Gene Pair Information
Gene Pair: IL1B, IFNG
Related Sentences
| # | PMID | Sentence |
| 1 | 1357793 | Rapid induction of intercellular adhesion molecule-1 on monocytes and myelomonocytic cell lines after interferon gamma treatment. |
| 2 | 1357793 | While previous work has emphasized the role of interferon gamma in inducing increased ICAM-1 expression on nonleukocytic cells, we have demonstrated time- and dose-dependent increases on human monocytes and two myelomonocytic cell lines (Rc2A & U937). |
| 3 | 1357793 | Class II MHC expression and IL-1 production were not elevated by IFNg treatment of these cells, indicating that other factors account for the remainder of the incremental activity observed following this treatment. |
| 4 | 1371640 | CD4/CD8 ratio and percentage CD4 were normal in peripheral blood. |
| 5 | 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. |
| 6 | 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. |
| 7 | 1404261 | Production of IL-2 was suppressed by 14.1-31.9%, and IFN-G was reduced by 8.7-57.0%. |
| 8 | 1404261 | Both IL-1 and TNF are endogenous pyrogens and activate polymorphonuclear leukocytes. |
| 9 | 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. |
| 10 | 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). |
| 11 | 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. |
| 12 | 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. |
| 13 | 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. |
| 14 | 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. |
| 15 | 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. |
| 16 | 2056245 | Developmental regulation of the cytokine repertoire in human macrophages: IL-1, IL-6, TNF-alpha, and M-CSF. |
| 17 | 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. |
| 18 | 2056245 | From the LPS-dependent cytokines, IL-1 beta and IL-6 were downregulated whereas TNF-alpha levels increased severalfold. |
| 19 | 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. |
| 20 | 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. |
| 21 | 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. |
| 22 | 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). |
| 23 | 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. |
| 24 | 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. |
| 25 | 8162754 | The effect of recombinant human interleukin 1B (IL-1B) and recombinant human gamma interferon (IFN-g), when given prophylactically, in a mouse model of septic acute lung injury was studied. |
| 26 | 8162754 | Mice were treated with various doses of IL-1B and IFN-g for 3 consecutive days prior to administration of lipopolysaccharide of Escherichia coli (1 mg/kg given intraperitoneally). |
| 27 | 8162754 | A significant reduction of edema and neutrophil accumulation into the lungs of mice was observed, especially at doses of 100 U per mouse and 10,000 U per mouse of IL-1B and IFN-g, respectively. |
| 28 | 8162754 | Prophylactic administration of IL-1B or IFN-g caused histologic changes, including marked reduction of edema and neutrophil accumulation in the interstitial and alveolar spaces. |
| 29 | 8162754 | Combined prophylactic administration of IL-1B and IFN-g provoked a marked decrease of neutrophil accumulation into the lungs, but was not accompanied by significant reduction of edema or hemorrhage. |
| 30 | 8162754 | These results provide evidence for the beneficial role of IL-1B and IFN-g in the abnormality of septic acute lung injury by reducing inflammatory lesions. |
| 31 | 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). |
| 32 | 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. |
| 33 | 8389732 | Although the expression of high affinity IL-2 receptors (IL-2R) (p75) was unaffected, exogenously added IL-2 failed to restore proliferation. |
| 34 | 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. |
| 35 | 8525128 | High gene expression of IL-4, IL-6, IL-10 and TNF-a was found in SLE patients as compared to normal subjects. |
| 36 | 8525128 | The expression of IL-1b, IL-2 and IFN-g genes was low or undetectable. |
| 37 | 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. |
| 38 | 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. |
| 39 | 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. |
| 40 | 17477815 | In these groups, we analyzed polymorphisms in TNFA by PCR and RFLP, polymorphisms of IFNG, IL1A, IL1B, IL1R1, TNFRSF1A, CASP1, and CRP by Sequenom MassArray (San Diego, CA), and polymorphisms in IL12B and IFNGR1 by fragment length analysis. |
| 41 | 17477815 | The polymorphisms at TNFA - 238 or in IFNG, IL1A, IL1B, IL12B, TNFRSF1A, IFNGR1, CASP1, and CRP were also not associated with typhoid or paratyphoid fever. |
| 42 | 23668260 | The infected mice displayed a significant up-regulation in the expression of chemokines (Cxcl1, Cxcl2 and Ccl2), numerous pro-inflammatory cytokines (Ifng, Il1b, Il6, and Il17f), as well as Il22 and a number of anti-microbial peptides (Defa1, Defa28, Defb1, Slpi and Reg3g) at the site(s) of infection. |
| 43 | 23668260 | However, CD4 T cells of the untreated and C. difficile-infected mice expressed similar levels of CD69 and CD25. |
| 44 | 23668260 | Neither tissue had up-regulated levels of Tbx21, Gata3 or Rorc. |
| 45 | 23668260 | They also displayed significantly higher phosphorylation of AKT and signal transducer and activator of transcription 3 (STAT3), an indication of pro-survival signalling. |
| 46 | 23668260 | These data underscore the local, innate, pro-inflammatory nature of the response to C. difficile and highlight eIF2α phosphorylation and the interleukin-22-pSTAT3-RegIIIγ axis as two of the pathways that could be used to contain and counteract the damage inflicted on the intestinal epithelium. |