ability to secrete IL-2 after expansion.
|
| 97 |
7663570
|
Lymph nodes containing microscopic tumor and shed mucin exhibited approximately 40-fold expansion in short-term (< 21 days) cultures with either IL-2 or IL-1 plus IL-2; the combination of IL-2/anti-CD3 monoclonal antibody (mAb) resulted in significantly higher expansion.
|
| 98 |
7663570
|
Cultures generated with IL-2 alone favored the expansion of CD8+ and CD56+ cells, whereas addition of IL-1 or anti-CD3 mAb to IL-2 promoted outgrowth of CD4+ T-cells.
|
| 99 |
7663570
|
However, CD4+ cells expanded in IL-2/anti-CD3 retained the ability to proliferate in response to TAG-72 mucin-expressing autologous tumor as well as bovine submaxillary mucin (BSM) a soluble TAG-72+ mucin.
|
| 100 |
7663570
|
In addition, CD4+ cells expressed mRNA for IL-2, IL-4, tumor necrosis factor-beta and IFNg, and retained the ability to secrete IL-2 after expansion.
|
| 101 |
7663570
|
Lymph nodes containing microscopic tumor and shed mucin exhibited approximately 40-fold expansion in short-term (< 21 days) cultures with either IL-2 or IL-1 plus IL-2; the combination of IL-2/anti-CD3 monoclonal antibody (mAb) resulted in significantly higher expansion.
|
| 102 |
7663570
|
Cultures generated with IL-2 alone favored the expansion of CD8+ and CD56+ cells, whereas addition of IL-1 or anti-CD3 mAb to IL-2 promoted outgrowth of CD4+ T-cells.
|
| 103 |
7663570
|
However, CD4+ cells expanded in IL-2/anti-CD3 retained the ability to proliferate in response to TAG-72 mucin-expressing autologous tumor as well as bovine submaxillary mucin (BSM) a soluble TAG-72+ mucin.
|
| 104 |
7663570
|
In addition, CD4+ cells expressed mRNA for IL-2, IL-4, tumor necrosis factor-beta and IFNg, and retained the ability to secrete IL-2 after expansion.
|
| 105 |
7663570
|
Lymph nodes containing microscopic tumor and shed mucin exhibited approximately 40-fold expansion in short-term (< 21 days) cultures with either IL-2 or IL-1 plus IL-2; the combination of IL-2/anti-CD3 monoclonal antibody (mAb) resulted in significantly higher expansion.
|
| 106 |
7663570
|
Cultures generated with IL-2 alone favored the expansion of CD8+ and CD56+ cells, whereas addition of IL-1 or anti-CD3 mAb to IL-2 promoted outgrowth of CD4+ T-cells.
|
| 107 |
7663570
|
However, CD4+ cells expanded in IL-2/anti-CD3 retained the ability to proliferate in response to TAG-72 mucin-expressing autologous tumor as well as bovine submaxillary mucin (BSM) a soluble TAG-72+ mucin.
|
| 108 |
7663570
|
In addition, CD4+ cells expressed mRNA for IL-2, IL-4, tumor necrosis factor-beta and IFNg, and retained the ability to secrete IL-2 after expansion.
|
| 109 |
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).
|
| 110 |
8018827
|
Lymphokines including IL-2, IL-3 and GM-CSF belong to type 1 and IFN-g, TNF and LT belong to type 2.
|
| 111 |
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).
|
| 112 |
8018827
|
Lymphokines including IL-2, IL-3 and GM-CSF belong to type 1 and IFN-g, TNF and LT belong to type 2.
|
| 113 |
8083651
|
Tumor necrosis factor, interleukin-2, and interferon-gamma in adult varicella.
|
| 114 |
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.
|
| 115 |
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.
|
| 116 |
8083651
|
Tumor necrosis factor, interleukin-2, and interferon-gamma in adult varicella.
|
| 117 |
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.
|
| 118 |
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.
|
| 119 |
8083651
|
Tumor necrosis factor, interleukin-2, and interferon-gamma in adult varicella.
|
| 120 |
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.
|
| 121 |
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.
|
| 122 |
8167691
|
Gene expression of IL2 and IFN-gamma in patients' T cells following antigenic stimulation was significantly reduced compared to controls, while IL-2R transcripts were normal.
|
| 123 |
8167691
|
Following stimulation with optimal (10 ng/ml p < 0.05) as well as suboptimal (1 ng/ml p < 0.0025) concentrations of staphylococcal enterotoxin A (SEA), proliferative response and cytokine release (IL-2 and IFNg) were significantly decreased in patients' T cells as compared to controls'.
|
| 124 |
8167691
|
Gene expression of IL2 and IFN-gamma in patients' T cells following antigenic stimulation was significantly reduced compared to controls, while IL-2R transcripts were normal.
|
| 125 |
8167691
|
Following stimulation with optimal (10 ng/ml p < 0.05) as well as suboptimal (1 ng/ml p < 0.0025) concentrations of staphylococcal enterotoxin A (SEA), proliferative response and cytokine release (IL-2 and IFNg) were significantly decreased in patients' T cells as compared to controls'.
|
| 126 |
8389732
|
1,25-Dihydroxyvitamin D3 (1,25-(OH)2D3) inhibits the proliferation of mitogen-stimulated human mononuclear cells (MNC) as well as the production of a number of proinflammatory cytokines, including interleukin (IL)-1 alpha, IL-6, tumour necrosis factor-alpha, IL-2, interferon-gamma (IFNg) and lymphotoxin (LT).
|
| 127 |
8389732
|
In the present study we have evaluated the ability of 1,25-(OH)2D3 to affect proliferation and cytokine production by human T cell lines stimulated by anti-CD3 antibodies or anti-CD3 plus anti-CD28 antibodies. 1,25-(OH)2D3 selectively reduced the supernatant levels of IL-2, while the IFNg and LT levels were unaffected.
|
| 128 |
8389732
|
Although the expression of high affinity IL-2 receptors (IL-2R) (p75) was unaffected, exogenously added IL-2 failed to restore proliferation.
|
| 129 |
8389732
|
1,25-Dihydroxyvitamin D3 (1,25-(OH)2D3) inhibits the proliferation of mitogen-stimulated human mononuclear cells (MNC) as well as the production of a number of proinflammatory cytokines, including interleukin (IL)-1 alpha, IL-6, tumour necrosis factor-alpha, IL-2, interferon-gamma (IFNg) and lymphotoxin (LT).
|
| 130 |
8389732
|
In the present study we have evaluated the ability of 1,25-(OH)2D3 to affect proliferation and cytokine production by human T cell lines stimulated by anti-CD3 antibodies or anti-CD3 plus anti-CD28 antibodies. 1,25-(OH)2D3 selectively reduced the supernatant levels of IL-2, while the IFNg and LT levels were unaffected.
|
| 131 |
8389732
|
Although the expression of high affinity IL-2 receptors (IL-2R) (p75) was unaffected, exogenously added IL-2 failed to restore proliferation.
|
| 132 |
8389732
|
1,25-Dihydroxyvitamin D3 (1,25-(OH)2D3) inhibits the proliferation of mitogen-stimulated human mononuclear cells (MNC) as well as the production of a number of proinflammatory cytokines, including interleukin (IL)-1 alpha, IL-6, tumour necrosis factor-alpha, IL-2, interferon-gamma (IFNg) and lymphotoxin (LT).
|
| 133 |
8389732
|
In the present study we have evaluated the ability of 1,25-(OH)2D3 to affect proliferation and cytokine production by human T cell lines stimulated by anti-CD3 antibodies or anti-CD3 plus anti-CD28 antibodies. 1,25-(OH)2D3 selectively reduced the supernatant levels of IL-2, while the IFNg and LT levels were unaffected.
|
| 134 |
8389732
|
Although the expression of high affinity IL-2 receptors (IL-2R) (p75) was unaffected, exogenously added IL-2 failed to restore proliferation.
|
| 135 |
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.
|
| 136 |
8525128
|
High gene expression of IL-4, IL-6, IL-10 and TNF-a was found in SLE patients as compared to normal subjects.
|
| 137 |
8525128
|
The expression of IL-1b, IL-2 and IFN-g genes was low or undetectable.
|
| 138 |
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.
|
| 139 |
8525128
|
High gene expression of IL-4, IL-6, IL-10 and TNF-a was found in SLE patients as compared to normal subjects.
|
| 140 |
8525128
|
The expression of IL-1b, IL-2 and IFN-g genes was low or undetectable.
|
| 141 |
8668918
|
ELISA assays were subsequently performed on supernatants for IL-4, IL-5, IL-2 and IFN-g.
|
| 142 |
8668918
|
The PPD1 induced IL-5 production, while the PPD2 induced high levels of IFN-gamma.
|
| 143 |
8755821
|
Graft-infiltrating cells (GIC) recovered from TH1-transfused animals contained large numbers of graft-reactive IL-2-producing cells (68-269/10(6) GIC), but no LDA-detectable IL-4-producing cells.
|
| 144 |
8755821
|
Infiltrating cells recovered from TH1-transfused allografts contained large numbers of graft-reactive (109-1458/10(6) GIC), LDA-detectable, IL-4-producing cells--indicating that the TH2 cells had arrived at the graft-but promoted acute allograft rejection rather than allograft acceptance.
|
| 145 |
8816327
|
In addition, the HSP and PGE2 treatment used inhibited the production of the Th1 cytokines IL-2 and IFNg but had a differential modulatory effect on Th2 cytokine production, namely enhancing the production of IL-6 whilst simultaneously impairing the synthesis of IL-4 and IL-10.
|
| 146 |
8993758
|
A Culture supernatants were collected and assayed for content of IL-2, IL-4, IL-10 and IFN-g.
|
| 147 |
8993758
|
Spleen cells from infected mice responded to concanavalin A and to HSV by secreting large amounts of IL-2 and IFN-g, modest amounts of IL-10, and no IL-4.
|
| 148 |
8993758
|
These mice, however, responded to HSV by secreting IFN-g, but no IL-2.
|
| 149 |
8993758
|
A Culture supernatants were collected and assayed for content of IL-2, IL-4, IL-10 and IFN-g.
|
| 150 |
8993758
|
Spleen cells from infected mice responded to concanavalin A and to HSV by secreting large amounts of IL-2 and IFN-g, modest amounts of IL-10, and no IL-4.
|
| 151 |
8993758
|
These mice, however, responded to HSV by secreting IFN-g, but no IL-2.
|
| 152 |
8993758
|
A Culture supernatants were collected and assayed for content of IL-2, IL-4, IL-10 and IFN-g.
|
| 153 |
8993758
|
Spleen cells from infected mice responded to concanavalin A and to HSV by secreting large amounts of IL-2 and IFN-g, modest amounts of IL-10, and no IL-4.
|
| 154 |
8993758
|
These mice, however, responded to HSV by secreting IFN-g, but no IL-2.
|
| 155 |
9209348
|
The spleen cells from the immunized mice produced a large amount of IFN-gamma and IL-2, whereas they released neither IL-4 or IL-10.
|
| 156 |
9272363
|
In an investigation of cell-mediated immunity against Bordetella pertussis, we found that B. pertussis infection in infants and in mice was associated with the induction of antigen-specific T cells that secrete IFN-g and IL-2, but not IL-4 or IL-5.
|
| 157 |
9272363
|
An examination of cytokine production following immunization with a three-component acellular vaccine, comprising inactive PT, FHA and pertactin adsorbed to alum, demonstrated that spleen cells from vaccinated mice produced high levels of IL-5, but no detectable IFN-g and low levels of IL-2.
|
| 158 |
9272363
|
In contrast, peripheral blood mononuclear cells from vaccinated infants produced IL-2, IL-5 and IFN-g.
|
| 159 |
9272363
|
In an investigation of cell-mediated immunity against Bordetella pertussis, we found that B. pertussis infection in infants and in mice was associated with the induction of antigen-specific T cells that secrete IFN-g and IL-2, but not IL-4 or IL-5.
|
| 160 |
9272363
|
An examination of cytokine production following immunization with a three-component acellular vaccine, comprising inactive PT, FHA and pertactin adsorbed to alum, demonstrated that spleen cells from vaccinated mice produced high levels of IL-5, but no detectable IFN-g and low levels of IL-2.
|
| 161 |
9272363
|
In contrast, peripheral blood mononuclear cells from vaccinated infants produced IL-2, IL-5 and IFN-g.
|
| 162 |
9272363
|
In an investigation of cell-mediated immunity against Bordetella pertussis, we found that B. pertussis infection in infants and in mice was associated with the induction of antigen-specific T cells that secrete IFN-g and IL-2, but not IL-4 or IL-5.
|
| 163 |
9272363
|
An examination of cytokine production following immunization with a three-component acellular vaccine, comprising inactive PT, FHA and pertactin adsorbed to alum, demonstrated that spleen cells from vaccinated mice produced high levels of IL-5, but no detectable IFN-g and low levels of IL-2.
|
| 164 |
9272363
|
In contrast, peripheral blood mononuclear cells from vaccinated infants produced IL-2, IL-5 and IFN-g.
|
| 165 |
9512760
|
During effective immune responses, the principal cytokine involved appears to be IL-2, with only small, controlled "bursts" of IFN gamma production.
|
| 166 |
9512760
|
However, IL-2 responsiveness is only transient in animals undergoing primary infection, while IFNg production is greatly elevated.
|
| 167 |
9512760
|
During effective immune responses, the principal cytokine involved appears to be IL-2, with only small, controlled "bursts" of IFN gamma production.
|
| 168 |
9512760
|
However, IL-2 responsiveness is only transient in animals undergoing primary infection, while IFNg production is greatly elevated.
|
| 169 |
9656453
|
In addition, the cytokine profiles support the T1rT2 differentiation with these immunizations, in that oxidized mannan antigen gives IFNg, IL-2 and IL-12 production, whereas in the absence of oxidization, IL-4 and not the other cytokines is produced.
|
| 170 |
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.
|
| 171 |
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.
|
| 172 |
10358183
|
We studied the expression of IFN-gamma, IL-2, IL-10, and IL-12 in the brains of SJL/J mice, B10.S mice, and the two lines of congenic mice during the first 2 wk following inoculation.
|
| 173 |
10358183
|
We found a greater expression of IFN-gamma and IL-2 mRNA in the brains of B10.S mice compared with those of SJL/J mice.
|
| 174 |
10358183
|
Also, the ratio of IL-12 to IL-10 mRNA levels was higher in B10.S mice.
|
| 175 |
10358183
|
We studied the expression of IFN-gamma, IL-2, IL-10, and IL-12 in the brains of SJL/J mice, B10.S mice, and the two lines of congenic mice during the first 2 wk following inoculation.
|
| 176 |
10358183
|
We found a greater expression of IFN-gamma and IL-2 mRNA in the brains of B10.S mice compared with those of SJL/J mice.
|
| 177 |
10358183
|
Also, the ratio of IL-12 to IL-10 mRNA levels was higher in B10.S mice.
|
| 178 |
11057100
|
[Secretion of interleukin-2 (IL-2) and interferon (IFN gamma)in whole blood cell culture stimulated with mitogens in patients with lung neoplasms].
|
| 179 |
11076653
|
The relationship between local treatment and tumour regression was supported by replacement of tumour cells by inflammatory cells in regressing lesions and marked induction of T and natural killer cell derived cytokines (IL-2, IL-4, IFNg ...) in post-therapeutic lesions analysed 28 days after the start of Vero-IL-2 administration.
|
| 180 |
11217546
|
This phase corresponds to early release of so-called inflammatory cytokines (IL1, IL6, IL8).
|
| 181 |
11217546
|
The second phase consists of recognition of bacterial antigens by helper CD4 lymphocytes, which mainly release IL2 and IFNg (Th1 response).
|
| 182 |
11259373
|
Human CD38 and its ligand CD31 define a unique lamina propria T lymphocyte signaling pathway.
|
| 183 |
11259373
|
Results are as follows: 1) LP T cells express an enzymatically active form of CD38, characterized by a modified ratio between cyclase and hydrolase functions; 2) LP T cells do not mobilize Ca2+ upon CD38 ligation, as seen in PB T cells (this condition is due to a lack in activation of PLC- g, constantly observed in PB T lymphocytes); 3) The early steps of CD38 signaling involve activation of lck, syk, and LAT; 4) Late events include synthesis and release of IL-2, IL-4, IL-5, IL-10, IFN-g and GM-CSF; 5) The uniqueness of the CD38 pathway in LP T cells is not caused by impaired interactions with the CD31 ligand.
|
| 184 |
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.
|
| 185 |
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.
|
| 186 |
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.
|
| 187 |
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.
|
| 188 |
12089714
|
Using amplification-refractory mutation system polymerase chain reaction, the following cytokine gene polymorphisms were determined: IL-2+166, IL-2-330, IL-15+13689, IL-15-80, TNF-A-308, TNFd3, IFN-G+874 (T(H)1-type cytokines), IL-4+33, IL-4-590, IL-6-174, IL-10-592, IL-10-819, IL-10-1082, IL-13+2043, IL-13-1055 (T(H)2 type cytokines), TGF-B1+869, and TGF-B1+915 (regulatory-type cytokines).
|
| 189 |
12089714
|
Univariate analysis showed that polymorphisms of IL-10-1082, TGF-B1+869, and HLA-DR6 were significantly related to liver graft rejection.
|
| 190 |
12089714
|
These findings suggest a role for the regulatory-type cytokine transforming growth factor-beta1 in human liver graft rejection.
|
| 191 |
12528636
|
The results obtained suggest that it is expedient for complex therapy of surgical sepsis to include immunocorrection aimed at the weakening of immunosuppresive action of antiinflammatory mediators and shift of the balance towards the reinforcement of activity of proinflammatory ones (IL-12, IL-1) and Th-1 cytokines (IL-2, IFN-g).
|
| 192 |
12849703
|
The cells were then analyzed for the effects of non-thermal ultrasound on cell growth and the presence of IL-2, IL-4 and IFN-g.
|
| 193 |
12849703
|
Cells pre-treated with 1 MHz and stimulated with ConA showed a significant increase in IL-4 and IFN-g.
|
| 194 |
12849703
|
Conversely, cells pre-treated with 3 MHz and stimulated with ConA show a significant decrease in IL-4 and IFN-g.
|
| 195 |
12849703
|
Interferon-gamma is known to stimulate production of collagen in fibroblasts, enhance debridement activity of macrophage and inhibit activity of the T cell subpopulation, T(H2).
|
| 196 |
14510669
|
The genes were natural resistance associated macrophage protein 1 (SLC11A1, previously known as NRAMP1), inhibitor of apoptosis protein 1 (IAP1), prosaposin (PSAP), Caspase-1 (CASP1), inducible nitric oxide production (iNOS), interferon-gamma (IFNG), interleukin-2 (IL2), immunoglobulin light chain (IGL), ZOV3, and transforming growth factors B2, B3 and B4 (TGFB2, B3 and B4).
|
| 197 |
14510669
|
Overall we found the most significant associations with caecum content, nine of 12 genes showed a significant association (SLC11A1, IAP1, PSAP, CASP1, iNOS, IL2, IGL, TGFB2 and TGFB4).
|
| 198 |
14510669
|
For liver, five genes (SLC11A1, CASP1, IL2, IGL, and TGFB4) and for spleen, only one gene (TGFB3) showed a significant association with SE load.
|
| 199 |
14510669
|
The genes were natural resistance associated macrophage protein 1 (SLC11A1, previously known as NRAMP1), inhibitor of apoptosis protein 1 (IAP1), prosaposin (PSAP), Caspase-1 (CASP1), inducible nitric oxide production (iNOS), interferon-gamma (IFNG), interleukin-2 (IL2), immunoglobulin light chain (IGL), ZOV3, and transforming growth factors B2, B3 and B4 (TGFB2, B3 and B4).
|
| 200 |
14510669
|
Overall we found the most significant associations with caecum content, nine of 12 genes showed a significant association (SLC11A1, IAP1, PSAP, CASP1, iNOS, IL2, IGL, TGFB2 and TGFB4).
|
| 201 |
14510669
|
For liver, five genes (SLC11A1, CASP1, IL2, IGL, and TGFB4) and for spleen, only one gene (TGFB3) showed a significant association with SE load.
|
| 202 |
14510669
|
The genes were natural resistance associated macrophage protein 1 (SLC11A1, previously known as NRAMP1), inhibitor of apoptosis protein 1 (IAP1), prosaposin (PSAP), Caspase-1 (CASP1), inducible nitric oxide production (iNOS), interferon-gamma (IFNG), interleukin-2 (IL2), immunoglobulin light chain (IGL), ZOV3, and transforming growth factors B2, B3 and B4 (TGFB2, B3 and B4).
|
| 203 |
14510669
|
Overall we found the most significant associations with caecum content, nine of 12 genes showed a significant association (SLC11A1, IAP1, PSAP, CASP1, iNOS, IL2, IGL, TGFB2 and TGFB4).
|
| 204 |
14510669
|
For liver, five genes (SLC11A1, CASP1, IL2, IGL, and TGFB4) and for spleen, only one gene (TGFB3) showed a significant association with SE load.
|
| 205 |
14628087
|
Both CD8+ and CD4+ T cells with specific activity against tumor antigens are needed for an efficient antitumor immune response.
|
| 206 |
14628087
|
DCs were obtained from peripheral blood mononuclear cells (PBMC) in the presence of IL-4 and GM-CSF.
|
| 207 |
14628087
|
Nonadherent peripheral blood mononuclear cells were cultured in the presence of Il-2 and IL-7.
|
| 208 |
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.
|
| 209 |
15021309
|
No SNPs at IFNG, IL2, IL12B, TNF, or CCL2 (MCP1) showed any association with HIV-related outcomes.
|
| 210 |
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.
|
| 211 |
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.
|
| 212 |
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.
|
| 213 |
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.
|
| 214 |
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.
|
| 215 |
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.
|
| 216 |
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.
|
| 217 |
15073568
|
CRH, 10(-7) M, significantly reversed the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of IFNg production.
|
| 218 |
15073568
|
CRH at all concentrations significantly blocked the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of TNFalpha production.
|
| 219 |
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.
|
| 220 |
15271977
|
A distal region in the interferon-gamma gene is a site of epigenetic remodeling and transcriptional regulation by interleukin-2.
|
| 221 |
15271977
|
IL-2 is another key immunoregulatory cytokine that is involved in T helper differentiation and is known to induce IFN-gamma expression in natural killer (NK) and T cells.
|
| 222 |
15271977
|
Despite concerted efforts to identify the one or more transcriptional control mechanisms by which IL-2 induces IFN-gamma mRNA expression, no such genomic regulatory regions have been described.
|
| 223 |
15271977
|
Within this distal region we found a Stat5-like motif, and in vitro DNA binding assays as well as in vivo chromosomal immunoprecipitation assays showed IL-2-induced binding of both Stat5a and Stat5b to this distal element in the IFNG gene.
|
| 224 |
15271977
|
We examined the function of this Stat5-binding motif by transfecting human peripheral blood mononuclear cells with -3.6 kb of IFNG-luciferase constructs and found that phorbol 12-myristate 13-acetate/ionomycin-induced transcription was augmented by IL-2 treatment.
|
| 225 |
15271977
|
The effect of IL-2 was lost when the Stat5 motif was disrupted.
|
| 226 |
15271977
|
These data led us to conclude that this distal region serves as both a target of chromatin remodeling in the IFNG locus as well as an IL-2-induced transcriptional enhancer that binds Stat5 proteins.
|
| 227 |
15271977
|
A distal region in the interferon-gamma gene is a site of epigenetic remodeling and transcriptional regulation by interleukin-2.
|
| 228 |
15271977
|
IL-2 is another key immunoregulatory cytokine that is involved in T helper differentiation and is known to induce IFN-gamma expression in natural killer (NK) and T cells.
|
| 229 |
15271977
|
Despite concerted efforts to identify the one or more transcriptional control mechanisms by which IL-2 induces IFN-gamma mRNA expression, no such genomic regulatory regions have been described.
|
| 230 |
15271977
|
Within this distal region we found a Stat5-like motif, and in vitro DNA binding assays as well as in vivo chromosomal immunoprecipitation assays showed IL-2-induced binding of both Stat5a and Stat5b to this distal element in the IFNG gene.
|
| 231 |
15271977
|
We examined the function of this Stat5-binding motif by transfecting human peripheral blood mononuclear cells with -3.6 kb of IFNG-luciferase constructs and found that phorbol 12-myristate 13-acetate/ionomycin-induced transcription was augmented by IL-2 treatment.
|
| 232 |
15271977
|
The effect of IL-2 was lost when the Stat5 motif was disrupted.
|
| 233 |
15271977
|
These data led us to conclude that this distal region serves as both a target of chromatin remodeling in the IFNG locus as well as an IL-2-induced transcriptional enhancer that binds Stat5 proteins.
|
| 234 |
15271977
|
A distal region in the interferon-gamma gene is a site of epigenetic remodeling and transcriptional regulation by interleukin-2.
|
| 235 |
15271977
|
IL-2 is another key immunoregulatory cytokine that is involved in T helper differentiation and is known to induce IFN-gamma expression in natural killer (NK) and T cells.
|
| 236 |
15271977
|
Despite concerted efforts to identify the one or more transcriptional control mechanisms by which IL-2 induces IFN-gamma mRNA expression, no such genomic regulatory regions have been described.
|
| 237 |
15271977
|
Within this distal region we found a Stat5-like motif, and in vitro DNA binding assays as well as in vivo chromosomal immunoprecipitation assays showed IL-2-induced binding of both Stat5a and Stat5b to this distal element in the IFNG gene.
|
| 238 |
15271977
|
We examined the function of this Stat5-binding motif by transfecting human peripheral blood mononuclear cells with -3.6 kb of IFNG-luciferase constructs and found that phorbol 12-myristate 13-acetate/ionomycin-induced transcription was augmented by IL-2 treatment.
|
| 239 |
15271977
|
The effect of IL-2 was lost when the Stat5 motif was disrupted.
|
| 240 |
15271977
|
These data led us to conclude that this distal region serves as both a target of chromatin remodeling in the IFNG locus as well as an IL-2-induced transcriptional enhancer that binds Stat5 proteins.
|
| 241 |
15271977
|
A distal region in the interferon-gamma gene is a site of epigenetic remodeling and transcriptional regulation by interleukin-2.
|
| 242 |
15271977
|
IL-2 is another key immunoregulatory cytokine that is involved in T helper differentiation and is known to induce IFN-gamma expression in natural killer (NK) and T cells.
|
| 243 |
15271977
|
Despite concerted efforts to identify the one or more transcriptional control mechanisms by which IL-2 induces IFN-gamma mRNA expression, no such genomic regulatory regions have been described.
|
| 244 |
15271977
|
Within this distal region we found a Stat5-like motif, and in vitro DNA binding assays as well as in vivo chromosomal immunoprecipitation assays showed IL-2-induced binding of both Stat5a and Stat5b to this distal element in the IFNG gene.
|
| 245 |
15271977
|
We examined the function of this Stat5-binding motif by transfecting human peripheral blood mononuclear cells with -3.6 kb of IFNG-luciferase constructs and found that phorbol 12-myristate 13-acetate/ionomycin-induced transcription was augmented by IL-2 treatment.
|
| 246 |
15271977
|
The effect of IL-2 was lost when the Stat5 motif was disrupted.
|
| 247 |
15271977
|
These data led us to conclude that this distal region serves as both a target of chromatin remodeling in the IFNG locus as well as an IL-2-induced transcriptional enhancer that binds Stat5 proteins.
|
| 248 |
15271977
|
A distal region in the interferon-gamma gene is a site of epigenetic remodeling and transcriptional regulation by interleukin-2.
|
| 249 |
15271977
|
IL-2 is another key immunoregulatory cytokine that is involved in T helper differentiation and is known to induce IFN-gamma expression in natural killer (NK) and T cells.
|
| 250 |
15271977
|
Despite concerted efforts to identify the one or more transcriptional control mechanisms by which IL-2 induces IFN-gamma mRNA expression, no such genomic regulatory regions have been described.
|
| 251 |
15271977
|
Within this distal region we found a Stat5-like motif, and in vitro DNA binding assays as well as in vivo chromosomal immunoprecipitation assays showed IL-2-induced binding of both Stat5a and Stat5b to this distal element in the IFNG gene.
|
| 252 |
15271977
|
We examined the function of this Stat5-binding motif by transfecting human peripheral blood mononuclear cells with -3.6 kb of IFNG-luciferase constructs and found that phorbol 12-myristate 13-acetate/ionomycin-induced transcription was augmented by IL-2 treatment.
|
| 253 |
15271977
|
The effect of IL-2 was lost when the Stat5 motif was disrupted.
|
| 254 |
15271977
|
These data led us to conclude that this distal region serves as both a target of chromatin remodeling in the IFNG locus as well as an IL-2-induced transcriptional enhancer that binds Stat5 proteins.
|
| 255 |
15271977
|
A distal region in the interferon-gamma gene is a site of epigenetic remodeling and transcriptional regulation by interleukin-2.
|
| 256 |
15271977
|
IL-2 is another key immunoregulatory cytokine that is involved in T helper differentiation and is known to induce IFN-gamma expression in natural killer (NK) and T cells.
|
| 257 |
15271977
|
Despite concerted efforts to identify the one or more transcriptional control mechanisms by which IL-2 induces IFN-gamma mRNA expression, no such genomic regulatory regions have been described.
|
| 258 |
15271977
|
Within this distal region we found a Stat5-like motif, and in vitro DNA binding assays as well as in vivo chromosomal immunoprecipitation assays showed IL-2-induced binding of both Stat5a and Stat5b to this distal element in the IFNG gene.
|
| 259 |
15271977
|
We examined the function of this Stat5-binding motif by transfecting human peripheral blood mononuclear cells with -3.6 kb of IFNG-luciferase constructs and found that phorbol 12-myristate 13-acetate/ionomycin-induced transcription was augmented by IL-2 treatment.
|
| 260 |
15271977
|
The effect of IL-2 was lost when the Stat5 motif was disrupted.
|
| 261 |
15271977
|
These data led us to conclude that this distal region serves as both a target of chromatin remodeling in the IFNG locus as well as an IL-2-induced transcriptional enhancer that binds Stat5 proteins.
|
| 262 |
15271977
|
A distal region in the interferon-gamma gene is a site of epigenetic remodeling and transcriptional regulation by interleukin-2.
|
| 263 |
15271977
|
IL-2 is another key immunoregulatory cytokine that is involved in T helper differentiation and is known to induce IFN-gamma expression in natural killer (NK) and T cells.
|
| 264 |
15271977
|
Despite concerted efforts to identify the one or more transcriptional control mechanisms by which IL-2 induces IFN-gamma mRNA expression, no such genomic regulatory regions have been described.
|
| 265 |
15271977
|
Within this distal region we found a Stat5-like motif, and in vitro DNA binding assays as well as in vivo chromosomal immunoprecipitation assays showed IL-2-induced binding of both Stat5a and Stat5b to this distal element in the IFNG gene.
|
| 266 |
15271977
|
We examined the function of this Stat5-binding motif by transfecting human peripheral blood mononuclear cells with -3.6 kb of IFNG-luciferase constructs and found that phorbol 12-myristate 13-acetate/ionomycin-induced transcription was augmented by IL-2 treatment.
|
| 267 |
15271977
|
The effect of IL-2 was lost when the Stat5 motif was disrupted.
|
| 268 |
15271977
|
These data led us to conclude that this distal region serves as both a target of chromatin remodeling in the IFNG locus as well as an IL-2-induced transcriptional enhancer that binds Stat5 proteins.
|
| 269 |
15688386
|
Simultaneous targeting of IL2 and IL12 to Hodgkin's lymphoma cells enhances activation of resting NK cells and tumor cell lysis.
|
| 270 |
15688386
|
To revert cellular anergy against H/RS cells, we generated an anti-CD30-antibody-interleukin-(IL)-2 and an anti-CD30-antibody-IL12 fusion protein that target IL2 and IL12, respectively, specifically to CD30+ H/RS cells.
|
| 271 |
15688386
|
Simultaneous targeting of IL2 and IL12 to Hodgkin's lymphoma cells enhances activation of resting NK cells and tumor cell lysis.
|
| 272 |
15688386
|
To revert cellular anergy against H/RS cells, we generated an anti-CD30-antibody-interleukin-(IL)-2 and an anti-CD30-antibody-IL12 fusion protein that target IL2 and IL12, respectively, specifically to CD30+ H/RS cells.
|
| 273 |
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.
|
| 274 |
15733644
|
No disease-causing mutations were identified in IL1A, IL1B, IL6 or TNFA.
|
| 275 |
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.
|
| 276 |
15799696
|
The mRNA expression of Il2 and Il4 decreased from day 5 to day 14 after irradiation.
|
| 277 |
15799696
|
Thereafter, the expression level of Il2 mRNA recovered to normal control levels; however, the expression of Il4 mRNA tended toward significantly low levels.
|
| 278 |
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.
|
| 279 |
15799696
|
The mRNA expression of Il2 and Il4 decreased from day 5 to day 14 after irradiation.
|
| 280 |
15799696
|
Thereafter, the expression level of Il2 mRNA recovered to normal control levels; however, the expression of Il4 mRNA tended toward significantly low levels.
|
| 281 |
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.
|
| 282 |
15799696
|
The mRNA expression of Il2 and Il4 decreased from day 5 to day 14 after irradiation.
|
| 283 |
15799696
|
Thereafter, the expression level of Il2 mRNA recovered to normal control levels; however, the expression of Il4 mRNA tended toward significantly low levels.
|
| 284 |
15840431
|
The levels of interleukin (IL)-2 and IL-4 were also decreased 22.6-58.4 and 10.2-36.6%, respectively, at high concentrations of beta-chlorolactic acid.
|
| 285 |
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.
|
| 286 |
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.
|
| 287 |
17073638
|
Decreased production of Interleukin(IL)-12, IL-2 and Interferon (IFN)-g accompanied by an increased secretion of IL-4 are the main features of this defective immunological response.
|
| 288 |
17994425
|
Interleukin (IL)-12, IL-2, interferon-gamma gene polymorphisms in subacute sclerosing panencephalitis patients.
|
| 289 |
17994425
|
Interleukin (IL)-2 -330 (rs2069 762) and +160 (rs2069 763), IL-12 p40 3' UTR (rs3213113), and interferon (IFN)-gamma +874 (rs2430561) polymorphisms are screened by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and PCR-sequence-specific priming (SSP) methods in 87 SSPE patients and 106 healthy controls (HCs) as candidate genes of susceptibility.
|
| 290 |
17994425
|
Interleukin (IL)-12, IL-2, interferon-gamma gene polymorphisms in subacute sclerosing panencephalitis patients.
|
| 291 |
17994425
|
Interleukin (IL)-2 -330 (rs2069 762) and +160 (rs2069 763), IL-12 p40 3' UTR (rs3213113), and interferon (IFN)-gamma +874 (rs2430561) polymorphisms are screened by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and PCR-sequence-specific priming (SSP) methods in 87 SSPE patients and 106 healthy controls (HCs) as candidate genes of susceptibility.
|
| 292 |
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.
|
| 293 |
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).
|
| 294 |
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.
|
| 295 |
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).
|
| 296 |
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.
|
| 297 |
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.
|
| 298 |
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).
|
| 299 |
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.
|
| 300 |
20213480
|
IL-2 and IFN-gamma in the retina of diabetic rats.
|
| 301 |
20421878
|
PHF11 is a transcriptional co-activator of the Th1 effector cytokine genes, interleukin-2 (IL2) and interferon-γ (IFNG), co-operating with nuclear factor kappa B (NF-κB).
|
| 302 |
20421878
|
Consistent with its presence in the nucleus, PHF11 was recruited to the IFNG promoter and over-expression of PHF11 increased the binding of NF-κB to the IFNG promoter and IFNG gene transcription.
|
| 303 |
20421878
|
Over-expression of PHF11 did not increase IL2 gene transcription, suggesting some specificity in promoter recognition.
|
| 304 |
20421878
|
In contrast, small-interfering RNA knock-down of PHF11 decreased transcription of both IFNG and IL2 and led to decreased CD28 cell-surface expression and reduced NF-κB nuclear import and DNA binding.
|
| 305 |
20421878
|
Knock-down of PHF11 also decreased cell viability and was accompanied by reduced expression of GIMAP4 and 5 genes required for T-cell differentiation, viability and homeostasis.
|
| 306 |
20421878
|
PHF11 is a transcriptional co-activator of the Th1 effector cytokine genes, interleukin-2 (IL2) and interferon-γ (IFNG), co-operating with nuclear factor kappa B (NF-κB).
|
| 307 |
20421878
|
Consistent with its presence in the nucleus, PHF11 was recruited to the IFNG promoter and over-expression of PHF11 increased the binding of NF-κB to the IFNG promoter and IFNG gene transcription.
|
| 308 |
20421878
|
Over-expression of PHF11 did not increase IL2 gene transcription, suggesting some specificity in promoter recognition.
|
| 309 |
20421878
|
In contrast, small-interfering RNA knock-down of PHF11 decreased transcription of both IFNG and IL2 and led to decreased CD28 cell-surface expression and reduced NF-κB nuclear import and DNA binding.
|
| 310 |
20421878
|
Knock-down of PHF11 also decreased cell viability and was accompanied by reduced expression of GIMAP4 and 5 genes required for T-cell differentiation, viability and homeostasis.
|
| 311 |
20421878
|
PHF11 is a transcriptional co-activator of the Th1 effector cytokine genes, interleukin-2 (IL2) and interferon-γ (IFNG), co-operating with nuclear factor kappa B (NF-κB).
|
| 312 |
20421878
|
Consistent with its presence in the nucleus, PHF11 was recruited to the IFNG promoter and over-expression of PHF11 increased the binding of NF-κB to the IFNG promoter and IFNG gene transcription.
|
| 313 |
20421878
|
Over-expression of PHF11 did not increase IL2 gene transcription, suggesting some specificity in promoter recognition.
|
| 314 |
20421878
|
In contrast, small-interfering RNA knock-down of PHF11 decreased transcription of both IFNG and IL2 and led to decreased CD28 cell-surface expression and reduced NF-κB nuclear import and DNA binding.
|
| 315 |
20421878
|
Knock-down of PHF11 also decreased cell viability and was accompanied by reduced expression of GIMAP4 and 5 genes required for T-cell differentiation, viability and homeostasis.
|
| 316 |
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.
|
| 317 |
21199392
|
For this purpose, serum concentration of interleukin 2 (IL2), interleukin 10 (IL10), interferon-gamma (IFNG), Toll-like receptor 2 (TLR2) and Toll-like receptor 9 (TLR9) were measured in blood samples obtained from F(2) piglets (n = 334) of a Duroc × Piétrain resource population (DUPI) after Mycoplasma hypopneumoniae (Mh), tetanus toxoid (TT) and Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) vaccination at 6, 9 and 15 weeks of age.
|
| 318 |
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.
|
| 319 |
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.
|
| 320 |
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.
|
| 321 |
21783593
|
Mice were treated with DNCB and TDI showed a preferential increase in the percentage of CD4+IL-2+ cells compared with vehicle and irritant-treated mice.
|
| 322 |
21783593
|
There was an increase in CD4+IFN-g+ cells of mice treated with DNCB and TDI, but no significant increases were observed in mice treated with SLS.
|
| 323 |
21783593
|
Mice were treated with DNCB and TDI showed an increase in the percentage of CD4+IL-4+ cells compared with vehicle and irritant-treated mice.
|
| 324 |
21783593
|
These results suggest that the population of interferon-gamma (IFN-g+) and IL-4+ cells on CD4+ cells and the mRNA expression for IL-4 in lymphocytes could be selectively modulated in allergen-treated mice.
|
| 325 |
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.
|
| 326 |
21876173
|
Such proliferation-dependent variation in cytokine production appears tied to the epigenetic signatures within the ifnG and tnfA proximal promoters.
|
| 327 |
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).
|
| 328 |
22407948
|
Previous studies have shown that short-term (4 weeks) or chronic (32 weeks) exposure to trichloroethylene (TCE) in drinking water of female MRL+/+ mice generated CD4(+) T cells that secreted increased levels of interferon (IFN)-γ and expressed an activated (CD44(hi)CD62L(lo)) phenotype.
|
| 329 |
22407948
|
Also observed was an increase in the expression of Dnmt1 (DNA methyltransferase-1) and decreased expression of several genes known to be downregulated by DNA methylation, namely Ifng, Il2, and Cdkn1a.
|
| 330 |
22407948
|
CD4(+) T cells from a second study in which MRL+/+ mice were treated for 17 weeks with TCE showed a similar increase in Iap and decrease in Cdkn1a.
|
| 331 |
22466669
|
The development and fate of follicular helper T cells defined by an IL-21 reporter mouse.
|
| 332 |
22466669
|
Germinal centers require CD4⁺ follicular helper T cells (TFH cells), whose hallmark is expression of the transcriptional repressor Bcl-6, the chemokine receptor CXCR5 and interleukin 21 (IL-21).
|
| 333 |
22466669
|
To track the development and fate of TFH cells, we generated an IL-21 reporter mouse by introducing sequence encoding green fluorescent protein (GFP) into the Il21 locus; these mice had expression of IL-21–GFP in CD4⁺CXCR5⁺PD-1⁺ TFH cells.
|
| 334 |
22466669
|
IL-21–GFP⁺ TFH cells were multifunctional helper cells that coexpressed several cytokines, including interferon-g (IFN-g), IL-2 and IL-4.
|
| 335 |
22660171
|
We have demonstrated that HMGB1 is detected at high levels in the serum of IL2-treated mice with translocation to the cytoplasm from the nucleus in the liver, consistent with HMGB1's release in response to stress, and ability to sustain autophagy.
|
| 336 |
22660171
|
Limiting autophagy in mice with coadministration of chloroquine (CQ) diminishes serum levels of HMGB1, cytokines (IFNG and IL6 but not IL18), and autophagic flux, attenuating weight gain, enhancing DC, T-cell and NK cell numbers, and promoting long-term tumor control in a murine hepatic metastases model.
|
| 337 |
22940185
|
A cytokine profile revealed the Th1- lineage development of dominant IFNg and IL-2 from RECD4T.
|
| 338 |
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.
|
| 339 |
23071669
|
MYC/MYCN, TGFB1, and IL2) and to 4 weeks (e.g.
|
| 340 |
23071669
|
IFNG, beta-estradiol, p53, NFKB, AKT, PRKCA, IL12, and HLA-C).
|
| 341 |
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.
|
| 342 |
23106526
|
The expression of cytokines mRNA, namely Ifng, Il2,Il4,Il10 and Il12, was quantitated by real-time PCR.
|
| 343 |
23106526
|
Moreover, Damghan strain elicited higher expression levels of Ifng and Il2 mRNA and the highest ratio of Ifng/Il4 mRNA expression compared with the other strains at 40 h and 8 weeks post-infection.
|
| 344 |
23106526
|
The expression of cytokines mRNA, namely Ifng, Il2,Il4,Il10 and Il12, was quantitated by real-time PCR.
|
| 345 |
23106526
|
Moreover, Damghan strain elicited higher expression levels of Ifng and Il2 mRNA and the highest ratio of Ifng/Il4 mRNA expression compared with the other strains at 40 h and 8 weeks post-infection.
|
| 346 |
23138119
|
IL-2 mRNA declined as pregnancy progressed, while IL-15, IFNG and TGFB1 transcripts increased on day 19 and/or 25.
|
| 347 |
23138119
|
Analyses of IL-4 and IL-12 mRNAs demonstrated the increase in these transcripts as pregnancy progressed.
|
| 348 |
23138119
|
Increase in CCR5 and CCR4 mRNAs indicated that both Th1 and Th2 cells coexisted in the day 25 pregnant endometrium.
|
| 349 |
23264404
|
DNA was isolated from peripheral blood and 22 polymorphisms were typed: IL1A -889, IL1B -511, IL1B +3962, IL1R pst1 1970, IL1RN mspa11100, IL4RA +1902, IL12 -1188, IFNG utr5644, TGF-β1 cdn10, TGF-β1 cdn25, TNF-α -308, TNF-α -238, IL-2 -330, IL-2 +166, IL-4 -1098, IL-4 -590, IL-4 -33, IL-6 -174, IL-6 565, IL-10 -1082, IL-10 -819, and IL-10 -592.
|
| 350 |
23264404
|
Fnd was negative and significantly different from 0 for IL-4 -590 (p of F=0.006), IL-10 -1082 (p of F=0.010), IFN utr5644 (p of F=0.024), IL-4 -1098 (p of F=0.026) and TGF-1 cdn25 (p of F=0.001) alleles, as well as for IL-2 haplotypes (p=0.025).
|
| 351 |
23264404
|
Several SNPs (IL-12B -1188, IL-2 -330, IL-4 -1098, IL-4 -590, and IL-10 -1082) were not in HWP (p<0.05).
|
| 352 |
23264404
|
A few SNPs (IL-12B -1188, IL-2 -330, IL-4 -1098, IL-4 -590, and IL-10 -1082) and several observed frequencies of cytokine diplotypes (IL-2/GG:TG, IL-2/TG:TG, IL-4/GCC:GCC, IL-4/TTC:TTC, IL-4/TTT:TTC, IL-10/GCC:GCC, IL-10/ATA:GCC, IL-10/ACC:GCC, and IL-10/ACC:ATA) were not in HWP and were significantly different from the expectations.
|
| 353 |
23264404
|
DNA was isolated from peripheral blood and 22 polymorphisms were typed: IL1A -889, IL1B -511, IL1B +3962, IL1R pst1 1970, IL1RN mspa11100, IL4RA +1902, IL12 -1188, IFNG utr5644, TGF-β1 cdn10, TGF-β1 cdn25, TNF-α -308, TNF-α -238, IL-2 -330, IL-2 +166, IL-4 -1098, IL-4 -590, IL-4 -33, IL-6 -174, IL-6 565, IL-10 -1082, IL-10 -819, and IL-10 -592.
|
| 354 |
23264404
|
Fnd was negative and significantly different from 0 for IL-4 -590 (p of F=0.006), IL-10 -1082 (p of F=0.010), IFN utr5644 (p of F=0.024), IL-4 -1098 (p of F=0.026) and TGF-1 cdn25 (p of F=0.001) alleles, as well as for IL-2 haplotypes (p=0.025).
|
| 355 |
23264404
|
Several SNPs (IL-12B -1188, IL-2 -330, IL-4 -1098, IL-4 -590, and IL-10 -1082) were not in HWP (p<0.05).
|
| 356 |
23264404
|
A few SNPs (IL-12B -1188, IL-2 -330, IL-4 -1098, IL-4 -590, and IL-10 -1082) and several observed frequencies of cytokine diplotypes (IL-2/GG:TG, IL-2/TG:TG, IL-4/GCC:GCC, IL-4/TTC:TTC, IL-4/TTT:TTC, IL-10/GCC:GCC, IL-10/ATA:GCC, IL-10/ACC:GCC, and IL-10/ACC:ATA) were not in HWP and were significantly different from the expectations.
|
| 357 |
23264404
|
DNA was isolated from peripheral blood and 22 polymorphisms were typed: IL1A -889, IL1B -511, IL1B +3962, IL1R pst1 1970, IL1RN mspa11100, IL4RA +1902, IL12 -1188, IFNG utr5644, TGF-β1 cdn10, TGF-β1 cdn25, TNF-α -308, TNF-α -238, IL-2 -330, IL-2 +166, IL-4 -1098, IL-4 -590, IL-4 -33, IL-6 -174, IL-6 565, IL-10 -1082, IL-10 -819, and IL-10 -592.
|
| 358 |
23264404
|
Fnd was negative and significantly different from 0 for IL-4 -590 (p of F=0.006), IL-10 -1082 (p of F=0.010), IFN utr5644 (p of F=0.024), IL-4 -1098 (p of F=0.026) and TGF-1 cdn25 (p of F=0.001) alleles, as well as for IL-2 haplotypes (p=0.025).
|
| 359 |
23264404
|
Several SNPs (IL-12B -1188, IL-2 -330, IL-4 -1098, IL-4 -590, and IL-10 -1082) were not in HWP (p<0.05).
|
| 360 |
23264404
|
A few SNPs (IL-12B -1188, IL-2 -330, IL-4 -1098, IL-4 -590, and IL-10 -1082) and several observed frequencies of cytokine diplotypes (IL-2/GG:TG, IL-2/TG:TG, IL-4/GCC:GCC, IL-4/TTC:TTC, IL-4/TTT:TTC, IL-10/GCC:GCC, IL-10/ATA:GCC, IL-10/ACC:GCC, and IL-10/ACC:ATA) were not in HWP and were significantly different from the expectations.
|
| 361 |
23264404
|
DNA was isolated from peripheral blood and 22 polymorphisms were typed: IL1A -889, IL1B -511, IL1B +3962, IL1R pst1 1970, IL1RN mspa11100, IL4RA +1902, IL12 -1188, IFNG utr5644, TGF-β1 cdn10, TGF-β1 cdn25, TNF-α -308, TNF-α -238, IL-2 -330, IL-2 +166, IL-4 -1098, IL-4 -590, IL-4 -33, IL-6 -174, IL-6 565, IL-10 -1082, IL-10 -819, and IL-10 -592.
|
| 362 |
23264404
|
Fnd was negative and significantly different from 0 for IL-4 -590 (p of F=0.006), IL-10 -1082 (p of F=0.010), IFN utr5644 (p of F=0.024), IL-4 -1098 (p of F=0.026) and TGF-1 cdn25 (p of F=0.001) alleles, as well as for IL-2 haplotypes (p=0.025).
|
| 363 |
23264404
|
Several SNPs (IL-12B -1188, IL-2 -330, IL-4 -1098, IL-4 -590, and IL-10 -1082) were not in HWP (p<0.05).
|
| 364 |
23264404
|
A few SNPs (IL-12B -1188, IL-2 -330, IL-4 -1098, IL-4 -590, and IL-10 -1082) and several observed frequencies of cytokine diplotypes (IL-2/GG:TG, IL-2/TG:TG, IL-4/GCC:GCC, IL-4/TTC:TTC, IL-4/TTT:TTC, IL-10/GCC:GCC, IL-10/ATA:GCC, IL-10/ACC:GCC, and IL-10/ACC:ATA) were not in HWP and were significantly different from the expectations.
|
| 365 |
23764468
|
Firstly, epigenetic enzyme gene expression (histone deacetylase (HDAC) and DNA methyltransferase (DNMT)) was measured after LPS stimulation.
|
| 366 |
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.
|
| 367 |
23777348
|
Expression levels of IFNG, IL2, IL12, IL4, and IL10 genes were estimated before infection and at 4, 8, and 12 MPI in stimulated peripheral blood mononuclear cells (PBMCs) of infected and control kids.
|
| 368 |
23777348
|
The study demonstrated the expression of IFNG and IL2 as classic Th1-like pro-inflammatory signatures; whereas, IL10 exhibited itself as classical Th2-like signature.
|
| 369 |
23777348
|
The study also reports unexpected lowered expression of the IL12 gene simultaneously with increased expression of IFNG, lowered expression of the IL2 gene (compared to IFNG), and suppressed expression of the IL4.
|
| 370 |
23777348
|
Expression levels of IFNG, IL2, IL12, IL4, and IL10 genes were estimated before infection and at 4, 8, and 12 MPI in stimulated peripheral blood mononuclear cells (PBMCs) of infected and control kids.
|
| 371 |
23777348
|
The study demonstrated the expression of IFNG and IL2 as classic Th1-like pro-inflammatory signatures; whereas, IL10 exhibited itself as classical Th2-like signature.
|
| 372 |
23777348
|
The study also reports unexpected lowered expression of the IL12 gene simultaneously with increased expression of IFNG, lowered expression of the IL2 gene (compared to IFNG), and suppressed expression of the IL4.
|
| 373 |
23777348
|
Expression levels of IFNG, IL2, IL12, IL4, and IL10 genes were estimated before infection and at 4, 8, and 12 MPI in stimulated peripheral blood mononuclear cells (PBMCs) of infected and control kids.
|
| 374 |
23777348
|
The study demonstrated the expression of IFNG and IL2 as classic Th1-like pro-inflammatory signatures; whereas, IL10 exhibited itself as classical Th2-like signature.
|
| 375 |
23777348
|
The study also reports unexpected lowered expression of the IL12 gene simultaneously with increased expression of IFNG, lowered expression of the IL2 gene (compared to IFNG), and suppressed expression of the IL4.
|
| 376 |
23847096
|
Interestingly, submicromolar doses of iPA stimulate resting human NK cells and synergize with IL-2 to induce a robust activation ex vivo with significant secretion of CCL5 and CCL3 and a large increase in TNF-α and IFN-γ production when compared with IL-2 single cytokine treatment.
|
| 377 |
23847096
|
Moreover, iPA promotes NK cell proliferation and up-regulates the expression of specific NK cell-activating receptors, as well as CD69 and CD107a expression.
|
| 378 |
23964278
|
The in vitro induced CD25(hi)TNFR2(+) T cells express a conventional regulatory T cells phenotype FOXP3(+)CTLA4(+)CD127(lo/-), but produce effector and immunoregulatory cytokines including IL-2, IL-10, and IFN-g.
|
| 379 |
23982206
|
Activation of the transcriptional function of the NF-κB protein c-Rel by O-GlcNAc glycosylation.
|
| 380 |
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.
|
| 381 |
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.
|
| 382 |
24030809
|
IFN-α8 and -α10 most potently enhanced expression of IFN-γ, IL-2, and IL-4.
|
| 383 |
24030809
|
While enhancement of IL-2 and IL-4 correlated with the time of preincubation with type I IFN, IFN-γ production was enhanced best when IFN-α was added immediately preceding or simultaneously with T-cell stimulation.
|
| 384 |
24030809
|
IFN-α8 and -α10 most potently enhanced expression of IFN-γ, IL-2, and IL-4.
|
| 385 |
24030809
|
While enhancement of IL-2 and IL-4 correlated with the time of preincubation with type I IFN, IFN-γ production was enhanced best when IFN-α was added immediately preceding or simultaneously with T-cell stimulation.
|
| 386 |
24055089
|
Statistical analysis indicated 6 genes, namely IFNG, IL2, XCL1, CD69, CSF2 and CXCL10, as significantly upregulated by PTx which was also demonstrated at the protein level for genes encoding secreted proteins.
|
| 387 |
24065520
|
Genetic variants in transforming growth factor-β gene (TGFB1) affect susceptibility to schizophrenia.
|
| 388 |
24065520
|
This study aimed at investigating the association between schizophrenia susceptibility and selected functional polymorphisms in genes encoding cytokines including: interleukin-2 (IL2 -330T>G, rs2069756), interleukin-6 (IL-6 -174G>C, rs1800795), interferon-γ (IFNG +874T>A, rs2430561) as well as for the first time transforming growth factor-β1 (TGFB1 +869T>C, rs1800470 and +916G>C, rs1800471).
|
| 389 |
24096714
|
The BiPN grade was associated with phytohemagglutinin-induced IL2, IFNG and TNFSF2, as well as with lipopolysaccharide-induced IL6 levels.
|
| 390 |
24118683
|
A combination of interferon-gamma and interleukin-2 production by Coxiella burnetii-stimulated circulating cells discriminates between chronic Q fever and past Q fever.
|
| 391 |
24134186
|
DNA microarray analysis and real-time PCR investigation revealed that cis-UCA, not trans-UCA, increased the expression of a gene encoding a β-galactoside-binding lectin, galectin-7, LGALS7B.
|
| 392 |
24134186
|
Galectin-7 administration upregulated apoptosis and inhibited the expression of interleukin-2 (IL2) and interferon-γ (IFNG) mRNA in Jurkat cells.
|
| 393 |
24296812
|
TNF-α(+) and IFN-γ(+) CD4(+) T cells expressed significantly higher levels of T-box transcription factors T-bet with graded loss of Eomesodermin (Eomes) expression (T-bet(Hi)Eomes(Hi/Lo)) when compared with TNF-α(+) CD4(+) T cells expressing lower levels of both T-bet and Eomes (T-bet(-)Eomes(-)).
|
| 394 |
24296812
|
Furthermore, TNF-α(+) and IFN-γ(+) CD4(+) T cells expressed significantly higher levels of perforin and interleukin (IL)-2 and displayed a terminally differentiated phenotype (CCR7(-)CD27(-)CD45RA(-)CD57(+)CD62L(-)).
|
| 395 |
24296812
|
In contrast, TNF-α(+) alone CMV-specific CD4(+) T cells were predominantly early-memory phenotype with a proportion of these cells displaying T memory stem-cell phenotype (CD95(+)CD45RA(+)CCR7(+)CD27(+)).
|
| 396 |
24296812
|
In vitro stimulation of CMV-specific CD4(+) T cells with viral antigen in the presence of IL-12 was sufficient to dramatically change the transcriptional and functional profile of TNF-α(+) CD4(+) T cells, whereas TNF-α(+) and IFN-γ(+) CD4(+) T cells remained unaltered.
|