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Gene Information
Gene symbol: IFNG
Gene name: interferon, gamma
HGNC ID: 5438
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 29088218 | Effector/memory CD4 T cells making either Th1 or Th2 cytokines commonly co-express T-bet and GATA-3. |
| 2 | 29088218 | Effector/memory CD4 T cells making either Th1 or Th2 cytokines commonly co-express T-bet and GATA-3. |
| 3 | 29088218 | Effector/memory CD4 T cells making either Th1 or Th2 cytokines commonly co-express T-bet and GATA-3. |
| 4 | 29088218 | Effector/memory CD4 T cells making either Th1 or Th2 cytokines commonly co-express T-bet and GATA-3. |
| 5 | 29088218 | Based on cytokine based polarization of NCD4T cells in vitro, programming for either 'Th1' (interferon-gamma [IFNg]) or 'Th2' (interleukin [IL]-4/5/13) cytokines is thought to occur via mutually exclusive expression and functioning of T-bet or GATA-3 transcription factors (TFs). |
| 6 | 29088218 | Based on cytokine based polarization of NCD4T cells in vitro, programming for either 'Th1' (interferon-gamma [IFNg]) or 'Th2' (interleukin [IL]-4/5/13) cytokines is thought to occur via mutually exclusive expression and functioning of T-bet or GATA-3 transcription factors (TFs). |
| 7 | 29088218 | Based on cytokine based polarization of NCD4T cells in vitro, programming for either 'Th1' (interferon-gamma [IFNg]) or 'Th2' (interleukin [IL]-4/5/13) cytokines is thought to occur via mutually exclusive expression and functioning of T-bet or GATA-3 transcription factors (TFs). |
| 8 | 29088218 | Based on cytokine based polarization of NCD4T cells in vitro, programming for either 'Th1' (interferon-gamma [IFNg]) or 'Th2' (interleukin [IL]-4/5/13) cytokines is thought to occur via mutually exclusive expression and functioning of T-bet or GATA-3 transcription factors (TFs). |
| 9 | 29088218 | However, we show that a high proportion of mouse and human memory-phenotype CD4 T (MCD4T) cells generated in vivo which expressed either Th1 or Th2 cytokines commonly co-expressed T-bet and GATA-3. |
| 10 | 29088218 | However, we show that a high proportion of mouse and human memory-phenotype CD4 T (MCD4T) cells generated in vivo which expressed either Th1 or Th2 cytokines commonly co-expressed T-bet and GATA-3. |
| 11 | 29088218 | However, we show that a high proportion of mouse and human memory-phenotype CD4 T (MCD4T) cells generated in vivo which expressed either Th1 or Th2 cytokines commonly co-expressed T-bet and GATA-3. |
| 12 | 29088218 | However, we show that a high proportion of mouse and human memory-phenotype CD4 T (MCD4T) cells generated in vivo which expressed either Th1 or Th2 cytokines commonly co-expressed T-bet and GATA-3. |
| 13 | 29088218 | While T-bet levels did not differ between IFNg-expressing and IL-4/5/13-expressing MCD4T cells, GATA-3 levels were higher in the latter. |
| 14 | 29088218 | While T-bet levels did not differ between IFNg-expressing and IL-4/5/13-expressing MCD4T cells, GATA-3 levels were higher in the latter. |
| 15 | 29088218 | While T-bet levels did not differ between IFNg-expressing and IL-4/5/13-expressing MCD4T cells, GATA-3 levels were higher in the latter. |
| 16 | 29088218 | While T-bet levels did not differ between IFNg-expressing and IL-4/5/13-expressing MCD4T cells, GATA-3 levels were higher in the latter. |
| 17 | 29088218 | Anti-CD3 and anti-CD28-mediated priming of polyclonal NCD4T cells in vitro without polarizing milieu generated cells that expressed either IFNg or IL-4/5/13 but not both, yet both IFNg- and IL-4/5/13-expressing cells showed upregulation of both TFs. |
| 18 | 29088218 | Anti-CD3 and anti-CD28-mediated priming of polyclonal NCD4T cells in vitro without polarizing milieu generated cells that expressed either IFNg or IL-4/5/13 but not both, yet both IFNg- and IL-4/5/13-expressing cells showed upregulation of both TFs. |
| 19 | 29088218 | Anti-CD3 and anti-CD28-mediated priming of polyclonal NCD4T cells in vitro without polarizing milieu generated cells that expressed either IFNg or IL-4/5/13 but not both, yet both IFNg- and IL-4/5/13-expressing cells showed upregulation of both TFs. |
| 20 | 29088218 | Anti-CD3 and anti-CD28-mediated priming of polyclonal NCD4T cells in vitro without polarizing milieu generated cells that expressed either IFNg or IL-4/5/13 but not both, yet both IFNg- and IL-4/5/13-expressing cells showed upregulation of both TFs. |
| 21 | 29088218 | TCR-transgenic NCD4T cells primed in vitro by cognate peptide in non-polarizing conditions which expressed either IFNg or IL-4/5/13 also showed a high proportion of cells co-expressing TFs, and their cytokine commitment varied depending on genetic background or priming conditions, without altering pattern of TF co-expression. |
| 22 | 29088218 | TCR-transgenic NCD4T cells primed in vitro by cognate peptide in non-polarizing conditions which expressed either IFNg or IL-4/5/13 also showed a high proportion of cells co-expressing TFs, and their cytokine commitment varied depending on genetic background or priming conditions, without altering pattern of TF co-expression. |
| 23 | 29088218 | TCR-transgenic NCD4T cells primed in vitro by cognate peptide in non-polarizing conditions which expressed either IFNg or IL-4/5/13 also showed a high proportion of cells co-expressing TFs, and their cytokine commitment varied depending on genetic background or priming conditions, without altering pattern of TF co-expression. |
| 24 | 29088218 | TCR-transgenic NCD4T cells primed in vitro by cognate peptide in non-polarizing conditions which expressed either IFNg or IL-4/5/13 also showed a high proportion of cells co-expressing TFs, and their cytokine commitment varied depending on genetic background or priming conditions, without altering pattern of TF co-expression. |
| 25 | 29088218 | Thus, the model of mutually antagonistic differentiation programs driven by mutually exclusively expressed T-bet or GATA-3 does not completely explain natural CD4 T cell priming outcomes. |
| 26 | 29088218 | Thus, the model of mutually antagonistic differentiation programs driven by mutually exclusively expressed T-bet or GATA-3 does not completely explain natural CD4 T cell priming outcomes. |
| 27 | 29088218 | Thus, the model of mutually antagonistic differentiation programs driven by mutually exclusively expressed T-bet or GATA-3 does not completely explain natural CD4 T cell priming outcomes. |
| 28 | 29088218 | Thus, the model of mutually antagonistic differentiation programs driven by mutually exclusively expressed T-bet or GATA-3 does not completely explain natural CD4 T cell priming outcomes. |
| 29 | 29070650 | The increased metastasis was independent of CD4+ and CD8+ T lymphocytes, but required NK cells and IFNγ. |
| 30 | 29070650 | We found that IL12-YFP reporter mice, whose lungs were injected with B16F10 melanoma, had increased numbers of IL12-expressing CD103+ DCs with enhanced CD86 expression. |
| 31 | 29070650 | Analysis of TCGA datasets revealed an association between high expression of BATF3 and IRF8 and improved survival of breast cancer patients; BATF3 expression also significantly correlated with NK-cell receptor genes, IL12, and IFNG Collectively, our findings show that IL12 from CD103+ DCs is critical for NK cell-mediated control of tumor metastasis. |
| 32 | 29039494 | Ten genes, SOS1, RAF1, IFNA2, IFNG, MTHFR, IGF1, CALM3, UBE2B, TP53 and BMP7 whose expression may be the key internal driving molecules, were selected using the online tool Anni 2.1. |
| 33 | 29032575 | Decreased Expression of IFNG-AS1, IFNG and IL-1B Inflammatory Genes in Medicated Schizophrenia and Bipolar Patients. |
| 34 | 29032575 | Decreased Expression of IFNG-AS1, IFNG and IL-1B Inflammatory Genes in Medicated Schizophrenia and Bipolar Patients. |
| 35 | 29032575 | Decreased Expression of IFNG-AS1, IFNG and IL-1B Inflammatory Genes in Medicated Schizophrenia and Bipolar Patients. |
| 36 | 29032575 | Decreased Expression of IFNG-AS1, IFNG and IL-1B Inflammatory Genes in Medicated Schizophrenia and Bipolar Patients. |
| 37 | 29032575 | Although aberrant expression of cytokines such as IL-1B and IFNG in blood from psychiatric patients supports a role of inflammation in the pathogenesis of the disease, little is known about mechanisms underlying their regulation. |
| 38 | 29032575 | Although aberrant expression of cytokines such as IL-1B and IFNG in blood from psychiatric patients supports a role of inflammation in the pathogenesis of the disease, little is known about mechanisms underlying their regulation. |
| 39 | 29032575 | Although aberrant expression of cytokines such as IL-1B and IFNG in blood from psychiatric patients supports a role of inflammation in the pathogenesis of the disease, little is known about mechanisms underlying their regulation. |
| 40 | 29032575 | Although aberrant expression of cytokines such as IL-1B and IFNG in blood from psychiatric patients supports a role of inflammation in the pathogenesis of the disease, little is known about mechanisms underlying their regulation. |
| 41 | 29032575 | We analysed the expression levels of IFNG-AS1 long non-coding RNA, and IFNG and IL-1B mRNAs in blood cells from 27 SZ- and 30 BP-medicated patients and in 32 healthy controls. |
| 42 | 29032575 | We analysed the expression levels of IFNG-AS1 long non-coding RNA, and IFNG and IL-1B mRNAs in blood cells from 27 SZ- and 30 BP-medicated patients and in 32 healthy controls. |
| 43 | 29032575 | We analysed the expression levels of IFNG-AS1 long non-coding RNA, and IFNG and IL-1B mRNAs in blood cells from 27 SZ- and 30 BP-medicated patients and in 32 healthy controls. |
| 44 | 29032575 | We analysed the expression levels of IFNG-AS1 long non-coding RNA, and IFNG and IL-1B mRNAs in blood cells from 27 SZ- and 30 BP-medicated patients and in 32 healthy controls. |
| 45 | 29032575 | No significant differences in the expression of IFNG-AS1, IFNG and IL-1B genes were found between patients with BP and SZ. |
| 46 | 29032575 | No significant differences in the expression of IFNG-AS1, IFNG and IL-1B genes were found between patients with BP and SZ. |
| 47 | 29032575 | No significant differences in the expression of IFNG-AS1, IFNG and IL-1B genes were found between patients with BP and SZ. |
| 48 | 29032575 | No significant differences in the expression of IFNG-AS1, IFNG and IL-1B genes were found between patients with BP and SZ. |
| 49 | 29017513 | Association between TNF, IL1B, IL6, IL10 and IFNG polymorphisms and recurrent miscarriage: a case control study. |
| 50 | 28972490 | Chronic lymphocytic leukaemia (CLL) is a lymphoproliferative disease characterised by accumulation of monoclonal CD19+CD5+CD23+ lymphocytes in the peripheral blood and bone marrow. |
| 51 | 28972490 | Chronic lymphocytic leukaemia (CLL) is a lymphoproliferative disease characterised by accumulation of monoclonal CD19+CD5+CD23+ lymphocytes in the peripheral blood and bone marrow. |
| 52 | 28972490 | Phagocytic function was assessed through the ability of freshly isolated monocytes to attach and to engulf intact or opsonized Staphylococcus aureus particles in vitro with or without Granulocyte/Macrophage Colony Stimulating Factor (GM-CSF) and Interferon g (IFNg). |
| 53 | 28972490 | Phagocytic function was assessed through the ability of freshly isolated monocytes to attach and to engulf intact or opsonized Staphylococcus aureus particles in vitro with or without Granulocyte/Macrophage Colony Stimulating Factor (GM-CSF) and Interferon g (IFNg). |
| 54 | 28972490 | Simultaneously, immunophenotyping for FcγRI (CD64), FcγRII (CD32), FcγRIII (CD16) and CD180 has been carried out. |
| 55 | 28972490 | Simultaneously, immunophenotyping for FcγRI (CD64), FcγRII (CD32), FcγRIII (CD16) and CD180 has been carried out. |
| 56 | 28972490 | Our results demonstrated that phagocytosis of the intact and opsonised or intact S. aureus by monocytes of CLL patients was significantly decreased in comparison with normal controls, with no recovery upon the treatment with GM-CSF and IFNg. |
| 57 | 28972490 | Our results demonstrated that phagocytosis of the intact and opsonised or intact S. aureus by monocytes of CLL patients was significantly decreased in comparison with normal controls, with no recovery upon the treatment with GM-CSF and IFNg. |
| 58 | 28972490 | A significant decrease in the expression of CD64 and CD180 has been detected on monocytes of CLL patients, with the drop in CD64 expression correlating with the disease progression and advanced Rai stages. |
| 59 | 28972490 | A significant decrease in the expression of CD64 and CD180 has been detected on monocytes of CLL patients, with the drop in CD64 expression correlating with the disease progression and advanced Rai stages. |
| 60 | 28972490 | No appreciable changes were detected in the expression of CD32 and CD16 throughout the experiments. |
| 61 | 28972490 | No appreciable changes were detected in the expression of CD32 and CD16 throughout the experiments. |
| 62 | 28972490 | The diminished expression of CD64 and CD180 provides possible explanation for the impaired phagocytic function of monocytes in CLL, as FcγRI receptor interaction with opsonising IgG1, and CD180 with the ligands on S. aureus might affect the ability of monocytes to attach and to engulf S. aureus particles and effectively eliminate the pathogen. |
| 63 | 28972490 | The diminished expression of CD64 and CD180 provides possible explanation for the impaired phagocytic function of monocytes in CLL, as FcγRI receptor interaction with opsonising IgG1, and CD180 with the ligands on S. aureus might affect the ability of monocytes to attach and to engulf S. aureus particles and effectively eliminate the pathogen. |
| 64 | 28966918 | C. trachomatis infection was associated with a strong upregulation of IFNG and IL22, the enrichment of Th1 and NK cell pathways and Th17 cell-associated cytokines. |
| 65 | 28966918 | C. trachomatis infection was associated with a strong upregulation of IFNG and IL22, the enrichment of Th1 and NK cell pathways and Th17 cell-associated cytokines. |
| 66 | 28966918 | C. trachomatis infection was associated with a strong upregulation of IFNG and IL22, the enrichment of Th1 and NK cell pathways and Th17 cell-associated cytokines. |
| 67 | 28966918 | In individuals with inflammation in the absence of infection the IFNG/IL22 and NK cell response was reduced, however, pro-inflammatory, growth and matrix factors remained upregulated and mucins were downregulated. |
| 68 | 28966918 | In individuals with inflammation in the absence of infection the IFNG/IL22 and NK cell response was reduced, however, pro-inflammatory, growth and matrix factors remained upregulated and mucins were downregulated. |
| 69 | 28966918 | In individuals with inflammation in the absence of infection the IFNG/IL22 and NK cell response was reduced, however, pro-inflammatory, growth and matrix factors remained upregulated and mucins were downregulated. |
| 70 | 28966918 | Our data suggest that, strong IFNG/IL22 responses, probably related to Th1 and NK cell involvement, is important for clearance of C. trachomatis and that the residual pro-inflammatory and pro-fibrotic phenotype that persists after infection might contribute to pathological scarring. |
| 71 | 28966918 | Our data suggest that, strong IFNG/IL22 responses, probably related to Th1 and NK cell involvement, is important for clearance of C. trachomatis and that the residual pro-inflammatory and pro-fibrotic phenotype that persists after infection might contribute to pathological scarring. |
| 72 | 28966918 | Our data suggest that, strong IFNG/IL22 responses, probably related to Th1 and NK cell involvement, is important for clearance of C. trachomatis and that the residual pro-inflammatory and pro-fibrotic phenotype that persists after infection might contribute to pathological scarring. |
| 73 | 28963929 | In present study, we evaluated adjuvant effect of separate or combined use of a TLR7/8 agonist, R848 and a TLR4 agonist, monophosphoryl lipid A (MPL) beside soluble Leishmania antigen (SLA) in BALB/c mice. |
| 74 | 28963929 | Mice were vaccinated three times by SLA with separate or combined TLR7/8 and TLR4 agonists and were then challenged by Leishmania major. |
| 75 | 28963929 | Delay type hypersensitivity, lesion development, parasite load, and cytokines (interferon gamma, and interleukin-10) response were assessed. |
| 76 | 28936833 | The top 10 important nodes of SAP overlapped with Salvianolate injection and aspirin included MAPK14, MAPK8, IL-6 and IL-8. |
| 77 | 28936833 | The important SAP nodes overlapped with Salvianolate injection alone included AKT1 and IFNG, and the important SAP nodes overlapped with aspirin included EPHB2 and TP53. |
| 78 | 28932637 | The results further demonstrate that targeting MUC1-C results in enhanced effector function of CD8+ tumor-infiltrating lymphocytes (TILs) as evidenced by increased expression of the activation marker CD69, the degranulation marker CD107α, and granzyme B. |
| 79 | 28932637 | Analysis of gene expression data sets further showed that overexpression of MUC1 in NSCLCs correlates negatively with CD8, IFNG and GZMB, and that decreases in CD8 and IFNG are associated with poor clinical outcomes. |
| 80 | 28867622 | Here, three single nucleotide polymorphisms (SNPs) in the IFNG gene (rs2069718), IRGM gene (rs10065172), and MBL2 gene (rs11003125) were genotyped among 183 PTB patients, 177 STB patients, and 360 healthy controls from the Chinese Han population. |
| 81 | 28736945 | Tim-1+ B cells suppress T cell interferon-gamma production and promote Foxp3 expression, but have impaired regulatory function in coronary artery disease. |
| 82 | 28736945 | Tim-1+ B cells suppress T cell interferon-gamma production and promote Foxp3 expression, but have impaired regulatory function in coronary artery disease. |
| 83 | 28736945 | In healthy individuals, IL-10-producing B cells were predominantly found in the Tim-1+ B cells. |
| 84 | 28736945 | In healthy individuals, IL-10-producing B cells were predominantly found in the Tim-1+ B cells. |
| 85 | 28736945 | Upon stimulation of the B cell receptor (BCR) and Toll-like receptor 9 (TLR-9) by anti-BCR antibodies and CpG, respectively, the Tim-1+ B cells could further upregulate IL-10 expression. |
| 86 | 28736945 | Upon stimulation of the B cell receptor (BCR) and Toll-like receptor 9 (TLR-9) by anti-BCR antibodies and CpG, respectively, the Tim-1+ B cells could further upregulate IL-10 expression. |
| 87 | 28736945 | In contrast, the Tim-1+ B cells were present at normal frequency in CAD patients, but showed impaired capacity to upregulate IL-10 with or without BCR + CpG stimulation. |
| 88 | 28736945 | In contrast, the Tim-1+ B cells were present at normal frequency in CAD patients, but showed impaired capacity to upregulate IL-10 with or without BCR + CpG stimulation. |
| 89 | 28736945 | The stimulated Tim-1+ B cells from healthy individuals also suppressed expression of interferon gamma (IFN-γ), an atherogenic cytokine in T cells, in an IL-10-dependent fashion, and strongly promoted the expression of Foxp3 in naive CD4+ CD45RO- T cells. |
| 90 | 28736945 | The stimulated Tim-1+ B cells from healthy individuals also suppressed expression of interferon gamma (IFN-γ), an atherogenic cytokine in T cells, in an IL-10-dependent fashion, and strongly promoted the expression of Foxp3 in naive CD4+ CD45RO- T cells. |
| 91 | 28736945 | In contrast, the Tim-1+ B cells from CAD patients were unable to suppress IFN-γ secretion, and only minimally increased the expression of Foxp3 in naive CD4+ CD45RO- T cells. |
| 92 | 28736945 | In contrast, the Tim-1+ B cells from CAD patients were unable to suppress IFN-γ secretion, and only minimally increased the expression of Foxp3 in naive CD4+ CD45RO- T cells. |
| 93 | 28736556 | Somatic mutation in NRAS or KRAS may cause a rare autoimmune disorder coupled with abnormal expansion of lymphocytes. |
| 94 | 28736556 | We also discovered that FTS therapy inhibited both the CFA-driven in vivo induction of Th17 and IL-17/IFN-γ producing "double positive" as well as the upregulation of serum levels of the Th17-associated cytokines IL-17A and IL-22. |
| 95 | 28736556 | By gene microarray analysis of effector CD4+ T cells from CFA-immunized rats, re-stimulated in vitro with the mycobacterium tuberculosis heat-shock protein 65 (Bhsp65), we determined that FTS abrogated the Bhsp65-induced transcription of a large list of genes (e.g., Il17a/f, Il22, Ifng, Csf2, Lta, and Il1a). |
| 96 | 28724658 | Objective: The aim of the study was to evaluate the effects of daily consumption of a tablet containing 5 mg FA on serum folate; number and cytotoxicity of natural killer (NK) cells; mRNA expression of dihydrofolate reductase (DHFR), methylenetetrahydrofolate reductase (MTHFR), interferon γ (IFNG), tumor necrosis factor α (TNFA), and interleukin 8 (IL8) genes; and concentrations of serum inflammatory markers. |
| 97 | 28724658 | Compared with baseline, DHFR mRNA expression was higher at 90 d (P = 0.006) and IL8 and TNFA mRNA expressions were higher at 45 and 90 d (P = 0.001 for both). |
| 98 | 28719267 | Children with coinfection had a significant decrease in Th1 cytokine production, interleukin 2 (IL-2) (P < 0.05), IL-12 (P < 0.05), and tumor necrosis factor alpha (P < 0.05) compared with Giardia-only infected children. |
| 99 | 28719267 | Coinfected children had an increase in IL-10/interferon gamma (IFN-γ) ratio compared with uninfected (P < 0.05) and Ascaris alone (P < 0.05). |
| 100 | 28715406 | Genetic polymorphisms of the IL6 and NOD2 genes are risk factors for inflammatory reactions in leprosy. |
| 101 | 28715406 | From the 15 single nucleotide polymorphisms (SNPs) at the 8 candidate genes genotyped (TNF/LTA, IFNG, IL10, TLR1, NOD2, SOD2, and IL6) we observed statistically different survival curves for rs751271 at the NOD2 and rs2069845 at the IL6 genes (log-rank p-values = 0.002 and 0.023, respectively), suggesting an influence on the amount of time before developing leprosy reactions. |
| 102 | 28715406 | Cox models showed associations between the SNPs rs751271 at NOD2 and rs2069845 at IL6 with leprosy reactions (HRGT = 0.45, p = 0.002; HRAG = 1.88, p = 0.0008, respectively). |
| 103 | 28715406 | Finally, IL-6 and IFN-γ levels were confirmed as high, while IL-10 titers were low in the sera of reactional patients. |
| 104 | 28715406 | From the results, we conclude that SNPs at the NOD2 and IL6 genes are associated with leprosy reactions as an outcome. |
| 105 | 28714020 | Transcription factor NFKB1 may activate miR‑146b and AKT may activate miR‑21. |
| 106 | 28714020 | Transcription factor NFKB1 may activate miR‑146b and AKT may activate miR‑21. |
| 107 | 28714020 | Transcription factor NFKB1 may activate miR‑146b and AKT may activate miR‑21. |
| 108 | 28714020 | In addition, miR‑21 had a regulatory effect on IFNG expression and miR‑146b may regulate the expression of BCL2, PTEN and IFNG. |
| 109 | 28714020 | In addition, miR‑21 had a regulatory effect on IFNG expression and miR‑146b may regulate the expression of BCL2, PTEN and IFNG. |
| 110 | 28714020 | In addition, miR‑21 had a regulatory effect on IFNG expression and miR‑146b may regulate the expression of BCL2, PTEN and IFNG. |
| 111 | 28714020 | Furthermore, target genes of miR‑146b and miR‑21 were significantly enriched in 14 Gene Ontology terms including regulation of cell proliferation (e.g., BCL2, PTEN and IFNG). |
| 112 | 28714020 | Furthermore, target genes of miR‑146b and miR‑21 were significantly enriched in 14 Gene Ontology terms including regulation of cell proliferation (e.g., BCL2, PTEN and IFNG). |
| 113 | 28714020 | Furthermore, target genes of miR‑146b and miR‑21 were significantly enriched in 14 Gene Ontology terms including regulation of cell proliferation (e.g., BCL2, PTEN and IFNG). |
| 114 | 28714020 | Furthermore, miR‑146b may be activated by NFKB1 and subsequently reduce the expression of BCL2, PTEN and IFNG in the progression of renal fibrosis. |
| 115 | 28714020 | Furthermore, miR‑146b may be activated by NFKB1 and subsequently reduce the expression of BCL2, PTEN and IFNG in the progression of renal fibrosis. |
| 116 | 28714020 | Furthermore, miR‑146b may be activated by NFKB1 and subsequently reduce the expression of BCL2, PTEN and IFNG in the progression of renal fibrosis. |
| 117 | 28707358 | CNS tissues from patients with MS and animals with experimental autoimmune encephalomyelitis (EAE) displayed reduced DHEA concentrations, accompanied by diminished expression of the DHEA-synthesizing enzyme CYP17A1 in oligodendrocytes (ODCs), in association with increased expression of inflammatory genes including interferon (IFN)-γ and interleukin (IL)-1β. |
| 118 | 28707358 | CNS tissues from patients with MS and animals with experimental autoimmune encephalomyelitis (EAE) displayed reduced DHEA concentrations, accompanied by diminished expression of the DHEA-synthesizing enzyme CYP17A1 in oligodendrocytes (ODCs), in association with increased expression of inflammatory genes including interferon (IFN)-γ and interleukin (IL)-1β. |
| 119 | 28707358 | Animals with EAE receiving DHEA-S treatment showed reduced Il1b and Ifng transcript levels in spinal cord compared to vehicle-treated animals with EAE. |
| 120 | 28707358 | Animals with EAE receiving DHEA-S treatment showed reduced Il1b and Ifng transcript levels in spinal cord compared to vehicle-treated animals with EAE. |
| 121 | 28705468 | Hence, our objective was to prospectively examine whether variations in cytokine genes (CRP, IFNG, IL1A, IL1B, IL4, IL6, IL10, IL18, TNF, and IL12A) play a role in MCR incidence in 530 community-dwelling Ashkenazi Jewish adults aged 65 years and older without MCR or dementia at baseline enrolled in the LonGenity study. |
| 122 | 28679952 | We show high levels of CXCL10 mRNA closely associated with IFNG levels in the BAL cells of 50% of severe asthmatics and also in the airways of mice subjected to a severe asthma model, both in the context of high-dose CS treatment. |
| 123 | 28679952 | We show high levels of CXCL10 mRNA closely associated with IFNG levels in the BAL cells of 50% of severe asthmatics and also in the airways of mice subjected to a severe asthma model, both in the context of high-dose CS treatment. |
| 124 | 28679952 | The inability of CS to dampen IFNG or CXCL10 expression was not because of impaired nuclear translocation of the glucocorticoid receptor (GR) or its transactivational functions. |
| 125 | 28679952 | The inability of CS to dampen IFNG or CXCL10 expression was not because of impaired nuclear translocation of the glucocorticoid receptor (GR) or its transactivational functions. |
| 126 | 28679952 | Rather, in the presence of CS and IFN-γ, STAT1 and GR were recruited on critical regulatory elements in the endogenous CXCL10 promoter in monocytes, albeit without any abatement of CXCL10 gene expression. |
| 127 | 28679952 | Rather, in the presence of CS and IFN-γ, STAT1 and GR were recruited on critical regulatory elements in the endogenous CXCL10 promoter in monocytes, albeit without any abatement of CXCL10 gene expression. |
| 128 | 28669671 | The MNV RC was marked by the microtubule-associated-protein-1-light-chain-3 (LC3) conjugation system of autophagy and then targeted by immunity-related GTPases (IRGs) and guanylate-binding proteins (GBPs) upon their induction by IFNG. |
| 129 | 28669671 | The MNV RC was marked by the microtubule-associated-protein-1-light-chain-3 (LC3) conjugation system of autophagy and then targeted by immunity-related GTPases (IRGs) and guanylate-binding proteins (GBPs) upon their induction by IFNG. |
| 130 | 28669671 | Further, the LC3 conjugation system and the IFN-inducible GTPases were necessary to inhibit MNV replication in mice and human cells. |
| 131 | 28669671 | Further, the LC3 conjugation system and the IFN-inducible GTPases were necessary to inhibit MNV replication in mice and human cells. |
| 132 | 28669385 | A transcriptomic analysis using RT-qPCR investigated the influence of IL-10 activity on expression of a suite of cytokine genes (IFNG, IL12B, IL10 and CXCL10) associated with antigen-stimulated production of IFN-γ. |
| 133 | 28669385 | A transcriptomic analysis using RT-qPCR investigated the influence of IL-10 activity on expression of a suite of cytokine genes (IFNG, IL12B, IL10 and CXCL10) associated with antigen-stimulated production of IFN-γ. |
| 134 | 28669385 | The IFNG and IL12B genes both experienced significant increases in expression in the presence of Anti-IL-10, while the expression of IL10 and CXCL10 remained unaffected. |
| 135 | 28669385 | The IFNG and IL12B genes both experienced significant increases in expression in the presence of Anti-IL-10, while the expression of IL10 and CXCL10 remained unaffected. |
| 136 | 28654216 | Many transcripts increased in stimulated NK cells were also increased in CD3-stimulated CD8 T cells (FDR < 0.05), including IFNG, CSF2, CCL3, CCL4, and XCL1. |
| 137 | 28654216 | CD160, XCL1, TNFRSF9, and IFNG were selective for TCR/CD3-activated T cells and CD16a-NK cells and all were strongly increased in ABMR and TCMR. |
| 138 | 28654216 | The molecules such as CD160 and XCL1 shared between NK cells in ABMR and effector T cells in TCMR may hold insights into important rejection mechanisms. |
| 139 | 28625883 | TCR+CD3+CD4-CD8- effector T cells in psoriasis. |
| 140 | 28625883 | TCR+CD3+CD4-CD8- "double negative" (DN) T cells can derive from CD8+ T cells through the down-regulation of CD8. |
| 141 | 28625883 | DN T cells from psoriasis patients are characterized by reduced DNA methylation of the IFNG gene and increased PD-1 expression. |
| 142 | 28611474 | p38α regulates cytokine-induced IFNγ secretion via the Mnk1/eIF4E pathway in Th1 cells. |
| 143 | 28611474 | The p38 mitogen-activated protein kinase (MAPK) pathway is involved in the regulation of immune and inflammatory processes. |
| 144 | 28611474 | We used p38α-conditional, p38β-deficient and p38α/β double-null mouse models to address the role of these two p38 MAPK in CD4+ T cells, and found that p38α deficiency causes these cells to hyperproliferate. |
| 145 | 28611474 | Our studies indicate that both p38α and p38β are dispensable for T helper cell type 1 (Th1) differentiation but, by controlling interferon (IFN)γ and tumor necrosis factor (TNF)α production, are critical for normal Th1 effector function. |
| 146 | 28611474 | Our results indicate that p38α regulates IFNγ secretion through the activation of the MNK1/eIF4E pathway of translation initiation and identify specific functions for p38α and p38β in T-cell proliferation. |
| 147 | 28581888 | Accordingly, we showed that IL17A and IFNG expression in lymphocytes from tuberculosis patients correlates with disease severity. |
| 148 | 28581888 | Accordingly, we showed that IL17A and IFNG expression in lymphocytes from tuberculosis patients correlates with disease severity. |
| 149 | 28581888 | Accordingly, we showed that IL17A and IFNG expression in lymphocytes from tuberculosis patients correlates with disease severity. |
| 150 | 28581888 | Accordingly, we showed that IL17A and IFNG expression in lymphocytes from tuberculosis patients correlates with disease severity. |
| 151 | 28581888 | Accordingly, we showed that IL17A and IFNG expression in lymphocytes from tuberculosis patients correlates with disease severity. |
| 152 | 28581888 | Here we investigate the role of IFNG and IL17A during autophagy in monocytes infected with Mt H37Rv or the mutant MtΔRD1. |
| 153 | 28581888 | Here we investigate the role of IFNG and IL17A during autophagy in monocytes infected with Mt H37Rv or the mutant MtΔRD1. |
| 154 | 28581888 | Here we investigate the role of IFNG and IL17A during autophagy in monocytes infected with Mt H37Rv or the mutant MtΔRD1. |
| 155 | 28581888 | Here we investigate the role of IFNG and IL17A during autophagy in monocytes infected with Mt H37Rv or the mutant MtΔRD1. |
| 156 | 28581888 | Here we investigate the role of IFNG and IL17A during autophagy in monocytes infected with Mt H37Rv or the mutant MtΔRD1. |
| 157 | 28581888 | IL17A augmented autophagy in infected monocytes from HR patients through a mechanism that activated MAPK1/ERK2-MAPK3/ERK1 but, during infection of monocytes from LR patients, IL17A had no effect on the autophagic response. |
| 158 | 28581888 | IL17A augmented autophagy in infected monocytes from HR patients through a mechanism that activated MAPK1/ERK2-MAPK3/ERK1 but, during infection of monocytes from LR patients, IL17A had no effect on the autophagic response. |
| 159 | 28581888 | IL17A augmented autophagy in infected monocytes from HR patients through a mechanism that activated MAPK1/ERK2-MAPK3/ERK1 but, during infection of monocytes from LR patients, IL17A had no effect on the autophagic response. |
| 160 | 28581888 | IL17A augmented autophagy in infected monocytes from HR patients through a mechanism that activated MAPK1/ERK2-MAPK3/ERK1 but, during infection of monocytes from LR patients, IL17A had no effect on the autophagic response. |
| 161 | 28581888 | IL17A augmented autophagy in infected monocytes from HR patients through a mechanism that activated MAPK1/ERK2-MAPK3/ERK1 but, during infection of monocytes from LR patients, IL17A had no effect on the autophagic response. |
| 162 | 28581888 | In contrast, addition of IFNG to infected monocytes, increased autophagy by activating MAPK14/p38 α both in HR and LR patients. |
| 163 | 28581888 | In contrast, addition of IFNG to infected monocytes, increased autophagy by activating MAPK14/p38 α both in HR and LR patients. |
| 164 | 28581888 | In contrast, addition of IFNG to infected monocytes, increased autophagy by activating MAPK14/p38 α both in HR and LR patients. |
| 165 | 28581888 | In contrast, addition of IFNG to infected monocytes, increased autophagy by activating MAPK14/p38 α both in HR and LR patients. |
| 166 | 28581888 | In contrast, addition of IFNG to infected monocytes, increased autophagy by activating MAPK14/p38 α both in HR and LR patients. |
| 167 | 28581888 | Interestingly, proteins codified in the RD1 region did not interfere with IFNG and IL17A autophagy induction. |
| 168 | 28581888 | Interestingly, proteins codified in the RD1 region did not interfere with IFNG and IL17A autophagy induction. |
| 169 | 28581888 | Interestingly, proteins codified in the RD1 region did not interfere with IFNG and IL17A autophagy induction. |
| 170 | 28581888 | Interestingly, proteins codified in the RD1 region did not interfere with IFNG and IL17A autophagy induction. |
| 171 | 28581888 | Interestingly, proteins codified in the RD1 region did not interfere with IFNG and IL17A autophagy induction. |
| 172 | 28581888 | In contrast, both IFNG and IL17A increased autophagy levels in patients with strong immunity to Mt, promoting mycobacterial killing. |
| 173 | 28581888 | In contrast, both IFNG and IL17A increased autophagy levels in patients with strong immunity to Mt, promoting mycobacterial killing. |
| 174 | 28581888 | In contrast, both IFNG and IL17A increased autophagy levels in patients with strong immunity to Mt, promoting mycobacterial killing. |
| 175 | 28581888 | In contrast, both IFNG and IL17A increased autophagy levels in patients with strong immunity to Mt, promoting mycobacterial killing. |
| 176 | 28581888 | In contrast, both IFNG and IL17A increased autophagy levels in patients with strong immunity to Mt, promoting mycobacterial killing. |
| 177 | 28581445 | Mice treated with glutamine also had higher numbers of HSV-specific IFN-γ-producing CD8 T cells in latently infected ganglia. |
| 178 | 28532492 | The pro-inflammatory cytokine genes IL1B and CXCL8 were up-regulated in monocytes and lymphocytes after Matrix-M exposure. |
| 179 | 28532492 | Matrix-M also induced IL12B, IL17A and IFNG in lymphocytes and IFN-α gene expression in MoDCs. |
| 180 | 28532492 | Granulocyte counts, serum amyloid A levels and transcription of IL18 and TLR2 coincided with disease progression in the pigs. |
| 181 | 28529323 | OVA-reactive CD8+ OT-I T cells were activated in vitro with OVA in the presence of either transforming growth factor-β1 (TGFB1) plus interleukin-10 (IL10), or IL2, to mimic normal or dysregulated uterine conditions, respectively, and transferred into pregnant mice on gestational day 3.5. |
| 182 | 28529323 | OT-I T cells activated with TGFB1 and IL10, like naive OT-I T cells, did not alter embryo implantation or fetal viability. |
| 183 | 28529323 | IL2-activated OT-I T cells expressed less FOXP3 and higher interferon-γ (IFNG) than cells activated with TGFB1 and IL10. |
| 184 | 28526442 | Comparative study of interleukin-17C (IL-17C) and IL-17D in large yellow croaker Larimichthys crocea reveals their similar but differential functional activity. |
| 185 | 28526442 | Here, we identified the IL-17C and IL-17D homologs from large yellow croaker (Larimichthys crocea), named LcIL-17C and LcIL-17D, respectively. |
| 186 | 28526442 | In the peripheral blood leukocytes (PBLs), the recombinant LcIL-17C (rLcIL-17C) could strongly promote the expression of chemokines (CXCL8, CXCL12, and CXCL13), proinflammatory factors (TNF-α, IL-1β, IL-6, and IFNg), and antibacterial peptide hepcidin, whereas rLcIL-17D induced a weaker expression of these chemokines. |
| 187 | 28507796 | LYG1 exerts antitumor function through promoting the activation, proliferation, and function of CD4+ T cells. |
| 188 | 28507796 | LYG1 recombinant protein (rhLYG1) could significantly suppress the growth of B16 tumors in WT B6 mice, but not in SCID-beige mice, Rag1-/- mice, CD4+- or CD8+ T cell-deleted mice. |
| 189 | 28507796 | It could increase the number of CD4+ and CD8+ T cells in tumor-infiltrating lymphocytes, tumor-draining lymph nodes, and spleens, and promote IFNγ production by T cells in tumor-bearing mice. |
| 190 | 28507796 | In vitro experiments demonstrated that rhLYG1 could directly enhance IFNγ secretion by CD4+ T cells, but not CD8+ T cells. |
| 191 | 28507796 | The tumor-inhibiting effect of LYG1 was eliminated in Ifng-/- mice. |
| 192 | 28507796 | In summary, our findings reveal a tumor-inhibiting role for LYG1 through promoting the activation, proliferation, and function of CD4+ T cells in antitumor immune responses, offering implications for novel tumor immunotherapy. |
| 193 | 28505074 | PCR array showed upregulation of some genes involved in lipid metabolism and anti-inflammatory activity (Cpt2, Ifng) and downregulation of some genes involved in pro-inflammatory response and in free fatty acid up-take (Fabp5, Socs3). |
| 194 | 28464285 | Elimination of GPR146-mediated antiviral function through IRF3/HES1-signalling pathway. |
| 195 | 28464285 | Here, we demonstrated that the expression of G-protein-coupled receptor 146 (GPR146) is highly increased by both IFN-β and IFN-γ in a signal transducer and activator of transcription 1-dependent signalling pathway. |
| 196 | 28464285 | Surprisingly, virus-activated IFN regulatory factor 3 (IRF3) signalling not only induces the expression of IFN but also represses GPR146 expression through HES1 (hairy and enhancer of split-1)-mediated transcriptional activity to establish a dynamic equilibrium between pro-viral and antiviral stages in host cells. |
| 197 | 28464285 | Taken together, these data reveal the antiviral role of GPR146 in fighting viral infection although the GPR146-mediated protection is eliminated by IRF3/HES1-signalling, which suggests a potential therapeutic significance of both GPR146 and HES1 signalling in viral infection. |
| 198 | 28459871 | On day 1 post-treatment, major upregulations of Ifng, Foxp3, Il1b, Il2, and Il6 genes in colon were only observed in the mice simultaneously treated with ampicillin. |
| 199 | 28459871 | A two-fold upregulation of colonic Foxp3 and Il1a was evident 25 days post-treatment. |
| 200 | 28453771 | The requirements for inflammation were examined in mice deficient in genes required (Ifng, Il6) or not required (Casp1) for mHgIA. |
| 201 | 28453771 | The requirements for inflammation were examined in mice deficient in genes required (Ifng, Il6) or not required (Casp1) for mHgIA. |
| 202 | 28453771 | The requirements for inflammation were examined in mice deficient in genes required (Ifng, Il6) or not required (Casp1) for mHgIA. |
| 203 | 28453771 | Additionally, lack of IFN-γ or IL-6 impacted expression of genes regulated by either IFN-γ or type I IFN. |
| 204 | 28453771 | Additionally, lack of IFN-γ or IL-6 impacted expression of genes regulated by either IFN-γ or type I IFN. |
| 205 | 28453771 | Additionally, lack of IFN-γ or IL-6 impacted expression of genes regulated by either IFN-γ or type I IFN. |
| 206 | 28453771 | Significantly, both IFN-γ and IL-6 were required for increased expression of IRF-1 which regulates IFN stimulated genes and is required for mHgIA. |
| 207 | 28453771 | Significantly, both IFN-γ and IL-6 were required for increased expression of IRF-1 which regulates IFN stimulated genes and is required for mHgIA. |
| 208 | 28453771 | Significantly, both IFN-γ and IL-6 were required for increased expression of IRF-1 which regulates IFN stimulated genes and is required for mHgIA. |
| 209 | 28453771 | Thus IRF-1 may be at the nexus of the interplay between IFN-γ and IL-6 in exacerbating a xenobiotic-induced inflammatory response, regulation of interferon responsive genes and autoimmunity. |
| 210 | 28453771 | Thus IRF-1 may be at the nexus of the interplay between IFN-γ and IL-6 in exacerbating a xenobiotic-induced inflammatory response, regulation of interferon responsive genes and autoimmunity. |
| 211 | 28453771 | Thus IRF-1 may be at the nexus of the interplay between IFN-γ and IL-6 in exacerbating a xenobiotic-induced inflammatory response, regulation of interferon responsive genes and autoimmunity. |
| 212 | 28448579 | IL-33 receptor ST2 regulates the cognitive impairments associated with experimental cerebral malaria. |
| 213 | 28448579 | We reported recently increased levels of IL-33 protein in brain undergoing ECM and the involvement of IL-33/ST2 pathway in ECM development. |
| 214 | 28448579 | PbA-induced neuroinflammation was reduced in ST2-deficient mice with low Ifng, Tnfa, Il1b, Il6, CXCL9, CXCL10 and Cd8a expression, associated with an absence of neurogenesis defects in hippocampus. |
| 215 | 28448579 | In vitro, IL-33/ST2 pathway induced microglia expression of IL-1β which in turn stimulated IL-33 expression by oligodendrocytes. |
| 216 | 28448579 | These results highlight the IL-33/ST2 pathway ability to orchestrate microglia and oligodendrocytes responses at an early stage of PbA-infection, with an amplification loop between IL-1β and IL-33, responsible for an exacerbated neuroinflammation context and associated neurological and cognitive defects. |
| 217 | 28444539 | The 2'5'-oligoadenylate synthetase (OAS) is an interferon (IFN)-induced protein that plays an important role in the antiviral action of IFN, with OAS3 being one of the four OAS classes (OAS1, OAS2, OAS3, OASL). |
| 218 | 28442041 | Genes with altered expression in sheep SCNT placentas included cytotoxic T-lymphocyte-associated protein 4 (CTLA4), interleukin 2 receptor alpha (IL2RA), cluster of differentiation 28 (CD28), interferon gamma (IFNG), interleukin 6 (IL6), interleukin 10 (IL10), transforming growth factor beta 1 (TGFB1), tumor necrosis factor alpha (TNF-α), interleukin 1 alpha (IL1A) and chemokine (C-X-C motif) ligand 8 (CXCL8). |
| 219 | 28424242 | mTORC1 Promotes T-bet Phosphorylation To Regulate Th1 Differentiation. |
| 220 | 28424242 | CD4+ T cells lacking the mTORC1 activator Rheb fail to secrete IFN-γ under Th1 polarizing conditions. |
| 221 | 28424242 | We hypothesized that this phenotype is due to defects in regulation of the canonical Th1 transcription factor T-bet at the level of protein phosphorylation downstream of mTORC1. |
| 222 | 28424242 | By analyzing activated murine wild-type and Rheb-deficient CD4+ T cells, as well as murine CD4+ T cells activated in the presence of rapamycin, a pharmacologic inhibitor of mTORC1, we were able to identify six T-bet phosphorylation sites. |
| 223 | 28424242 | Five of these are novel, and four sites are consistently dephosphorylated in both Rheb-deficient CD4+ T cells and T cells treated with rapamycin, suggesting mTORC1 signaling controls their phosphorylation. |
| 224 | 28424242 | The reduced activity of the triple mutant T-bet is associated with its failure to recruit chromatin remodeling complexes to the Ifng gene promoter. |
| 225 | 28424242 | These results establish a novel mechanism by which mTORC1 regulates Th1 differentiation, through control of T-bet phosphorylation. |
| 226 | 28419180 | Placentas exposed to nicotine shifted to a neutral environment, with equivalent levels of interferon gamma (IFNG) and IL10. |
| 227 | 28419180 | Both IL6 and tumor necrosis factor (TNF) levels in amniotic fluid were highly elevated when both nicotine and infection were present. |
| 228 | 28407008 | RQ-PCR validation of important genes representative for the dataset, including apoptosis (XIAP, CASP1, BCLAF1 and CFLAR), proliferation/development (ID3) and inflammation (CD28, CCR7, CX3CR1 and IFNG) processes largely confirmed the dysregulation in proliferation and apoptosis. |
| 229 | 28384236 | As a result, 85 novel genes were inferred, among which eleven genes (e.g., MYD88, FGFR2, NF-κBIA) were identified by both the RWR-based and SP-based methods, 70 genes (e.g., BMP4, IFNG, KITLG) were discovered only by the RWR-based method and four genes (L1R1, MCM6, NOG and CXCR3) were predicted only by the SP-based method. |
| 230 | 28317093 | In this study, impaired non-specific antibody-dependent CD56+ NK cell responses were observed in chronic HCV infection, as shown by decreased degranulation (extracellular CD107a expression) and interferon (IFN)-γ production in response to antibody-bound P815 cells. |
| 231 | 28316372 | The expression of genes, including IL10, JAK1, STAT3, SOCS3, IP10, ICAM1, IFNA, IFNG, STAT1, and IRF1, was investigated by RT-qPCR. |
| 232 | 28316372 | Patients with dyslipidemia demonstrated statistically higher expression of the IL10 and IFNA genes, while IFNG, IP10, IRF1, JAK1, and STAT3 were lower in comparison with nondyslipidemic patients. |
| 233 | 28288138 | Immunotherapeutic approaches, particularly programmed death 1/programmed death ligand 1 (PD-1/PD-L1) blockade, have improved the treatment of non-small-cell lung cancer (NSCLC), supporting the premise that evasion of immune destruction is of importance for NSCLC progression. |
| 234 | 28288138 | We show that MUC1-C increases NF-κB p65 occupancy on the CD274/PD-L1 promoter and thereby drives CD274 transcription. |
| 235 | 28288138 | Moreover, we demonstrate that MUC1-C-induced activation of NF-κB→︀ZEB1 signaling represses the TLR9 (toll-like receptor 9), IFNG, MCP-1 (monocyte chemoattractant protein-1) and GM-CSF genes, and that this signature is associated with decreases in overall survival. |
| 236 | 28262634 | Mutant-infected cod leucocytes presented higher interleukin 1 beta (il1β) and interleukin 8 (il8) transcription than wild-type (WT)-infected cells. |
| 237 | 28262634 | Immunized fish had lower interleukin 6 (il6) and il8 transcription in kidney and prolonged interferon-gamma (ifng) transcription in spleens after challenge compared with non-immunized fish. |
| 238 | 28257599 | Immunosuppressive drugs affect interferon (IFN)-γ and programmed cell death 1 (PD-1) kinetics in patients with newly diagnosed autoimmune hepatitis. |
| 239 | 28257599 | Immunosuppressive drugs affect interferon (IFN)-γ and programmed cell death 1 (PD-1) kinetics in patients with newly diagnosed autoimmune hepatitis. |
| 240 | 28257599 | Herein we investigate the in-vitro effects of prednisolone, 6-mercaptopurine, cyclosporin, tacrolimus, mycophenolic acid (MPA) and rapamycin, immunosuppressive drugs (ISDs) used in AIH treatment, on the expression of proinflammatory cytokines, co-inhibitory molecules and ability to proliferate of CD4+ CD25- cells, isolated from the peripheral blood of treatment-naive patients with AIH. |
| 241 | 28257599 | Herein we investigate the in-vitro effects of prednisolone, 6-mercaptopurine, cyclosporin, tacrolimus, mycophenolic acid (MPA) and rapamycin, immunosuppressive drugs (ISDs) used in AIH treatment, on the expression of proinflammatory cytokines, co-inhibitory molecules and ability to proliferate of CD4+ CD25- cells, isolated from the peripheral blood of treatment-naive patients with AIH. |
| 242 | 28257599 | We note that in healthy subjects (HS) following polyclonal stimulation and in the absence of ISDs, the expression of interferon (IFN)-γ, interleukin (IL)-17 and tumour necrosis factor (TNF)-α by CD4 effectors peaks at 48 h and decreases at 96 h to reach baseline levels. |
| 243 | 28257599 | We note that in healthy subjects (HS) following polyclonal stimulation and in the absence of ISDs, the expression of interferon (IFN)-γ, interleukin (IL)-17 and tumour necrosis factor (TNF)-α by CD4 effectors peaks at 48 h and decreases at 96 h to reach baseline levels. |
| 244 | 28257599 | Levels of programmed cell death-1 (PD-1), T cell immunoglobulin and mucin domain-containing molecule-3 (TIM-3) and cytotoxic T lymphocyte antigen-4 (CTLA-4) increase over 96-h culture both in HS and AIH, although with faster kinetics in the latter. |
| 245 | 28257599 | Levels of programmed cell death-1 (PD-1), T cell immunoglobulin and mucin domain-containing molecule-3 (TIM-3) and cytotoxic T lymphocyte antigen-4 (CTLA-4) increase over 96-h culture both in HS and AIH, although with faster kinetics in the latter. |
| 246 | 28257599 | Exposure to ISDs contains IFN-γ and PD-1 expression in AIH, where control over CD4+ CD25- cell proliferation is also noted upon exposure to MPA. |
| 247 | 28257599 | Exposure to ISDs contains IFN-γ and PD-1 expression in AIH, where control over CD4+ CD25- cell proliferation is also noted upon exposure to MPA. |
| 248 | 28257599 | Treatment with tacrolimus and cyclosporin render CD4+ CD25- cells more susceptible to Treg control. |
| 249 | 28257599 | Treatment with tacrolimus and cyclosporin render CD4+ CD25- cells more susceptible to Treg control. |
| 250 | 28250252 | Association of IL10, IL4, IFNG, and CTLA4 Gene Polymorphisms with Efavirenz Hypersensitivity Reaction in Patients Infected with Human Immunodeficiency Virus. |
| 251 | 28250252 | Association of IL10, IL4, IFNG, and CTLA4 Gene Polymorphisms with Efavirenz Hypersensitivity Reaction in Patients Infected with Human Immunodeficiency Virus. |
| 252 | 28250252 | We evaluated interleukin-10 (IL10) －592 C/A, IL4－589 C/T, interferon gamma (IFNG)＋874 A/T, cytotoxic T-lymphocyte-associated antigen 4 (CTLA4)＋49 A/G gene polymorphisms associated with efavirenz hypersensitivity reaction. |
| 253 | 28250252 | We evaluated interleukin-10 (IL10) －592 C/A, IL4－589 C/T, interferon gamma (IFNG)＋874 A/T, cytotoxic T-lymphocyte-associated antigen 4 (CTLA4)＋49 A/G gene polymorphisms associated with efavirenz hypersensitivity reaction. |
| 254 | 28250252 | A significant inverse correlation was observed when comparing the CTLA4＋49A/G and IL4 －589 C/T polymorphisms (r＝－0.650, p＝0.001); that is, the CTLA4 +49GG genotype, involved with the lowest capacity of inhibition, was inversely correlated IL4－589TT genotype, which induces high production of IL-4. |
| 255 | 28250252 | A significant inverse correlation was observed when comparing the CTLA4＋49A/G and IL4 －589 C/T polymorphisms (r＝－0.650, p＝0.001); that is, the CTLA4 +49GG genotype, involved with the lowest capacity of inhibition, was inversely correlated IL4－589TT genotype, which induces high production of IL-4. |
| 256 | 28248972 | Novel CD28 antagonist mPEG PV1-Fab' mitigates experimental autoimmune uveitis by suppressing CD4+ T lymphocyte activation and IFN-γ production. |
| 257 | 28248972 | A decrease in the activation profile of both T CD4+ and T CD8+ eye-infiltrating lymphocytes was evidenced. |
| 258 | 28248972 | In the periphery, T CD4+ cells from PV1-treated mice also showed a decrease in their activation status, with reduced expression of CD69, CD25, and PD-1 molecules. |
| 259 | 28248972 | In addition, frequency of CD4+IFN-γ+ T cells was significantly lower in PV1-treated group, but not of IL-17-producing T cells. |
| 260 | 28248972 | Moreover, after specific restimulation, PV1 blockade selectively blocked IFN-γ production by CD4+ lymphocytes Taken together, our data suggest that mPEG PV1-Fab' acts mainly on IFN-γ-producing CD4+ T cells and emphasize that this specific CD28 blockade strategy is a potential specific and alternative tool for the treatment of autoimmune disorders in the eye. |
| 261 | 28239238 | Bioinformatics analysis indicated that the cytokine imbalance relevant to key molecules (such as extracellular signal-regulated kinase 1/2 (ERK1/2), p38 mitogen-activated protein kinase (MAPK), tumor necrosis factor (TNF), colony-stimulating factor 3 (CSF3), interleukin- (IL-) 6, and interferon gene (IFNG)) and canonical signaling pathways (such as the complement system, antigen presentation, macropinocytosis signaling, nuclear factor-kappa B (NF-κB) signaling, and IL-17 signaling) was responsible for the common comprehensive mechanism of PS and RA. |
| 262 | 28238791 | Subsequently, Selol protected against LPS-induced up-regulation of proinflammatory cytokines (Tnfa, Ifng, Il6) in rat brain cortex. |
| 263 | 28238791 | The molecular mechanisms through which Selol prevented the neuroinflammation were associated with the inhibition of oxidized glutathione (GSSG) accumulation and with an increase of glutathione-associated enzymes: glutathione peroxidase (Se-GPx), glutathione reductase (GR) as well as thioredoxin reductase (TrxR) activity and expression. |
| 264 | 28220815 | Here, we demonstrate that in CD8+ T cells, Cbx3/HP1γ insufficiency leads to chromatin remodeling accompanied by enhanced Prf1, Gzmb and Ifng expression. |
| 265 | 28220815 | In tumors obtained from Cbx3/HP1γ-insufficient mice or wild type mice treated with Cbx3/HP1γ-insufficient CD8+ T cells, there is an increase of CD8+ effector T cells expressing the stimulatory receptor Klrk1/NKG2D, a decrease in CD4+ CD25+ FOXP3+ regulatory T cells (Treg cells) as well as CD25+ CD4+ T cells expressing the inhibitory receptor CTLA4. |
| 266 | 28186087 | These antitumor effects were CD8+ T-cell and NK cell dependent; however, they were found to be CD4+ T-cell independent. |
| 267 | 28186087 | We found that BV directly stimulated NK cells, induced the expression of the activation marker CD69 and promoted interferon-gamma (IFN-γ) production and cytotoxicity. |
| 268 | 28158541 | Accordingly, copper- and zinc levels and expressions of the infection biomarkers Cxcl2 and Ifng increased in the liver on day 4 with a tendency of increased of copper, zinc and Ifng on day 20. |
| 269 | 28143527 | Immune interferon (IFN), also known as IFN-γ, promotes not only immunomodulation but also antimicrobial and anticancer activity. |
| 270 | 28139755 | Genetically determined high activity of IL-12 and IL-18 in ulcerative colitis and TLR5 in Crohns disease were associated with non-response to anti-TNF therapy. |
| 271 | 28139755 | A recent study indicated that genetically determined high activity of pro-inflammatory cytokines, including interleukin-1β (IL-1β), IL-6 and interferon gamma (IFN-γ), are associated with non-response to anti-TNF therapy. |
| 272 | 28139755 | Eight functional SNPs were associated with anti-TNF response either among patients with CD (TLR5 (rs5744174) and IFNGR2 (rs8126756)), UC (IL12B (rs3212217), IL18 (rs1946518), IFNGR1 (rs2234711), TBX21 (rs17250932) and JAK2 (rs12343867)) or in the combined cohort of patient with CD and UC (IBD) (NLRP3 (rs10754558), IL12B (rs3212217) and IFNGR1 (rs2234711)) (P<0.05). |
| 273 | 28139755 | In conclusion, Our results suggest that SNPs associated with genetically determined high activity of TLR5 among patients with CD and genetically determined high IL-12 and IL-18 levels among patients with UC were associated with non-response. |
| 274 | 28042206 | Increased IL17A, IFNG, and FOXP3 Transcripts in Moderate-Severe Psoriasis: A Major Influence Exerted by IL17A in Disease Severity. |
| 275 | 28042206 | Increased IL17A, IFNG, and FOXP3 Transcripts in Moderate-Severe Psoriasis: A Major Influence Exerted by IL17A in Disease Severity. |
| 276 | 28042206 | Therefore, we sought to analyse skin transcript levels of IL17A, IL22, RORC, IL8, IFNG, IL33, IL36A, FOXP3, and IL10 and correlate with clinic of patients with plaque-type psoriasis. |
| 277 | 28042206 | Therefore, we sought to analyse skin transcript levels of IL17A, IL22, RORC, IL8, IFNG, IL33, IL36A, FOXP3, and IL10 and correlate with clinic of patients with plaque-type psoriasis. |
| 278 | 28042206 | The main results revealed increased transcripts levels of IL17A, IFNG, and FOXP3 in moderate-severe patients. |
| 279 | 28042206 | The main results revealed increased transcripts levels of IL17A, IFNG, and FOXP3 in moderate-severe patients. |
| 280 | 27984087 | HLA and non-HLA studies showed that particular alleles in the HLA-DRB1, HLA-DQB1, HLA-DQA1, HLA-DPB1 genes and variants in STAT4, IRF5 and CD247 are frequently associated with SSc. |
| 281 | 27984087 | STRING10 analysis showed that NFKB1, CSF3R, STAT4, IFNG, PRL and ILs are the main "hubs" of interaction network of the non-HLA genes associated with SSc. |
| 282 | 27983725 | We defined an 8-genes signature (IL8, IL10, IL17A, CCL3, CCL5, VEGFA, EBI3 and NOS2) identifying each condition (MGUS/smoldering/symptomatic-MM) with 84% accuracy. |
| 283 | 27983725 | We defined an 8-genes signature (IL8, IL10, IL17A, CCL3, CCL5, VEGFA, EBI3 and NOS2) identifying each condition (MGUS/smoldering/symptomatic-MM) with 84% accuracy. |
| 284 | 27983725 | Moreover, six genes (IFNG, IL2, LTA, CCL2, VEGFA, CCL3) were found independently correlated with patients' survival. |
| 285 | 27983725 | Moreover, six genes (IFNG, IL2, LTA, CCL2, VEGFA, CCL3) were found independently correlated with patients' survival. |
| 286 | 27983725 | Patients whose MM cells expressed high levels of Th1 cytokines (IFNG/LTA/IL2/CCL2) and low levels of CCL3 and VEGFA, experienced the longest survival. |
| 287 | 27983725 | Patients whose MM cells expressed high levels of Th1 cytokines (IFNG/LTA/IL2/CCL2) and low levels of CCL3 and VEGFA, experienced the longest survival. |
| 288 | 27933160 | Anaphylactic shock symptoms, acute allergic skin responses and serum specific IgE, mMCP-1 and galectin-9 were measured upon OVA challenge. |
| 289 | 27933160 | Unstimulated splenocyte cultures produced increased levels of IL10 and IFNg in mice fed the scFOSlcFOS + B. breve diet. |
| 290 | 27901113 | In the present study, to determine if necroptosis participates in bovine structural luteolysis, we investigated RIPK1 and RIPK3 expression throughout the estrous cycle, during prostaglandin F2α (PGF)-induced luteolysis in the bovine corpus luteum (CL), and in cultured luteal steroidogenic cells (LSCs) after treatment with selected luteolytic factors. |
| 291 | 27901113 | In addition, effects of a RIPK1 inhibitor (necrostatin-1, Nec-1; 50 μM) on cell viability, progesterone secretion, apoptosis related factors and RIPKs expression, were evaluated. |
| 292 | 27901113 | Expression of RIPK1 and RIPK3 increased in the CL tissue during both spontaneous and PGF-induced luteolysis (P < 0.05). |
| 293 | 27901113 | In cultured LSCs, tumor necrosis factor α (TNF; 2.3 nM) in combination with interferon γ (IFNG; 2.5 nM) up-regulated RIPK1 mRNA and protein expression (P < 0.05). |
| 294 | 27901113 | Although Nec-1 prevented TNF + IFNG-induced cell death (P < 0.05), it did not affect CASP3 and CASP8 expression. |
| 295 | 27901113 | Nec-1 decreased both RIPK1 and RIPK3 protein expression (P < 0.05). |
| 296 | 27855206 | However, whereas IFNAR KO mice showed infiltration by neutrophils and macrophages and higher expression of IL-1, IL-6 and Cox2, B6 WT mice show a cellular infiltration in the CNS composed predominantly of T cells, particularly CD8+ T cells, and increased mRNA expression levels of IFNg, GzmB and Prf1 at peak of disease. |
| 297 | 27837027 | Programmed cell death protein-1 (PD-1)/programmed death ligand-1 (PD-L1) checkpoint blockade has led to remarkable and durable objective responses in a number of different tumor types. |
| 298 | 27837027 | In the current study, we analyzed PD-L1, PD-L2, PD-1, and cytolytic activity (CYT) expression, as well as mutational density from melanoma and eight other solid tumor types using The Cancer Genome Atlas database. |
| 299 | 27837027 | We found that in some tumor types, PD-L2 expression is more closely linked to Th1/IFNG expression and PD-1 and CD8 signaling than PD-L1 In contrast, mutational load was not correlated with a Th1/IFNG gene signature in any tumor type. |
| 300 | 27837027 | PD-L1, PD-L2, PD-1, CYT expression, and mutational density are all positive prognostic features in melanoma, and conditional inference modeling revealed PD-1/CYT expression (i.e., an inflamed tumor microenvironment) as the most impactful feature, followed by mutational density. |
| 301 | 27742586 | The intramuscular injection of an expression plasmid encoding turbot Ifng (pMCV1.4-ifng) was not able to affect the transcription of numerous immune genes directly related to the activity of IFN-gamma, with the exception of macrophage-colony stimulating factor (csf1). |
| 302 | 27742586 | The intramuscular injection of an expression plasmid encoding turbot Ifng (pMCV1.4-ifng) was not able to affect the transcription of numerous immune genes directly related to the activity of IFN-gamma, with the exception of macrophage-colony stimulating factor (csf1). |
| 303 | 27742586 | On the other hand, some macrophage markers, such as the macrophage receptor with collagenous structure (marco), were down-regulated by Ifng during the viral infection. |
| 304 | 27742586 | On the other hand, some macrophage markers, such as the macrophage receptor with collagenous structure (marco), were down-regulated by Ifng during the viral infection. |
| 305 | 27806943 | Incubation of the chorioamniotic membranes with HMGB1 1) induced the release of mature IL-1beta and IL-6; 2) upregulated the mRNA expression of the pro-inflammatory mediators NFKB1, IL6, TNF, IL1A, IFNG, and HMGB1 receptors RAGE and TLR2; 3) upregulated the mRNA expression of the inflammasome components NLRP3 and AIM2 as well as NOD proteins (NOD1 and NOD2); 4) increased the protein concentrations of NLRP3 and NOD2; 5) increased the concentration of caspase-1 and the quantity of its active form (p20); and 6) upregulated the mRNA expression and active form of MMP-9. |
| 306 | 27803923 | The results showed that both the recombinant proteins, either alone or in combination, could elicit strong humoral and cellular immune responses with a higher level of IgG antibodies, IFN-γ, IL-2, CD4+, and CD8+ T cells as compared to those in mice from control groups. |
| 307 | 27799486 | We investigated the involvement of sphingosine kinase 1 and 2 (SphK1 and SphK2), which phosphorylate sphingosine to produce sphingosine 1-phosphate, in kidney fibrosis induced by folic acid (FA) or unilateral ischemia-reperfusion injury. |
| 308 | 27799486 | We investigated the involvement of sphingosine kinase 1 and 2 (SphK1 and SphK2), which phosphorylate sphingosine to produce sphingosine 1-phosphate, in kidney fibrosis induced by folic acid (FA) or unilateral ischemia-reperfusion injury. |
| 309 | 27799486 | Analysis of Masson trichrome staining and fibrotic marker protein and mRNA expression 14 days after AKI revealed that wild-type (WT) and Sphk1-/- mice exhibited more kidney fibrosis than Sphk2-/- mice. |
| 310 | 27799486 | Analysis of Masson trichrome staining and fibrotic marker protein and mRNA expression 14 days after AKI revealed that wild-type (WT) and Sphk1-/- mice exhibited more kidney fibrosis than Sphk2-/- mice. |
| 311 | 27799486 | Furthermore, kidneys of FA-treated WT and Sphk1-/- mice had greater immune cell infiltration and expression of fibrotic and inflammatory markers than kidneys of FA-treated Sphk2-/- mice. |
| 312 | 27799486 | Furthermore, kidneys of FA-treated WT and Sphk1-/- mice had greater immune cell infiltration and expression of fibrotic and inflammatory markers than kidneys of FA-treated Sphk2-/- mice. |
| 313 | 27799486 | In contrast, kidneys of Sphk2-/- mice exhibited greater expression of Ifng and IFN-γ-responsive genes (Cxcl9 and Cxcl10) than kidneys of WT or Sphk1-/- mice did at this time point. |
| 314 | 27799486 | In contrast, kidneys of Sphk2-/- mice exhibited greater expression of Ifng and IFN-γ-responsive genes (Cxcl9 and Cxcl10) than kidneys of WT or Sphk1-/- mice did at this time point. |
| 315 | 27799486 | Splenic T cells from untreated Sphk2-/- mice were hyperproliferative and produced more IFN-γ than did those of WT or Sphk1-/- mice. |
| 316 | 27799486 | Splenic T cells from untreated Sphk2-/- mice were hyperproliferative and produced more IFN-γ than did those of WT or Sphk1-/- mice. |
| 317 | 27799486 | IFN-γ blocking antibody administered to Sphk2-/- mice or deletion of Ifng (Sphk2-/-Ifng-/- mice) blocked the protective effect of SphK2 deficiency in fibrosis. |
| 318 | 27799486 | IFN-γ blocking antibody administered to Sphk2-/- mice or deletion of Ifng (Sphk2-/-Ifng-/- mice) blocked the protective effect of SphK2 deficiency in fibrosis. |
| 319 | 27799486 | Moreover, adoptive transfer of Sphk2-/- (but not Sphk2-/-Ifng-/- ) CD4 T cells into WT mice blocked FA-induced fibrosis. |
| 320 | 27799486 | Moreover, adoptive transfer of Sphk2-/- (but not Sphk2-/-Ifng-/- ) CD4 T cells into WT mice blocked FA-induced fibrosis. |
| 321 | 27708054 | Instead, LDHA maintains high concentrations of acetyl-coenzyme A to enhance histone acetylation and transcription of Ifng Ablation of LDHA in T cells protects mice from immunopathology triggered by excessive IFN-γ expression or deficiency of regulatory T cells. |
| 322 | 27774523 | To test how perforin (Prf1), granzyme B (GzmB) and interferon-gamma (IFNg) impact tumor occurrence and progression, we bred the TgMISIIR-TAg transgene into Prf1-/-, GzmB-/-, and IFNgR1-/- mice. |
| 323 | 27774523 | In contrast, loss of function of Prf1 or GzmB did not significantly impact tumor progression and host survival. |
| 324 | 27759021 | Focusing on LPS exposure, we demonstrate that the key molecular indices of maternal inflammatory stress, notably high levels of RANTES, MIP-1α, CCL2, KC, and G-CSF (granulocyte colony-stimulating factor) in gestational tissues/serum, are abrogated by OM85 pretreatment. |
| 325 | 27759021 | Systems-level analyses conducted in parallel using RNASeq revealed that OM85 pretreatment selectively tunes LPS-induced activation in maternal gestational tissues for attenuated expression of TNF, IL1, and IFNG-driven proinflammatory networks, without constraining Type1-IFN-associated networks central to first-line antimicrobial defense. |
| 326 | 27670768 | Microarray revealed changes in gene expression: four genes were downregulated (B3GNT3, ZNF683, IFNG and TNF) and seven upregulated (DEFA4, CTSG, DEFA8P, AZU1, MPO, ELANE and PRTN3). |
| 327 | 27670768 | Comparison with previously published data on in vitro methylprednisolone-regulated genes showed that SMAD7, TNF and CHI3L1 were also downregulated in vivo in relapsing-remitting multiple sclerosis patients. |
| 328 | 27668605 | Carriage frequencies of alleles and genotypes of polymorphic loci of inflammation genes (49A>G CTLA4, 41G>A and 87C>T PDE4D, -590C>T IL4, -308A>G TNF, 252G>A LTA, 874A>T IFNG, -509С>Т, 869T>C and 915G>C TGFB1) were determined in a sample of 200 patients diagnosed with ischemic stroke and in the control group similar in gender and age (146 individuals), all ethnic Russians. |
| 329 | 27655794 | However, CCR7 deficiency did lead to the preferential accumulation of CD8+ ATT cells, which was further exacerbated by HFD feeding. |
| 330 | 27655794 | Finally, expression of inflammatory cytokines/chemokines, such as Tnf, Il6, Il1β, Ccl2, and Ccl3, was equally elevated in AT by HFD feeding in CCR7-/- and WT mice, while Ifng and Il18 were elevated by HFD feeding in CCR7-/- but not in WT mice. |
| 331 | 27655794 | Together, these data suggest that CCR7 plays a role in CD8+ATT cell egress, but does not influence ATM accumulation or the metabolic impact of diet-induced obesity. |
| 332 | 27641098 | However, in Rag2-/-γc-/- mice, lacking lymphocytes and NK cells, and in Ifng-/- mice, Ldhalow and control cells formed tumors at similar rates. |
| 333 | 27580107 | The DNA microarray data were validated by use of a real-time reverse-transcription PCR assay, and expression of the genes FOS, NFKBI, IFNG, CXCR6, CCR5, ITGB2, CCR7, and SELL was assessed. |
| 334 | 27580107 | Profile analysis also revealed that FOS and NFKBI (genes of transcription factors) were involved in most cell-signaling pathways and that expression of these genes was significantly higher in colostral T cells than in peripheral blood T cells. |
| 335 | 27580107 | Furthermore, CCR7 and SELL (genes of T-cell differentiation markers) in colostral T cells had expression patterns extremely similar to those found in effector or effector memory T cells. |
| 336 | 27553676 | Chronic exposure to trichloroethylene increases DNA methylation of the Ifng promoter in CD4+ T cells. |
| 337 | 27553676 | Chronic exposure to trichloroethylene increases DNA methylation of the Ifng promoter in CD4+ T cells. |
| 338 | 27553676 | Chronic exposure to trichloroethylene increases DNA methylation of the Ifng promoter in CD4+ T cells. |
| 339 | 27553676 | Chronic exposure to trichloroethylene increases DNA methylation of the Ifng promoter in CD4+ T cells. |
| 340 | 27553676 | Chronic exposure to trichloroethylene increases DNA methylation of the Ifng promoter in CD4+ T cells. |
| 341 | 27553676 | A time-dependent effect of TCE exposure on both Ifng gene expression and IFN-γ protein production was observed in effector/memory CD4+ T cells, with an increase after 22 weeks of exposure and a decrease after 40 weeks of exposure. |
| 342 | 27553676 | A time-dependent effect of TCE exposure on both Ifng gene expression and IFN-γ protein production was observed in effector/memory CD4+ T cells, with an increase after 22 weeks of exposure and a decrease after 40 weeks of exposure. |
| 343 | 27553676 | A time-dependent effect of TCE exposure on both Ifng gene expression and IFN-γ protein production was observed in effector/memory CD4+ T cells, with an increase after 22 weeks of exposure and a decrease after 40 weeks of exposure. |
| 344 | 27553676 | A time-dependent effect of TCE exposure on both Ifng gene expression and IFN-γ protein production was observed in effector/memory CD4+ T cells, with an increase after 22 weeks of exposure and a decrease after 40 weeks of exposure. |
| 345 | 27553676 | A time-dependent effect of TCE exposure on both Ifng gene expression and IFN-γ protein production was observed in effector/memory CD4+ T cells, with an increase after 22 weeks of exposure and a decrease after 40 weeks of exposure. |
| 346 | 27553676 | A cumulative increase in DNA methylation in the CpG sites of the promoter of the Ifng gene was observed in effector/memory, but not naïve, CD4+ T cells over time. |
| 347 | 27553676 | A cumulative increase in DNA methylation in the CpG sites of the promoter of the Ifng gene was observed in effector/memory, but not naïve, CD4+ T cells over time. |
| 348 | 27553676 | A cumulative increase in DNA methylation in the CpG sites of the promoter of the Ifng gene was observed in effector/memory, but not naïve, CD4+ T cells over time. |
| 349 | 27553676 | A cumulative increase in DNA methylation in the CpG sites of the promoter of the Ifng gene was observed in effector/memory, but not naïve, CD4+ T cells over time. |
| 350 | 27553676 | A cumulative increase in DNA methylation in the CpG sites of the promoter of the Ifng gene was observed in effector/memory, but not naïve, CD4+ T cells over time. |
| 351 | 27553676 | Also unique to the Ifng promoter was an increase in methylation variance in effector/memory compared to naïve CD4+ T cells. |
| 352 | 27553676 | Also unique to the Ifng promoter was an increase in methylation variance in effector/memory compared to naïve CD4+ T cells. |
| 353 | 27553676 | Also unique to the Ifng promoter was an increase in methylation variance in effector/memory compared to naïve CD4+ T cells. |
| 354 | 27553676 | Also unique to the Ifng promoter was an increase in methylation variance in effector/memory compared to naïve CD4+ T cells. |
| 355 | 27553676 | Also unique to the Ifng promoter was an increase in methylation variance in effector/memory compared to naïve CD4+ T cells. |
| 356 | 27553676 | Taken together, the CpG sites of the Ifng promoter in effector/memory CD4+ T cells were especially sensitive to the effects of TCE exposure, which may help explain the regulatory effect of the chemical on this gene. |
| 357 | 27553676 | Taken together, the CpG sites of the Ifng promoter in effector/memory CD4+ T cells were especially sensitive to the effects of TCE exposure, which may help explain the regulatory effect of the chemical on this gene. |
| 358 | 27553676 | Taken together, the CpG sites of the Ifng promoter in effector/memory CD4+ T cells were especially sensitive to the effects of TCE exposure, which may help explain the regulatory effect of the chemical on this gene. |
| 359 | 27553676 | Taken together, the CpG sites of the Ifng promoter in effector/memory CD4+ T cells were especially sensitive to the effects of TCE exposure, which may help explain the regulatory effect of the chemical on this gene. |
| 360 | 27553676 | Taken together, the CpG sites of the Ifng promoter in effector/memory CD4+ T cells were especially sensitive to the effects of TCE exposure, which may help explain the regulatory effect of the chemical on this gene. |
| 361 | 27543773 | Furthermore, AF which contains Lycopodine, Serratidine, Lycoposerramine-G and (probably) Cermizine B completely inhibited the SNP-induced expression of interferon-γ (Ifng) and cyclooxygenase 2 (Ptgs2) as well as significantly down-regulated the expression of 12/15-lipoxygenase (Alox12) and tended to decrease the mRNA level of interleukin-6 gene (Il6). |
| 362 | 27536272 | Cytokine assays confirmed these results on protein level exemplarily for two key inflammatory cytokines, interferon gamma and interleukin 6. |
| 363 | 27536272 | Cytokine assays confirmed these results on protein level exemplarily for two key inflammatory cytokines, interferon gamma and interleukin 6. |
| 364 | 27536272 | The hypothetic gene regulatory network revealed a positive feedback loop of Ifng, Stat1, and Tlr3 gene signaling that was triggered by the HA-G222 variant and correlated with a clinical symptom score indicating disease severity. |
| 365 | 27536272 | The hypothetic gene regulatory network revealed a positive feedback loop of Ifng, Stat1, and Tlr3 gene signaling that was triggered by the HA-G222 variant and correlated with a clinical symptom score indicating disease severity. |
| 366 | 27492330 | Jurkat T cells were activated by PMA/ionomycin subsequently interferon-γ (IFNG) and tumor necrosis factor (TNF)-α protein levels were assessed by ELISA. |
| 367 | 27492330 | Jurkat T cells were activated by PMA/ionomycin subsequently interferon-γ (IFNG) and tumor necrosis factor (TNF)-α protein levels were assessed by ELISA. |
| 368 | 27492330 | IFNG-AS1 was one of these differentially expressed lncRNAs in UC patients and found to regulate the key inflammatory cytokine, IFNG, in CD4 T cells. |
| 369 | 27492330 | IFNG-AS1 was one of these differentially expressed lncRNAs in UC patients and found to regulate the key inflammatory cytokine, IFNG, in CD4 T cells. |
| 370 | 27477919 | More specifically, heme inhibited the M1 phenotype of microglia, hampered the activation of astrocytes, and decreased the cerebral expression of Ifng, Tnfa and Ip10. |
| 371 | 27477919 | Heme might that way alter the migration of pathogenic CD4 and CD8 T lymphocytes within the brain observed during cerebral malaria. |
| 372 | 27454382 | Importantly, heme significantly reduced mortality from 40.9% to 6.3% (P <0.005) and gene expression of pro-inflammatory cytokines (Ccl5, Cxcl10, IL-1b, and Ifng). |
| 373 | 27451029 | Gene expression analysis of a chosen set of radiation response genes in irradiated PBMC revealed a similar profile for DNA damage response and repair genes including FDXR, XPC, DDB2, and GADD45 in DNC-treated cells compared to IR control. |
| 374 | 27451029 | However, in response to radiation, an altered profile of expression was noticed for CDKN1A (p21), MDM2, IFNG, and BBC3 (PUMA) genes after DNC treatment. |
| 375 | 27447180 | Here we engineered targeted deletions of parasite secreted effector proteins using a genetically tractable Δku80 vaccine strain to show that the secretion of specific rhoptry (ROP) and dense granule (GRA) proteins by uracil auxotrophic mutants of T. gondii in conjunction with host cell invasion activates antitumor immunity through host responses involving CD8α+ dendritic cells, the IL-12/interferon-gamma (IFN-γ) TH1 axis, as well as CD4+ and CD8+ T cells. |
| 376 | 27441275 | We identified a number of uncharacterized genes (ZNF300, NUP1333, KLK1 and others) and confirmed previous studies demonstrating specific genes/genesets that are important mediators of host immune responses and that displayed associations with antibody response to influenza A/H1N1 vaccine. |
| 377 | 27441275 | These included interferon-regulatory transcription factors (IRF1/IRF2/IRF6/IRF7/IRF9), chemokine/chemokine receptors (CCR5/CCR9/CCL5), cytokine/cytokine receptors (IFNG/IL10RA/TNFRSF1A), protein kinases (MAP2K4/MAPK3), growth factor receptor (TGFBR1). |
| 378 | 27424131 | Association of Promoter Polymorphisms of Interleukin-10 and Interferon-Gamma Genes with Tuberculosis in Azeri Population of Iran. |
| 379 | 27424131 | Association of Promoter Polymorphisms of Interleukin-10 and Interferon-Gamma Genes with Tuberculosis in Azeri Population of Iran. |
| 380 | 27424131 | Association of Promoter Polymorphisms of Interleukin-10 and Interferon-Gamma Genes with Tuberculosis in Azeri Population of Iran. |
| 381 | 27424131 | In this study, we investigated a possible association between interleukin-10 (IL-10) -1082A⁄G (rs1800896) and interferon (IFN)-gamma +874T/A (rs2430561) promoter polymorphisms and tuberculosis (TB) in the Azeri population of Iran. |
| 382 | 27424131 | In this study, we investigated a possible association between interleukin-10 (IL-10) -1082A⁄G (rs1800896) and interferon (IFN)-gamma +874T/A (rs2430561) promoter polymorphisms and tuberculosis (TB) in the Azeri population of Iran. |
| 383 | 27424131 | In this study, we investigated a possible association between interleukin-10 (IL-10) -1082A⁄G (rs1800896) and interferon (IFN)-gamma +874T/A (rs2430561) promoter polymorphisms and tuberculosis (TB) in the Azeri population of Iran. |
| 384 | 27424131 | IL-10 -1082G/A and IFN-gamma +874T/A single nucleotide polymorphisms (SNPs) were genotyped by amplification refractory mutation system (ARMS)-PCR in 200 healthy controls and 124 tuberculosis patients. |
| 385 | 27424131 | IL-10 -1082G/A and IFN-gamma +874T/A single nucleotide polymorphisms (SNPs) were genotyped by amplification refractory mutation system (ARMS)-PCR in 200 healthy controls and 124 tuberculosis patients. |
| 386 | 27424131 | IL-10 -1082G/A and IFN-gamma +874T/A single nucleotide polymorphisms (SNPs) were genotyped by amplification refractory mutation system (ARMS)-PCR in 200 healthy controls and 124 tuberculosis patients. |
| 387 | 27414498 | Toxoplasma Effector Recruits the Mi-2/NuRD Complex to Repress STAT1 Transcription and Block IFN-γ-Dependent Gene Expression. |
| 388 | 27382192 | Pretransplant blood mRNA expression of apoptosis-related genes (CASP3, FAS, and IL-18) and Th1-derived cytokine gene IFNG correlated positively with short- (6-month GFR CASP3: P = 0.027, FAS: P = 0.021, and IFNG: P = 0.029) and long-term graft function (24-month GFR CASP3: P = 0.003, FAS: P = 0.033, IL-18: P = 0.044, and IFNG: P = 0.04). |
| 389 | 27382192 | Pretransplant blood mRNA expression of apoptosis-related genes (CASP3, FAS, and IL-18) and Th1-derived cytokine gene IFNG correlated positively with short- (6-month GFR CASP3: P = 0.027, FAS: P = 0.021, and IFNG: P = 0.029) and long-term graft function (24-month GFR CASP3: P = 0.003, FAS: P = 0.033, IL-18: P = 0.044, and IFNG: P = 0.04). |
| 390 | 27382192 | The pretransplant IFNG and CASP3 and FAS and IL-18 genes' expression in the recipients' peripheral blood is the possible candidate for novel biomarker of short- and long-term allograft function. |
| 391 | 27382192 | The pretransplant IFNG and CASP3 and FAS and IL-18 genes' expression in the recipients' peripheral blood is the possible candidate for novel biomarker of short- and long-term allograft function. |
| 392 | 27378243 | We show here that the dietary phytochemical apigenin inhibited interferon (IFN)-γ-induced PD-L1 upregulation by triple-negative MDA-MB-468 BC cells, HER2(+) SK-BR-3 BC cells, and 4T1 mouse mammary carcinoma cells, as well as human mammary epithelial cells, but did not affect constitutive PD-L1 expression by triple-negative MDA-MB-231 BC cells. |
| 393 | 27378243 | Apigenin-mediated inhibition of IFN-γ-induced PD-L1 expression by MDA-MB-468 and 4T1 cells was associated with reduced phosphorylation of STAT1, which was early and transient at Tyr701 and sustained at Ser727. |
| 394 | 27378243 | Apigenin-mediated inhibition of IFN-γ-induced PD-L1 expression by MDA-MB-468 cells also increased proliferation and interleukin-2 synthesis by PD-1-expressing Jurkat T cells that were co-cultured with MDA-MB-468 cells. |
| 395 | 27370973 | However, the vaccine up-regulated the expression of genes related to the cell-mediated cytotoxicity (CMC; tcrb and cd8a) and the interferon pathway (IFN; ifn, mx and ifng). |
| 396 | 27320704 | Blood samples were collected and gene expression was analyzed by reverse transcriptase polymerase chain reaction for IFNg, IL1b, IL6, IL8, TNFa, TGFb1 and iNOS. |
| 397 | 27320704 | We found an association between BMI and inflammatory expression at all the points of time checked, a slight inverse association occurs with low BMI for mRNA IL1b, IL6, TNFa, TGFb1 and iNOS, and there was a more pronounced positive association for obese patients for all tested genes. |
| 398 | 27297388 | As a proof of principle that AMs are useful for investigation of C. burnetii replication, we performed experiments with AMs from Nos2(-/-) or Ifng(-/-) mice. |
| 399 | 27288995 | Several investigators addressed the possibility that disturbed cytokine production of TNF, IL-6, IFN-γ and IL-10, among a variety of others, may be implicated in CVID. |
| 400 | 27288995 | Several investigators addressed the possibility that disturbed cytokine production of TNF, IL-6, IFN-γ and IL-10, among a variety of others, may be implicated in CVID. |
| 401 | 27288995 | Several investigators addressed the possibility that disturbed cytokine production of TNF, IL-6, IFN-γ and IL-10, among a variety of others, may be implicated in CVID. |
| 402 | 27288995 | The aim of this study was to test the hypothesis that genetic polymorphisms involving TNF (-308G/A), IFNG (+874 T/A), IL10 (-1082G/A, -819T/C and -592A/C), and IL6 (-174G/C) cytokine genes might contribute to susceptibility to CVID. |
| 403 | 27288995 | The aim of this study was to test the hypothesis that genetic polymorphisms involving TNF (-308G/A), IFNG (+874 T/A), IL10 (-1082G/A, -819T/C and -592A/C), and IL6 (-174G/C) cytokine genes might contribute to susceptibility to CVID. |
| 404 | 27288995 | The aim of this study was to test the hypothesis that genetic polymorphisms involving TNF (-308G/A), IFNG (+874 T/A), IL10 (-1082G/A, -819T/C and -592A/C), and IL6 (-174G/C) cytokine genes might contribute to susceptibility to CVID. |
| 405 | 27288995 | Thirty five patients with CVID and 250 healthy controls were genotyped for indicated single nucleotide polymorphisms (SNP) in TNF, IL6, IFNG and IL10 using Taqman-based assays. |
| 406 | 27288995 | Thirty five patients with CVID and 250 healthy controls were genotyped for indicated single nucleotide polymorphisms (SNP) in TNF, IL6, IFNG and IL10 using Taqman-based assays. |
| 407 | 27288995 | Thirty five patients with CVID and 250 healthy controls were genotyped for indicated single nucleotide polymorphisms (SNP) in TNF, IL6, IFNG and IL10 using Taqman-based assays. |
| 408 | 27288995 | CVID patients had significantly higher frequency of TNF A allele and AA genotype than in healthy subjects (p=0.006; OR=2.27; 95%CI=1.24-4.17 and p=0.038, OR=15.64; 95%CI=1.38-177.20, respectively). |
| 409 | 27288995 | CVID patients had significantly higher frequency of TNF A allele and AA genotype than in healthy subjects (p=0.006; OR=2.27; 95%CI=1.24-4.17 and p=0.038, OR=15.64; 95%CI=1.38-177.20, respectively). |
| 410 | 27288995 | CVID patients had significantly higher frequency of TNF A allele and AA genotype than in healthy subjects (p=0.006; OR=2.27; 95%CI=1.24-4.17 and p=0.038, OR=15.64; 95%CI=1.38-177.20, respectively). |
| 411 | 27288995 | Genetic analysis of IL6 SNP showed that allele G confers increased risk for CVID (p=0.037, OR=1.78, 95% CI=1.03-3.08) while IFNG allele T was associated with splenomegaly in CVID (p=0.032; OR=2.86; 95% CI=1.08-7.56). |
| 412 | 27288995 | Genetic analysis of IL6 SNP showed that allele G confers increased risk for CVID (p=0.037, OR=1.78, 95% CI=1.03-3.08) while IFNG allele T was associated with splenomegaly in CVID (p=0.032; OR=2.86; 95% CI=1.08-7.56). |
| 413 | 27288995 | Genetic analysis of IL6 SNP showed that allele G confers increased risk for CVID (p=0.037, OR=1.78, 95% CI=1.03-3.08) while IFNG allele T was associated with splenomegaly in CVID (p=0.032; OR=2.86; 95% CI=1.08-7.56). |
| 414 | 27288995 | We observed no association between genotypes, alleles and haplotypes of IL-10 gene and CVID or its clinical complications. |
| 415 | 27288995 | We observed no association between genotypes, alleles and haplotypes of IL-10 gene and CVID or its clinical complications. |
| 416 | 27288995 | We observed no association between genotypes, alleles and haplotypes of IL-10 gene and CVID or its clinical complications. |
| 417 | 27288995 | In conclusion, our results indicated association between CVID and cytokine gene polymorphisms -308G/A TNF and -174G/C IL6. |
| 418 | 27288995 | In conclusion, our results indicated association between CVID and cytokine gene polymorphisms -308G/A TNF and -174G/C IL6. |
| 419 | 27288995 | In conclusion, our results indicated association between CVID and cytokine gene polymorphisms -308G/A TNF and -174G/C IL6. |
| 420 | 27288334 | The levels of four of them, including vascular endothelial growth factor receptor-3 (VEGFR3), basic fibroblast growth factor (bFGF), interferon gamma (IFNG) and matrix metalloproteinase 1 (MMP1), were quantified using western blot analysis. |
| 421 | 27276061 | In addition to pathogen associated lipopolysaccharides (LPS), iNOS gene expression is dependent on numerous proinflammatory cytokines in the cellular microenvironment of the macrophage, two of which include interferon gamma (IFN-γ) and tumor necrosis factor alpha (TNF-α). |
| 422 | 27276061 | Results from our theoretical studies indicated that IFN-γ and subsequent activation of IRF1 are essential in consequential production of iNOS upon LPS stimulation. |
| 423 | 27226296 | Bhlhe40 alone shows no significant effects on Ifng promoter activities but contributes to enhance T-box transcription factor Tbx21 (T-bet)-mediated Ifng promoter activation. |
| 424 | 27226296 | Bhlhe40 alone shows no significant effects on Ifng promoter activities but contributes to enhance T-box transcription factor Tbx21 (T-bet)-mediated Ifng promoter activation. |
| 425 | 27226296 | Chromatin immunoprecipitation analysis revealed that Bhlhe40 accumulates in the T-box region of the Ifng locus and contributes to histone H3-lysine 9 acetylation of the Ifng locus, which is impaired without T-bet conditions. |
| 426 | 27226296 | Chromatin immunoprecipitation analysis revealed that Bhlhe40 accumulates in the T-box region of the Ifng locus and contributes to histone H3-lysine 9 acetylation of the Ifng locus, which is impaired without T-bet conditions. |
| 427 | 27223631 | Polymorphisms on IFNG, IL12B and IL12RB1 genes and paracoccidioidomycosis in the Brazilian population. |
| 428 | 27223631 | Polymorphisms on IFNG, IL12B and IL12RB1 genes and paracoccidioidomycosis in the Brazilian population. |
| 429 | 27223631 | We included 156 patients with PCM (40 with the acute form, 99 with the chronic multifocal and 17 with the chronic unifocal form) and assayed their DNA samples for IFNG +874 T/A SNP by PCR-ARMS (Amplification Refractory Mutational System), IL12B +1188 A/C SNP on 3' UTR and IL12RB1 641 A/G SNP on exon 7 by PCR-RFLP (Restriction Fragment Length Polymorphism). |
| 430 | 27223631 | We included 156 patients with PCM (40 with the acute form, 99 with the chronic multifocal and 17 with the chronic unifocal form) and assayed their DNA samples for IFNG +874 T/A SNP by PCR-ARMS (Amplification Refractory Mutational System), IL12B +1188 A/C SNP on 3' UTR and IL12RB1 641 A/G SNP on exon 7 by PCR-RFLP (Restriction Fragment Length Polymorphism). |
| 431 | 27216712 | Moreover, the immunostimulatory activity of B7H6 was demonstrated by the secretion of the pro-inflammatory cytokines tumor necrosis factor-alfa (TNF-α) and interferon gamma (IFN-γ) by the human NK cell line. |
| 432 | 27183578 | Analysis of this process showed differential gene expression along with protein levels of proinflammatory markers, including IL-1β, IL-6, IL-12p40, and TNF-α. |
| 433 | 27183578 | These cytokine genes included chemokines (Cxcl1, Cxcl3, Cxcl5, Ccl2, and Ccl3), ILs (Il1b and Ifng), growth factors (Csf2 and Csf3), and TNF family members (Cd40lg). |
| 434 | 27183578 | However, every hemocyanin maintains downregulated key M2 cytokine genes, including Il4 and Il5 Collectively, our data demonstrate that hemocyanins are able to trigger the release of proinflammatory factors with different patterns of cytokine expression, suggesting differential signaling pathways and transcriptional network mechanisms that lead to the activation of M1-polarized macrophages. |
| 435 | 27179873 | Genes that were differentially expressed over the transition period included those involved in neutrophil adhesion (SELL, ITGB2, and ITGBX), mediation of the immune response (TLR4, HLA-DRA, and CXCR2), maturation, cell cycle progression, apoptosis (MCL1, BCL2, FASLG, and RIPK1), and control of gene expression (PPARG, PPARD, and STAT3). |
| 436 | 27179873 | We noted reduced gene expression of proinflammatory cytokines (IFNG, TNF, IL12, and CCL2) on the day of calving, whereas anti-inflammatory cytokine gene expression (IL10) was upregulated. |
| 437 | 27179873 | Increased gene expression of antimicrobial peptides (BNBD4, DEFB10, and DEFB1) occurred on the day of calving. |
| 438 | 27172324 | We recently demonstrated that the LC3 conjugation system (ATG7, ATG3, and ATG12-ATG5-ATG16L1) is required to target LC3 and IFNG (interferon, gamma)-inducible GTPases to the parasitophorus vacuole membrane (PVM) of a protist parasite Toxoplasma gondii and consequently for IFNG to control T. gondii infection. |
| 439 | 27172324 | Here we show that not only LC3, but also its homologs (GABARAP, GABARAPL1, and GABARAPL2) localize on the PVM of T. gondii in a conjugation-dependent manner. |
| 440 | 27118638 | Genes exclusively upregulated in CD4(+) T cells of aP+LpxL1-vaccinated mice included Th1 and Th17 signature cytokine genes Ifng and Il17a respectively. |
| 441 | 27101784 | Acute inflammation and Th1 response are important in the early clearance of the bacteria as it was emphasized by the association between immune genes (i.e.: HLA, IFNG, TNF, NRPAM1, IL10) variants and the development of active pulmonary TB. |
| 442 | 27071061 | HPAI H5N1 virus induced excessive expression of type I IFNs (IFNA and IFNG), cytokines (IL1B, IL18, IL22, IL13, and IL12B), chemokines (CCL4, CCL19, CCL10, and CX3CL1) and IFN stimulated genes (OASL, MX1, RSAD2, IFITM5, IFIT5, GBP 1, and EIF2AK) in lung tissues. |
| 443 | 27053161 | Th2 cells produce Th2 cytokines such as IL-4, IL-5 and IL-13, but repress Th1 cytokine IFNγ. |
| 444 | 27053161 | We herein show that phosphorylation of Gata3 at Ser308, Thr315 and Ser316 induces dissociation of a histone deacetylase Hdac2 from the Gata3/Chd4 repressive complex in Th2 cells. |
| 445 | 27053161 | We also identify Akt1 as a Gata3-phosphorylating kinase, and the activation of Akt1 induces derepression of Tbx21 and Ifng expression in Th2 cells. |
| 446 | 27040810 | Association of Interleukin-2, but not Interferon-Gamma, single nucleotide polymorphisms with juvenile idiopathic arthritis. |
| 447 | 27027442 | Following colonization with Helicobacter hepaticus Cd11ccreIl10rafl/fl mice developed severe large intestinal inflammation characterized by infiltrating T cells and increased levels of Il17a, Ifng, and Il12p40. |
| 448 | 26921287 | The mechanism of fibrin-mediated fibrosis was linked to interferon (IFN)γ induction of inducible nitric oxide synthase (iNOS), a gene linked to bile duct hyperplasia and liver fibrosis. |
| 449 | 26916970 | Evidence for genetic association of TBX21 and IFNG with systemic lupus erythematosus in a Chinese Han population. |
| 450 | 26916970 | Evidence for genetic association of TBX21 and IFNG with systemic lupus erythematosus in a Chinese Han population. |
| 451 | 26916970 | Evidence for genetic association of TBX21 and IFNG with systemic lupus erythematosus in a Chinese Han population. |
| 452 | 26916970 | Evidence for genetic association of TBX21 and IFNG with systemic lupus erythematosus in a Chinese Han population. |
| 453 | 26916970 | TBX21 recode T-bet which is an important transcription factor that drives the Th1 immune response primarily by promoting expression of the interferon-gamma (IFNG) gene. |
| 454 | 26916970 | TBX21 recode T-bet which is an important transcription factor that drives the Th1 immune response primarily by promoting expression of the interferon-gamma (IFNG) gene. |
| 455 | 26916970 | TBX21 recode T-bet which is an important transcription factor that drives the Th1 immune response primarily by promoting expression of the interferon-gamma (IFNG) gene. |
| 456 | 26916970 | TBX21 recode T-bet which is an important transcription factor that drives the Th1 immune response primarily by promoting expression of the interferon-gamma (IFNG) gene. |
| 457 | 26916970 | Recent studies have shown that genetic variants in TBX21 and IFNG are connected with risk of systemic lupus erythematosus (SLE). |
| 458 | 26916970 | Recent studies have shown that genetic variants in TBX21 and IFNG are connected with risk of systemic lupus erythematosus (SLE). |
| 459 | 26916970 | Recent studies have shown that genetic variants in TBX21 and IFNG are connected with risk of systemic lupus erythematosus (SLE). |
| 460 | 26916970 | Recent studies have shown that genetic variants in TBX21 and IFNG are connected with risk of systemic lupus erythematosus (SLE). |
| 461 | 26916970 | Genotyping of 3 variants (rs4794067 in TBX21, rs2069705 and rs2069718 in IFNG) was performed. |
| 462 | 26916970 | Genotyping of 3 variants (rs4794067 in TBX21, rs2069705 and rs2069718 in IFNG) was performed. |
| 463 | 26916970 | Genotyping of 3 variants (rs4794067 in TBX21, rs2069705 and rs2069718 in IFNG) was performed. |
| 464 | 26916970 | Genotyping of 3 variants (rs4794067 in TBX21, rs2069705 and rs2069718 in IFNG) was performed. |
| 465 | 26896749 | Moreover, the expression of Ifng, Il4, Il10 and Il12 mRNA levels in the draining lymph nodes of the treated mice were compared to the control mice using real-time PCR. |
| 466 | 26896749 | Moreover, the expression of Ifng, Il4, Il10 and Il12 mRNA levels in the draining lymph nodes of the treated mice were compared to the control mice using real-time PCR. |
| 467 | 26896749 | The ratio of Ifng/Il4 mRNA was also higher in Zn sulfate-treated mice compared to Glucantime-treated animals. |
| 468 | 26896749 | The ratio of Ifng/Il4 mRNA was also higher in Zn sulfate-treated mice compared to Glucantime-treated animals. |
| 469 | 26840694 | Hepatic gene expression of type III IFNs (IFNL1, IFNL3, IFNL4-ΔG) similarly decreased with treatment, while IFNA2 expression, undetectable in all subjects pretreatment, was detected post-treatment in three subjects who achieved a SVR. |
| 470 | 26840694 | Hepatic gene expression of type III IFNs (IFNL1, IFNL3, IFNL4-ΔG) similarly decreased with treatment, while IFNA2 expression, undetectable in all subjects pretreatment, was detected post-treatment in three subjects who achieved a SVR. |
| 471 | 26840694 | Other IFNs had no change in gene expression (IFNG, IFNB1, IFNA5) or could not be detected. |
| 472 | 26840694 | Other IFNs had no change in gene expression (IFNG, IFNB1, IFNA5) or could not be detected. |
| 473 | 26836235 | DNA microarray analysis showed that the expression of Ccl24, Xcl1, Ifng, and Ccl17 in the ear tissues was lower in the soy-treated mice than in the positive controls. |
| 474 | 26768126 | At the cellular level, IL-2, IFN gamma and IL-10 levels did not significantly differ using either route of vaccination and the distribution of T cell subsets was comparable along with a relative decrease of regulatory T-cells after both ways of administration. |
| 475 | 26758063 | Here, we approach this problem from an immunological perspective by examining CD19(+)CD24(hi)CD38(hi) B cells, an important participant in acute and chronic inflammation. |
| 476 | 26758063 | We find that elderly pneumonia patients have elevated CD19(+)CD24(hi)CD38(hi) B cell frequency compared to healthy individuals. |
| 477 | 26758063 | This B cell population may express a higher level of IL-10, which has been was shown to suppress CD4(+) T cell-mediated proinflammatory cytokine interferon gamma (IFNg) and tumor necrosis factor alpha (TNFa) production, through an IL-10-dependent mechanism. |
| 478 | 26758063 | We also observe that the frequency of CD19(+)CD24(hi)CD38(hi) B cell is positively correlated with the frequency of CD4(+)CD25(+)Foxp3(+)Tregs in peripheral blood. |
| 479 | 26758063 | Moreover, consistent with CD19(+)CD24(hi)CD38(hi) B cell's anti-inflammatory role, we find that pneumonia patients who later developed ALI have reduced level of CD19(+)CD24(hi)CD38(hi) B cells. |
| 480 | 26758063 | Together, our results demonstrated that CD19(+)CD24(hi)CD38(hi) B cells in pneumonia patients possess regulatory function in vivo, and are associated with a reduced ALI risk. |
| 481 | 26749212 | Eomesodermin promotes interferon-γ expression and binds to multiple conserved noncoding sequences across the Ifng locus in mouse thymoma cell lines. |
| 482 | 26749212 | Eomesodermin promotes interferon-γ expression and binds to multiple conserved noncoding sequences across the Ifng locus in mouse thymoma cell lines. |
| 483 | 26749212 | Eomesodermin promotes interferon-γ expression and binds to multiple conserved noncoding sequences across the Ifng locus in mouse thymoma cell lines. |
| 484 | 26749212 | Eomesodermin promotes interferon-γ expression and binds to multiple conserved noncoding sequences across the Ifng locus in mouse thymoma cell lines. |
| 485 | 26749212 | Eomesodermin promotes interferon-γ expression and binds to multiple conserved noncoding sequences across the Ifng locus in mouse thymoma cell lines. |
| 486 | 26749212 | The T-box transcription factors T-bet and eomesodermin (Eomes) have been shown to regulate the lineage-specific expression of interferon-γ (IFN-γ). |
| 487 | 26749212 | The T-box transcription factors T-bet and eomesodermin (Eomes) have been shown to regulate the lineage-specific expression of interferon-γ (IFN-γ). |
| 488 | 26749212 | The T-box transcription factors T-bet and eomesodermin (Eomes) have been shown to regulate the lineage-specific expression of interferon-γ (IFN-γ). |
| 489 | 26749212 | The T-box transcription factors T-bet and eomesodermin (Eomes) have been shown to regulate the lineage-specific expression of interferon-γ (IFN-γ). |
| 490 | 26749212 | The T-box transcription factors T-bet and eomesodermin (Eomes) have been shown to regulate the lineage-specific expression of interferon-γ (IFN-γ). |
| 491 | 26749212 | However, in contrast to T-bet, the role of Eomes in the expression of IFN-γ remains unclear. |
| 492 | 26749212 | However, in contrast to T-bet, the role of Eomes in the expression of IFN-γ remains unclear. |
| 493 | 26749212 | However, in contrast to T-bet, the role of Eomes in the expression of IFN-γ remains unclear. |
| 494 | 26749212 | However, in contrast to T-bet, the role of Eomes in the expression of IFN-γ remains unclear. |
| 495 | 26749212 | However, in contrast to T-bet, the role of Eomes in the expression of IFN-γ remains unclear. |
| 496 | 26749212 | In this study, we investigated the Eomes-dependent expression of IFN-γ in the mouse thymoma BW5147 and EL4 cells, which do not express T-bet or Eomes. |
| 497 | 26749212 | In this study, we investigated the Eomes-dependent expression of IFN-γ in the mouse thymoma BW5147 and EL4 cells, which do not express T-bet or Eomes. |
| 498 | 26749212 | In this study, we investigated the Eomes-dependent expression of IFN-γ in the mouse thymoma BW5147 and EL4 cells, which do not express T-bet or Eomes. |
| 499 | 26749212 | In this study, we investigated the Eomes-dependent expression of IFN-γ in the mouse thymoma BW5147 and EL4 cells, which do not express T-bet or Eomes. |
| 500 | 26749212 | In this study, we investigated the Eomes-dependent expression of IFN-γ in the mouse thymoma BW5147 and EL4 cells, which do not express T-bet or Eomes. |
| 501 | 26749212 | In BW5147 cells, Eomes augmented luciferase activity driven by the Ifng promoter encoding from -2500 to +113 bp; however, it was not increased by a stimulation with PMA and IM. |
| 502 | 26749212 | In BW5147 cells, Eomes augmented luciferase activity driven by the Ifng promoter encoding from -2500 to +113 bp; however, it was not increased by a stimulation with PMA and IM. |
| 503 | 26749212 | In BW5147 cells, Eomes augmented luciferase activity driven by the Ifng promoter encoding from -2500 to +113 bp; however, it was not increased by a stimulation with PMA and IM. |
| 504 | 26749212 | In BW5147 cells, Eomes augmented luciferase activity driven by the Ifng promoter encoding from -2500 to +113 bp; however, it was not increased by a stimulation with PMA and IM. |
| 505 | 26749212 | In BW5147 cells, Eomes augmented luciferase activity driven by the Ifng promoter encoding from -2500 to +113 bp; however, it was not increased by a stimulation with PMA and IM. |
| 506 | 26749212 | A chromatin immunoprecipitation assay showed that Eomes bound to the Ifng promoter and conserved noncoding sequence (CNS) -22 kb across the Ifng locus with high efficacy in BW5147 cells. |
| 507 | 26749212 | A chromatin immunoprecipitation assay showed that Eomes bound to the Ifng promoter and conserved noncoding sequence (CNS) -22 kb across the Ifng locus with high efficacy in BW5147 cells. |
| 508 | 26749212 | A chromatin immunoprecipitation assay showed that Eomes bound to the Ifng promoter and conserved noncoding sequence (CNS) -22 kb across the Ifng locus with high efficacy in BW5147 cells. |
| 509 | 26749212 | A chromatin immunoprecipitation assay showed that Eomes bound to the Ifng promoter and conserved noncoding sequence (CNS) -22 kb across the Ifng locus with high efficacy in BW5147 cells. |
| 510 | 26749212 | A chromatin immunoprecipitation assay showed that Eomes bound to the Ifng promoter and conserved noncoding sequence (CNS) -22 kb across the Ifng locus with high efficacy in BW5147 cells. |
| 511 | 26749212 | Moreover, Eomes increased permissive histone modifications in the Ifng promoter and multiple CNSs. |
| 512 | 26749212 | Moreover, Eomes increased permissive histone modifications in the Ifng promoter and multiple CNSs. |
| 513 | 26749212 | Moreover, Eomes increased permissive histone modifications in the Ifng promoter and multiple CNSs. |
| 514 | 26749212 | Moreover, Eomes increased permissive histone modifications in the Ifng promoter and multiple CNSs. |
| 515 | 26749212 | Moreover, Eomes increased permissive histone modifications in the Ifng promoter and multiple CNSs. |
| 516 | 26749212 | These results indicated that Eomes bound to the Ifng promoter and multiple CNSs in stimulation-dependent and stimulation-independent manners. |
| 517 | 26749212 | These results indicated that Eomes bound to the Ifng promoter and multiple CNSs in stimulation-dependent and stimulation-independent manners. |
| 518 | 26749212 | These results indicated that Eomes bound to the Ifng promoter and multiple CNSs in stimulation-dependent and stimulation-independent manners. |
| 519 | 26749212 | These results indicated that Eomes bound to the Ifng promoter and multiple CNSs in stimulation-dependent and stimulation-independent manners. |
| 520 | 26749212 | These results indicated that Eomes bound to the Ifng promoter and multiple CNSs in stimulation-dependent and stimulation-independent manners. |
| 521 | 26748724 | Liver fibrosis was induced in Socs1(-/-)Ifng(-/-) mice with dimethylnitrosamine or carbon tetrachloride. |
| 522 | 26748724 | Liver fibrosis was induced in Socs1(-/-)Ifng(-/-) mice with dimethylnitrosamine or carbon tetrachloride. |
| 523 | 26748724 | Following fibrogenic treatments, Socs1(-/-)Ifng(-/-) mice showed elevated serum ALT levels and increased liver fibrosis compared to Ifng(-/-) mice. |
| 524 | 26748724 | Following fibrogenic treatments, Socs1(-/-)Ifng(-/-) mice showed elevated serum ALT levels and increased liver fibrosis compared to Ifng(-/-) mice. |
| 525 | 26748724 | The livers of SOCS1-deficient mice showed bridging fibrosis, which was associated with increased accumulation of myofibroblasts and abundant collagen deposition. |
| 526 | 26748724 | The livers of SOCS1-deficient mice showed bridging fibrosis, which was associated with increased accumulation of myofibroblasts and abundant collagen deposition. |
| 527 | 26748724 | SOCS1-deficient livers showed increased expression of genes coding for smooth muscle actin, collagen, and enzymes involved in remodeling the extracellular matrix, namely matrix metalloproteinases and tissue inhibitor of metalloproteinases. |
| 528 | 26748724 | SOCS1-deficient livers showed increased expression of genes coding for smooth muscle actin, collagen, and enzymes involved in remodeling the extracellular matrix, namely matrix metalloproteinases and tissue inhibitor of metalloproteinases. |
| 529 | 26748724 | Primary HSCs from SOCS1-deficient mice showed increased proliferation in response to growth factors such as HGF, EGF and PDGF, and the fibrotic livers of SOCS1-deficient mice showed increased expression of the Pdgfb gene. |
| 530 | 26748724 | Primary HSCs from SOCS1-deficient mice showed increased proliferation in response to growth factors such as HGF, EGF and PDGF, and the fibrotic livers of SOCS1-deficient mice showed increased expression of the Pdgfb gene. |
| 531 | 26723120 | The H-AMIR cows produced more IL-4 protein than H-CMIR cows at 48 h; however, no difference in gene expression of type-2 transcription factor GATA3 or IL4 was noted. |
| 532 | 26723120 | Further, H-CMIR cows had increased expression of the IFNG gene at 16, 24, and 48 h post-treatment with ConA, although expression of the type-1 transcription factor gene TBX21 did not differ between immune response groups. |
| 533 | 26697438 | Compared to mock-inoculated PBMCs, WNV-stimulated PBMCs expressed high levels of interferon (IFN) alpha (IFNA), gamma (IFNG), IL6, IL12, IL22, CXCL10, and pentraxin 3 (PTX3) mRNA. |
| 534 | 26697438 | Compared to mock-inoculated PBMCs, WNV-stimulated PBMCs expressed high levels of interferon (IFN) alpha (IFNA), gamma (IFNG), IL6, IL12, IL22, CXCL10, and pentraxin 3 (PTX3) mRNA. |
| 535 | 26697438 | Compared to mock-inoculated PBMCs, WNV-stimulated PBMCs expressed high levels of interferon (IFN) alpha (IFNA), gamma (IFNG), IL6, IL12, IL22, CXCL10, and pentraxin 3 (PTX3) mRNA. |
| 536 | 26697438 | TLRs-signaling downstream genes (MyD88, STAT1, TRAF3, IRF7, and IRF9) subsequently became up-regulated. |
| 537 | 26697438 | TLRs-signaling downstream genes (MyD88, STAT1, TRAF3, IRF7, and IRF9) subsequently became up-regulated. |
| 538 | 26697438 | TLRs-signaling downstream genes (MyD88, STAT1, TRAF3, IRF7, and IRF9) subsequently became up-regulated. |
| 539 | 26697438 | The high expression of IFNs, TLR3, TLR4, TRAF3, STAT1, IRF7, and IRF9 are in accordance with antiviral activities, while expression of TNFA, HO1, iNOS, caspase 3, and caspase 9 transcripts suggests the involvement of oxidative stress and apoptosis in WNV-stimulated rabbit PBMCs, respectively. |
| 540 | 26697438 | The high expression of IFNs, TLR3, TLR4, TRAF3, STAT1, IRF7, and IRF9 are in accordance with antiviral activities, while expression of TNFA, HO1, iNOS, caspase 3, and caspase 9 transcripts suggests the involvement of oxidative stress and apoptosis in WNV-stimulated rabbit PBMCs, respectively. |
| 541 | 26697438 | The high expression of IFNs, TLR3, TLR4, TRAF3, STAT1, IRF7, and IRF9 are in accordance with antiviral activities, while expression of TNFA, HO1, iNOS, caspase 3, and caspase 9 transcripts suggests the involvement of oxidative stress and apoptosis in WNV-stimulated rabbit PBMCs, respectively. |
| 542 | 26697438 | Higher expression of IFNA, IFN beta (IFNB), IFNG, TNFA, IL6, IL22, PTX3, TLR3 and TLR4, IRF7, IRF9, STST1, TRAF3, caspase 3, and caspase 9 were seen in PBMCs from WNV-infected rabbits on day 3 post-intradermal virus inoculation compared to PBMCs from uninfected control rabbits. |
| 543 | 26697438 | Higher expression of IFNA, IFN beta (IFNB), IFNG, TNFA, IL6, IL22, PTX3, TLR3 and TLR4, IRF7, IRF9, STST1, TRAF3, caspase 3, and caspase 9 were seen in PBMCs from WNV-infected rabbits on day 3 post-intradermal virus inoculation compared to PBMCs from uninfected control rabbits. |
| 544 | 26697438 | Higher expression of IFNA, IFN beta (IFNB), IFNG, TNFA, IL6, IL22, PTX3, TLR3 and TLR4, IRF7, IRF9, STST1, TRAF3, caspase 3, and caspase 9 were seen in PBMCs from WNV-infected rabbits on day 3 post-intradermal virus inoculation compared to PBMCs from uninfected control rabbits. |
| 545 | 26690514 | Expression of EGR1/2/3, IL8, CXCL1, PTGS2, CD69, IFNG, FASLG, CCL4, CDC42, DDX58, NFKBID and NR4A2 genes were independently validated; EGR1/2/3 and IL8 showed >8-fold higher expression in cases relative to the controls implying their important role in CAD. |
| 546 | 26658491 | IFNG and IL2 mRNA production was assayed by FISH-Flow. |
| 547 | 26658491 | IFNG and IL2 mRNA production was assayed by FISH-Flow. |
| 548 | 26658491 | An association was found between donor LTBI status and antigen-specific induction of IFNG and IL2 transcripts. |
| 549 | 26658491 | An association was found between donor LTBI status and antigen-specific induction of IFNG and IL2 transcripts. |
| 550 | 26646149 | IFN-γ and IL-21 Double Producing T Cells Are Bcl6-Independent and Survive into the Memory Phase in Plasmodium chabaudi Infection. |
| 551 | 26646149 | IFN-γ and IL-21 Double Producing T Cells Are Bcl6-Independent and Survive into the Memory Phase in Plasmodium chabaudi Infection. |
| 552 | 26646149 | IFN-γ and IL-21 Double Producing T Cells Are Bcl6-Independent and Survive into the Memory Phase in Plasmodium chabaudi Infection. |
| 553 | 26646149 | IFN-γ and IL-21 Double Producing T Cells Are Bcl6-Independent and Survive into the Memory Phase in Plasmodium chabaudi Infection. |
| 554 | 26646149 | In Plasmodium chabaudi infection, one specific CD4 T cell subset generates anti-parasitic IFN-γ and the antibody-promoting cytokine, IL-21. |
| 555 | 26646149 | In Plasmodium chabaudi infection, one specific CD4 T cell subset generates anti-parasitic IFN-γ and the antibody-promoting cytokine, IL-21. |
| 556 | 26646149 | In Plasmodium chabaudi infection, one specific CD4 T cell subset generates anti-parasitic IFN-γ and the antibody-promoting cytokine, IL-21. |
| 557 | 26646149 | In Plasmodium chabaudi infection, one specific CD4 T cell subset generates anti-parasitic IFN-γ and the antibody-promoting cytokine, IL-21. |
| 558 | 26646149 | While Ifng+ Teff expanded, the level of the Th1 lineage-determining transcription factor T-bet only peaked briefly. |
| 559 | 26646149 | While Ifng+ Teff expanded, the level of the Th1 lineage-determining transcription factor T-bet only peaked briefly. |
| 560 | 26646149 | While Ifng+ Teff expanded, the level of the Th1 lineage-determining transcription factor T-bet only peaked briefly. |
| 561 | 26646149 | While Ifng+ Teff expanded, the level of the Th1 lineage-determining transcription factor T-bet only peaked briefly. |
| 562 | 26646149 | Ifng+ Teff also co-express ICOS, the B cell area homing molecule CXCR5, and other Tfh lineage-associated molecules including Bcl6, the transcription factor required for germinal center (GC) T follicular helper cells (Tfh) differentiation. |
| 563 | 26646149 | Ifng+ Teff also co-express ICOS, the B cell area homing molecule CXCR5, and other Tfh lineage-associated molecules including Bcl6, the transcription factor required for germinal center (GC) T follicular helper cells (Tfh) differentiation. |
| 564 | 26646149 | Ifng+ Teff also co-express ICOS, the B cell area homing molecule CXCR5, and other Tfh lineage-associated molecules including Bcl6, the transcription factor required for germinal center (GC) T follicular helper cells (Tfh) differentiation. |
| 565 | 26646149 | Ifng+ Teff also co-express ICOS, the B cell area homing molecule CXCR5, and other Tfh lineage-associated molecules including Bcl6, the transcription factor required for germinal center (GC) T follicular helper cells (Tfh) differentiation. |
| 566 | 26646149 | Because Bcl6 and T-bet co-localize to the nucleus of Ifng+ Teff, we hypothesized that Bcl6 controls the Tfh-like phenotype of Ifng+ Teff cells in P. chabaudi infection. |
| 567 | 26646149 | Because Bcl6 and T-bet co-localize to the nucleus of Ifng+ Teff, we hypothesized that Bcl6 controls the Tfh-like phenotype of Ifng+ Teff cells in P. chabaudi infection. |
| 568 | 26646149 | Because Bcl6 and T-bet co-localize to the nucleus of Ifng+ Teff, we hypothesized that Bcl6 controls the Tfh-like phenotype of Ifng+ Teff cells in P. chabaudi infection. |
| 569 | 26646149 | Because Bcl6 and T-bet co-localize to the nucleus of Ifng+ Teff, we hypothesized that Bcl6 controls the Tfh-like phenotype of Ifng+ Teff cells in P. chabaudi infection. |
| 570 | 26646149 | Bcl6-deficient T cells did not develop into GC Tfh, but they still generated CXCR5+ IFN-γ+ IL-21+ IL-10+ Teff, suggesting that this predominant population is not of the Tfh-lineage. |
| 571 | 26646149 | Bcl6-deficient T cells did not develop into GC Tfh, but they still generated CXCR5+ IFN-γ+ IL-21+ IL-10+ Teff, suggesting that this predominant population is not of the Tfh-lineage. |
| 572 | 26646149 | Bcl6-deficient T cells did not develop into GC Tfh, but they still generated CXCR5+ IFN-γ+ IL-21+ IL-10+ Teff, suggesting that this predominant population is not of the Tfh-lineage. |
| 573 | 26646149 | Bcl6-deficient T cells did not develop into GC Tfh, but they still generated CXCR5+ IFN-γ+ IL-21+ IL-10+ Teff, suggesting that this predominant population is not of the Tfh-lineage. |
| 574 | 26646149 | IL-10 deficient mice, which have increased IFN-γ and T-bet expression, demonstrated expansion of both IFN-γ+ IL-21+ CXCR5+ cells and IFN-γ+ GC Tfh cells, suggesting a Th1 lineage for the former. |
| 575 | 26646149 | IL-10 deficient mice, which have increased IFN-γ and T-bet expression, demonstrated expansion of both IFN-γ+ IL-21+ CXCR5+ cells and IFN-γ+ GC Tfh cells, suggesting a Th1 lineage for the former. |
| 576 | 26646149 | IL-10 deficient mice, which have increased IFN-γ and T-bet expression, demonstrated expansion of both IFN-γ+ IL-21+ CXCR5+ cells and IFN-γ+ GC Tfh cells, suggesting a Th1 lineage for the former. |
| 577 | 26646149 | IL-10 deficient mice, which have increased IFN-γ and T-bet expression, demonstrated expansion of both IFN-γ+ IL-21+ CXCR5+ cells and IFN-γ+ GC Tfh cells, suggesting a Th1 lineage for the former. |
| 578 | 26646149 | In the memory phase, all Ifng+ T cells produced IL-21, but only a small percentage of highly proliferative Ifng+ T cells maintained a T-bethi phenotype. |
| 579 | 26646149 | In the memory phase, all Ifng+ T cells produced IL-21, but only a small percentage of highly proliferative Ifng+ T cells maintained a T-bethi phenotype. |
| 580 | 26646149 | In the memory phase, all Ifng+ T cells produced IL-21, but only a small percentage of highly proliferative Ifng+ T cells maintained a T-bethi phenotype. |
| 581 | 26646149 | In the memory phase, all Ifng+ T cells produced IL-21, but only a small percentage of highly proliferative Ifng+ T cells maintained a T-bethi phenotype. |
| 582 | 26634912 | The proportion of circulating Th1 cells and the level of T-bet, IFNG mRNA were increased in HT patients, the expression of IFNG-AS1 was upregulated and positively correlated with the proportion of circulating Th1 cells or T-bet, and IFNG expression, or serum level of anti-thyroglobulin antibody/thyroperoxidase antibody in HT patients. |
| 583 | 26634912 | The proportion of circulating Th1 cells and the level of T-bet, IFNG mRNA were increased in HT patients, the expression of IFNG-AS1 was upregulated and positively correlated with the proportion of circulating Th1 cells or T-bet, and IFNG expression, or serum level of anti-thyroglobulin antibody/thyroperoxidase antibody in HT patients. |
| 584 | 26634912 | The proportion of circulating Th1 cells and the level of T-bet, IFNG mRNA were increased in HT patients, the expression of IFNG-AS1 was upregulated and positively correlated with the proportion of circulating Th1 cells or T-bet, and IFNG expression, or serum level of anti-thyroglobulin antibody/thyroperoxidase antibody in HT patients. |
| 585 | 26634912 | IFNG-AS1 regulated the expression of IFNG at both transcriptional and translational level in human CD4(+) T cells. |
| 586 | 26634912 | IFNG-AS1 regulated the expression of IFNG at both transcriptional and translational level in human CD4(+) T cells. |
| 587 | 26634912 | IFNG-AS1 regulated the expression of IFNG at both transcriptional and translational level in human CD4(+) T cells. |
| 588 | 26634912 | Furthermore, strong positive correlations between the increased transcript level of IFNG-AS1 and the increased transcript level of T-bet or IFNG were revealed in thyroid tissues from HT patients. |
| 589 | 26634912 | Furthermore, strong positive correlations between the increased transcript level of IFNG-AS1 and the increased transcript level of T-bet or IFNG were revealed in thyroid tissues from HT patients. |
| 590 | 26634912 | Furthermore, strong positive correlations between the increased transcript level of IFNG-AS1 and the increased transcript level of T-bet or IFNG were revealed in thyroid tissues from HT patients. |
| 591 | 26632437 | Mice with EAE exhibited an increased frequency of Th1 cells in the spleen, with concomitant increases in the mRNA levels of Tbet and Ifng and increased IFN-γ production by activated splenocytes; the frequency of Treg cells, as well as mRNA levels of Foxp3 and Tgfb, was reduced, as was TGF-β production by activated splenocytes. |
| 592 | 26625258 | In the complete response (CR) cases, 999 overexpressed genes including at least 234 tumor-specific CTL-activation associated genes such as IFNG, PRF1, and GZMB, were found in post-treatment biopsy specimens. |
| 593 | 26625258 | Furthermore, NK cells, which were activated by neutrophils-producing S100A8/S100A9, and CTLs were suggested to cooperatively enhance the effect of CRT in the CDH2-negative I-type. |
| 594 | 26621862 | In this study, we examined the roles of inflammatory cytokines such as IFN-γ, IL-17A, and type I IFNs to understand the mechanism underlying the phenotype in D34A mice. mRNAs for IFN-γ and IL-I7A in CD4(+) T cells increased, but inflammatory phenotype manifesting as thrombocytopenia and splenomegaly was still observed in Ifng(-/-) or Il17a(-/-) D34A mice. |
| 595 | 26601495 | The variability of potentially important functional polymorphic variants rs2069705 (5'UTR of the IFNG gene), rs17880053 (near 5'UTR of the IFNGR2), rs11126176 (LOC100287361 pseudogene), and rs804271 (near 5'UTR of the NEIL2 gene) was characterized in representatives of four ethnic groups living in the Siberian region. |
| 596 | 26589234 | Evidence for Epigenetic Regulation of Pro-Inflammatory Cytokines, Interleukin-12 and Interferon Gamma, in Peripheral Blood Mononuclear Cells from PTSD Patients. |
| 597 | 26589234 | Evidence for Epigenetic Regulation of Pro-Inflammatory Cytokines, Interleukin-12 and Interferon Gamma, in Peripheral Blood Mononuclear Cells from PTSD Patients. |
| 598 | 26589234 | Evidence for Epigenetic Regulation of Pro-Inflammatory Cytokines, Interleukin-12 and Interferon Gamma, in Peripheral Blood Mononuclear Cells from PTSD Patients. |
| 599 | 26589234 | Evidence for Epigenetic Regulation of Pro-Inflammatory Cytokines, Interleukin-12 and Interferon Gamma, in Peripheral Blood Mononuclear Cells from PTSD Patients. |
| 600 | 26589234 | Evidence for Epigenetic Regulation of Pro-Inflammatory Cytokines, Interleukin-12 and Interferon Gamma, in Peripheral Blood Mononuclear Cells from PTSD Patients. |
| 601 | 26589234 | While overall DNA methylation level did not differ significantly between control and PTSD, the promoters of several individual genes (e.g., Interferon gamma (IFNG) and Interleukin (IL)-12B) were differentially methylated. |
| 602 | 26589234 | While overall DNA methylation level did not differ significantly between control and PTSD, the promoters of several individual genes (e.g., Interferon gamma (IFNG) and Interleukin (IL)-12B) were differentially methylated. |
| 603 | 26589234 | While overall DNA methylation level did not differ significantly between control and PTSD, the promoters of several individual genes (e.g., Interferon gamma (IFNG) and Interleukin (IL)-12B) were differentially methylated. |
| 604 | 26589234 | While overall DNA methylation level did not differ significantly between control and PTSD, the promoters of several individual genes (e.g., Interferon gamma (IFNG) and Interleukin (IL)-12B) were differentially methylated. |
| 605 | 26589234 | While overall DNA methylation level did not differ significantly between control and PTSD, the promoters of several individual genes (e.g., Interferon gamma (IFNG) and Interleukin (IL)-12B) were differentially methylated. |
| 606 | 26589234 | ChIP-seq data revealed that the promoter of IFNG and TBX-21 was associated with the activation marker H3K4me3 in PTSD. |
| 607 | 26589234 | ChIP-seq data revealed that the promoter of IFNG and TBX-21 was associated with the activation marker H3K4me3 in PTSD. |
| 608 | 26589234 | ChIP-seq data revealed that the promoter of IFNG and TBX-21 was associated with the activation marker H3K4me3 in PTSD. |
| 609 | 26589234 | ChIP-seq data revealed that the promoter of IFNG and TBX-21 was associated with the activation marker H3K4me3 in PTSD. |
| 610 | 26589234 | ChIP-seq data revealed that the promoter of IFNG and TBX-21 was associated with the activation marker H3K4me3 in PTSD. |
| 611 | 26589234 | The transcript levels of both IFNG and TBX-21 were higher in PTSD correlating well with the altered methylation patterns. |
| 612 | 26589234 | The transcript levels of both IFNG and TBX-21 were higher in PTSD correlating well with the altered methylation patterns. |
| 613 | 26589234 | The transcript levels of both IFNG and TBX-21 were higher in PTSD correlating well with the altered methylation patterns. |
| 614 | 26589234 | The transcript levels of both IFNG and TBX-21 were higher in PTSD correlating well with the altered methylation patterns. |
| 615 | 26589234 | The transcript levels of both IFNG and TBX-21 were higher in PTSD correlating well with the altered methylation patterns. |
| 616 | 26589234 | Knockdown of lysine (K)-specific demethylase 5B (KDM5B), or inhibition of DNA (Cytosine-5-)-methyltransferase 1 (DNMT1) caused up-regulation of IL-12. |
| 617 | 26589234 | Knockdown of lysine (K)-specific demethylase 5B (KDM5B), or inhibition of DNA (Cytosine-5-)-methyltransferase 1 (DNMT1) caused up-regulation of IL-12. |
| 618 | 26589234 | Knockdown of lysine (K)-specific demethylase 5B (KDM5B), or inhibition of DNA (Cytosine-5-)-methyltransferase 1 (DNMT1) caused up-regulation of IL-12. |
| 619 | 26589234 | Knockdown of lysine (K)-specific demethylase 5B (KDM5B), or inhibition of DNA (Cytosine-5-)-methyltransferase 1 (DNMT1) caused up-regulation of IL-12. |
| 620 | 26589234 | Knockdown of lysine (K)-specific demethylase 5B (KDM5B), or inhibition of DNA (Cytosine-5-)-methyltransferase 1 (DNMT1) caused up-regulation of IL-12. |
| 621 | 26589234 | Our miRNA microarray identified many downregulated miRNAs in PTSD that are predicted to target IFNG and IL-12. |
| 622 | 26589234 | Our miRNA microarray identified many downregulated miRNAs in PTSD that are predicted to target IFNG and IL-12. |
| 623 | 26589234 | Our miRNA microarray identified many downregulated miRNAs in PTSD that are predicted to target IFNG and IL-12. |
| 624 | 26589234 | Our miRNA microarray identified many downregulated miRNAs in PTSD that are predicted to target IFNG and IL-12. |
| 625 | 26589234 | Our miRNA microarray identified many downregulated miRNAs in PTSD that are predicted to target IFNG and IL-12. |
| 626 | 26589234 | Consequently, we showed that up-regulation of hsa-miR-193a-5p could decrease the expression of IL-12. |
| 627 | 26589234 | Consequently, we showed that up-regulation of hsa-miR-193a-5p could decrease the expression of IL-12. |
| 628 | 26589234 | Consequently, we showed that up-regulation of hsa-miR-193a-5p could decrease the expression of IL-12. |
| 629 | 26589234 | Consequently, we showed that up-regulation of hsa-miR-193a-5p could decrease the expression of IL-12. |
| 630 | 26589234 | Consequently, we showed that up-regulation of hsa-miR-193a-5p could decrease the expression of IL-12. |
| 631 | 26580078 | Exposure of M.tb-infected MDM to AgNP suppressed M.tb-induced expression of IL1B, IL10, and TNFA mRNA. |
| 632 | 26580078 | AgNP exposure suppressed M.tb-induced expression of a subset of NF-κB mediated genes (CSF2, CSF3, IFNG, IL1A, IL1B, IL6, IL10, TNFA, NFKB1A). |
| 633 | 26559095 | Many genes involved in tuberculosis susceptibility (e.g., NRAMP1 (SLC11A1), IFNG, NOS2A, VDR, ISG15, TACO, TLR1, TLR, IL18R1, chemokines, PADI, DUSP14, MBL, and MASP-2) have been subjected to epigenetic modification. |
| 634 | 26546406 | Earlier, in our immunoproteomic analysis, we found that peptidyl-prolyl cis-trans isomerase A (PpiA) protein-containing fractions induced significantly higher interferon-gamma (IFN-γ) response in LTBI than in PTB. |
| 635 | 26491197 | In this study, we found that PPARα functions within CD4(+) and CD8(+) T lymphocytes and NKT cells to negatively regulate IFN-γ responses in male mice and identified Ifng as the gene target of PPARα repression. |
| 636 | 26491197 | In this study, we found that PPARα functions within CD4(+) and CD8(+) T lymphocytes and NKT cells to negatively regulate IFN-γ responses in male mice and identified Ifng as the gene target of PPARα repression. |
| 637 | 26491197 | Treatment of male CD4(+) T cells with the PPARα agonist fenofibrate induced the recruitment of PPARα and the nuclear receptor-interacting protein, nuclear receptor corepressor 1, to specific cis-regulatory elements in the Ifng locus. |
| 638 | 26491197 | Treatment of male CD4(+) T cells with the PPARα agonist fenofibrate induced the recruitment of PPARα and the nuclear receptor-interacting protein, nuclear receptor corepressor 1, to specific cis-regulatory elements in the Ifng locus. |
| 639 | 26491197 | Finally, we investigated the effects of IS001 on IFN-γ responses in mice during infection with the Th1-associated pathogen Listeria monocytogenes and observed that IS001 enhanced IFN-γ production by NKT, CD4(+), and CD8(+) T cells and improved the survival of male, but not female, mice. |
| 640 | 26491197 | Finally, we investigated the effects of IS001 on IFN-γ responses in mice during infection with the Th1-associated pathogen Listeria monocytogenes and observed that IS001 enhanced IFN-γ production by NKT, CD4(+), and CD8(+) T cells and improved the survival of male, but not female, mice. |
| 641 | 26481684 | Oct1 and OCA-B are selectively required for CD4 memory T cell function. |
| 642 | 26481684 | ChIPseq identifies ∼50 differentially expressed direct Oct1 and OCA-B targets. |
| 643 | 26481684 | We identify an underlying mechanism involving OCA-B recruitment of the histone lysine demethylase Jmjd1a to targets such as Il2, Ifng, and Zbtb32. |
| 644 | 26481684 | The findings pinpoint Oct1 and OCA-B as central mediators of CD4(+) T cell memory. |
| 645 | 26473437 | The following genes have been studied in populations of trauma patients: CD14, HMGB1, IFNG, IL1A, IL1B, IL1RN, IL4, IL6, IL8, IL10, IL17F, IL18, MBL2, MASP2, FCN2, TLR1, TLR2, TLR4, TLR9, TNF, LTA, GR, MYLK, NLRP3, PRDX6, RAGE, HSPA1B, HSPA1L, HSP90, SERPINE1, IRAK1, IRAK3, VEGFA, LY96, ANGPT2, LBP, MicroRNA, and mtDNA. |
| 646 | 26373652 | Erratum to: Pathogenesis of intracranial aneurysm is mediated by proinflammatory cytokine TNFA and IFNG and through stochastic regulation of IL10 and TGFB1 by comorbid factors. |
| 647 | 26373614 | Twelve inflammatory factors [interleukin (IL)-2, IL-4, IL-6, IL-8, IL-10, vascular endothelial growth factor, interferon-gamma (IFN-γ), tumour necrosis factor-alpha, IL-1α, IL-1β, monocyte chemoattractant protein-1 (MCP-1), epidermal growth factor (EGF)] were analysed from serum samples. |
| 648 | 26373614 | The stepwise regression analysis showed that IFN-γ explained 27·5%, and IFN-γ and IL-6 together explained 39·8% of the variability of FFM, while IFN-γ explained 21·1%, and IFN-γ together with EGF explained 36·6% of the variability of muscle mass in male rowers. |
| 649 | 26373614 | Serum IL-8 (r = -0·65) and VEGF (r = -0·48) correlated (P<0·05) with VO2 max kg-1 . |
| 650 | 26300430 | Using data integration of genome-wide TF binding profiles, we defined regions with combinatorial binding of lineage-specific master TFs (T-BET, GATA3, and ROR-γt) and STATs (STAT1 and STAT4, STAT6, and STAT3) in murine T helper (Th) 1, Th2, and Th17 cells, respectively. |
| 651 | 26300430 | Genes associated with super-enhancers, including relevant Th-cell genes (such as Ifng in Th1, Il13 in Th2, and Il17a in Th17 cells), showed strong transcriptional activity. |
| 652 | 26278786 | We herein report that pro-inflammatory cytokines, IFNG and TNFA, synergistically activated transcription of RNF213 both in vitro and in vivo. |
| 653 | 26278786 | Using various chemical inhibitors, we found that AKT and PKR pathways contributed to the transcriptional activation of RNF213. |
| 654 | 26278786 | Chemical inhibitors for AKT (LY294002) and PKR (C16) disrupted their angiogenic potentials, suggesting that RNF213 and its upstream pathways cooperatively organize the process of angiogenesis. |
| 655 | 26268241 | We performed targeted resequencing on 92 cases of PTCL and identified frequent mutations affecting RHOA, TET2, DNMT3A, and isocitrate dehydrogenase 2 (IDH2). |
| 656 | 26268241 | Strikingly, AITL cases with IDH2(R172) mutations demonstrated a distinct gene expression signature characterized by downregulation of genes associated with TH1 differentiation (eg, STAT1 and IFNG) and a striking enrichment of an interleukin 12-induced gene signature. |
| 657 | 26268241 | Ectopic expression of IDH2(R172K) in the Jurkat cell line and CD4(+) T cells led to markedly increased levels of 2-hydroxyglutarate, histone-3 lysine methylation, and 5-methylcytosine and a decrease of 5-hydroxymethylcytosine. |
| 658 | 26261529 | Association between PD-1/PD-L1 and T regulate cells in early recurrent miscarriage. |
| 659 | 26261529 | In this study, we try to testify the relationship between the programmed cell death receptor-1 (PD-1)/programmed cell death ligand 1 (PD-L1) passway and Treg cells in maternal-fetal immune regulation through PD-1 blockade on lymphocytes of normal early pregnancy in vitro and investigation of the PD-1 and PD-L1 changes in early recurrent miscarriage patients. |
| 660 | 26261529 | CD4+ CD25+ Treg cells and PD-1 (CD279) positive cell were detected in deciduas in early recurrent miscarriage patients by flow cytometry. |
| 661 | 26261529 | Meanwhile the mRNA level of PD-1 and molecular expression of PD-L1 in deciduas of early recurrent miscarriage patients were detected by real time RT-PCR test and Immunohistochemical staining respectively. |
| 662 | 26261529 | Also through antibody blocking assay to block PD-1 on lymphocytes of normal early pregnancy in vitro further testify the relationship between PD-1/PD-L1 and Treg cells, the results were analyzed by flow cytometry. |
| 663 | 26261529 | CD4+ CD25+ Treg cells decreased both in deciduas in RM (P < 0.05), and for all almost 100% Treg cells (CD4+ CD25+) expressed PD-1, but there was no difference between the PD-1 positive cells in decidual lymphocytes in RM and that in normal pregnancy women (P > 0.05). |
| 664 | 26261529 | PD-L1 mRNA in deciduas decreased in RM (P < 0.001), but PD-1 mRNA no difference (P > 0.1). |
| 665 | 26261529 | After PD-1 blockade there was no change in CD4+ CD25+ Treg cells percentage, while the CD4+ T cell percentage increased (P < 0.01), as well as the level of IFN-gamma in cells supernatant (P < 0.01). |
| 666 | 26261529 | PD-1 blockade has a little influence on the number of Treg cells, and may lead to impaired Treg cells function, the decrease of PD-L1 may closely relates to the occurrence of early recurrent miscarriage and implies that Treg cells may through PD-1/PD-L1 pathway play a role of immunosuppression regulation, and the impairment of Treg cells function in recurrent early abortion cases may be due to PD-L1 decrease in deciduas or trophoblast cells rather than PD-1 change. |
| 667 | 26261240 | V75M, one of many disease-causing mutations occurring in SUMO*motif (72-ψψψψKDxxxxSY-83) of WASp, compromises WASp-SUMOylation, associates with COMMD1 to attenuate NF-κB signaling, and recruits histone deacetylases-6 (HDAC6) to p300-marked promoters of NF-κB response genes that pattern immunity but not inflammation. |
| 668 | 26261240 | Consequently, proteins mediating adaptive immunity (IFNG, STAT1, TLR1) are deficient, whereas those mediating auto-inflammation (GM-CSF, TNFAIP2, IL-1β) are paradoxically increased in TH1 cells expressing SUMOylation-deficient WASp. |
| 669 | 26261240 | Moreover, SUMOylation-deficient WASp favors ectopic development of the TH17-like phenotype (↑IL17A, IL21, IL22, IL23R, RORC, and CSF2) under TH1-skewing conditions, suggesting a role for WASp in modulating TH1/TH17 plasticity. |
| 670 | 26253701 | CD3+ICOS+ T cells show differences in the synthesis of nitric oxide, IFN-γ, and IL-10 in patients with pulmonary tuberculosis or in healthy household contacts. |
| 671 | 26253701 | Moreover, T cells synthesise nitric oxide (NO), interferon gamma (IFN-γ), and interleukin (IL)-10, which help regulate the immune response to tuberculosis. |
| 672 | 26253701 | Therefore, we assessed the synthesis of NO, IFN-γ, and IL-10 in CD3+ICOS+ T cells from healthy individuals, household contacts (HHC), and patients with active pulmonary tuberculosis (PTB), previously stimulated with the antigen H37Rv. |
| 673 | 26253701 | Our results indicated a significant increase in both the percentage of ICOS+ cells and CD3+ICOS+ T cells producing NO, IFN-γ, and IL-10 in cells obtained from patients with PTB (p < 0.01). |
| 674 | 26253701 | In conclusion, results show that the CD3+ICOS+ T cells obtained from PTB patients are the main producers of NO, IFN-γ, and IL-10. |
| 675 | 26242990 | Genetic variants were identified by sequencing the promoter regions and all exons of IFNG, IFNGR1, IFNGR2, IRF1, IL12A, IL12B, IL12RB1, IL12RB2, IL23A, IL23R, IL27, EBI3, IL27RA, IL6ST, SOCS1, STAT1, STAT4, JAK2, TYK2 and TBX21 in 69 DNA samples from Ghana. |
| 676 | 26237955 | [Agonists of µ- and δ-Opioid Receptors in the Regulation of IL-2, IL-4 and IFN-γ Production by Peripheral Blood Cells in vitro]. |
| 677 | 26237955 | It was found that β-endorphin stimulates the PHA (phytohemagglutinin)-induced production of interleukin-4 and has no affect on the production of interferon-gamma in unfractionated leukocytic suspension. |
| 678 | 26237955 | In the culture of purified CD4+ T cells, β-endorphin does not affect the concentration of IL-2, IL-4, and IFN-γ, but stimulates the production of IL-4 and inhibits the production of IFN-γ when adding monocytes to the culture. |
| 679 | 26237955 | Selective δ-agonist DADLE enhances the PHA-induced production of IL-4 in unfractionated leukocytic suspension and in CD4+ lymphocytes+monocytes system. |
| 680 | 26224007 | Here, we show that Il10 null mutant (Il10(-/-)) mice exhibit altered local T cell responses in pregnancy, exhibiting pronounced hyperplasia in para-aortic lymph nodes draining the uterus with >6-fold increased CD4(+) and CD8(+) T cells compared with wild-type controls. |
| 681 | 26224007 | Among these CD4(+) cells, Foxp3(+) T regulatory (Treg) cells were substantially enriched, with 11-fold higher numbers at Day 9.5 postcoitum. |
| 682 | 26224007 | Lymph node hypertrophy in Il10(-/-) mice was associated with more activated phenotypes in dendritic cells and macrophages, with elevated expression of MHCII, scavenger receptor, and CD80. |
| 683 | 26224007 | Affymetrix microarray revealed an altered transcriptional profile in Treg cells from pregnant Il10(-/-) mice, with elevated expression of Ctse (cathepsin E), Il1r1, Il12rb2, and Ifng. |
| 684 | 26224007 | In vitro, Il10(-/-) Treg cells showed reduced steady-state Foxp3 expression, and polyclonal stimulation caused greater loss of Foxp3 and reduced capacity to suppress IL17 in CD4(+)Foxp3(-) T cells. |
| 685 | 26198819 | Pathogenesis of intracranial aneurysm is mediated by proinflammatory cytokine TNFA and IFNG and through stochastic regulation of IL10 and TGFB1 by comorbid factors. |
| 686 | 26170288 | Opposing roles of STAT1 and STAT3 in IL-21 function in CD4+ T cells. |
| 687 | 26170288 | Opposing roles of STAT1 and STAT3 in IL-21 function in CD4+ T cells. |
| 688 | 26170288 | Although IL-21 can activate several STAT family transcription factors, previous studies focused mainly on the role of STAT3 in IL-21 signaling. |
| 689 | 26170288 | Although IL-21 can activate several STAT family transcription factors, previous studies focused mainly on the role of STAT3 in IL-21 signaling. |
| 690 | 26170288 | Here, we investigated the role of STAT1 and show that STAT1 and STAT3 have at least partially opposing roles in IL-21 signaling in CD4(+) T cells. |
| 691 | 26170288 | Here, we investigated the role of STAT1 and show that STAT1 and STAT3 have at least partially opposing roles in IL-21 signaling in CD4(+) T cells. |
| 692 | 26170288 | IL-21 induced STAT1 phosphorylation, and this was augmented in Stat3-deficient CD4(+) T cells. |
| 693 | 26170288 | IL-21 induced STAT1 phosphorylation, and this was augmented in Stat3-deficient CD4(+) T cells. |
| 694 | 26170288 | RNA-Seq analysis of CD4(+) T cells from Stat1- and Stat3-deficient mice revealed that both STAT1 and STAT3 are critical for IL-21-mediated gene regulation. |
| 695 | 26170288 | RNA-Seq analysis of CD4(+) T cells from Stat1- and Stat3-deficient mice revealed that both STAT1 and STAT3 are critical for IL-21-mediated gene regulation. |
| 696 | 26170288 | Expression of some genes, including Tbx21 and Ifng, was differentially regulated by STAT1 and STAT3. |
| 697 | 26170288 | Expression of some genes, including Tbx21 and Ifng, was differentially regulated by STAT1 and STAT3. |
| 698 | 26170288 | Moreover, opposing actions of STAT1 and STAT3 on IFN-γ expression in CD4(+) T cells were demonstrated in vivo during chronic lymphocytic choriomeningitis infection. |
| 699 | 26170288 | Moreover, opposing actions of STAT1 and STAT3 on IFN-γ expression in CD4(+) T cells were demonstrated in vivo during chronic lymphocytic choriomeningitis infection. |
| 700 | 26170288 | Finally, IL-21-mediated induction of STAT1 phosphorylation, as well as IFNG and TBX21 expression, were higher in CD4(+) T cells from patients with autosomal dominant hyper-IgE syndrome, which is caused by STAT3 deficiency, as well as in cells from STAT1 gain-of-function patients. |
| 701 | 26170288 | Finally, IL-21-mediated induction of STAT1 phosphorylation, as well as IFNG and TBX21 expression, were higher in CD4(+) T cells from patients with autosomal dominant hyper-IgE syndrome, which is caused by STAT3 deficiency, as well as in cells from STAT1 gain-of-function patients. |
| 702 | 26170288 | These data indicate an interplay between STAT1 and STAT3 in fine-tuning IL-21 actions. |
| 703 | 26170288 | These data indicate an interplay between STAT1 and STAT3 in fine-tuning IL-21 actions. |
| 704 | 26158463 | In the present study, caprine MDMs were induced with LPS and ConA and the expression profile of immune response (IR) genes, namely, Tumor Necrosis Factor Alpha (TNFA), Interferon Gamma (IFNG), Interleukin 2 (IL2), Granulocyte Macrophage Colony Stimulating Factor (GMCSF), Interleukin 10 (IL10), Transforming Growth Factor Beta (TGFB), Natural Resistance-Associated Macrophage Protein-1 (NRAMP1), inducible nitric oxide synthase (NOS2), and caspase1 (CASP1) were studied to compare the potential of LPS and ConA in initiating immune responses in goat macrophages. |
| 705 | 26158463 | In the present study, caprine MDMs were induced with LPS and ConA and the expression profile of immune response (IR) genes, namely, Tumor Necrosis Factor Alpha (TNFA), Interferon Gamma (IFNG), Interleukin 2 (IL2), Granulocyte Macrophage Colony Stimulating Factor (GMCSF), Interleukin 10 (IL10), Transforming Growth Factor Beta (TGFB), Natural Resistance-Associated Macrophage Protein-1 (NRAMP1), inducible nitric oxide synthase (NOS2), and caspase1 (CASP1) were studied to compare the potential of LPS and ConA in initiating immune responses in goat macrophages. |
| 706 | 26158463 | Real Time quantitative PCR (RT-qPCR) analysis revealed that both LPS and ConA caused an upregulation (p < 0.05) of GMCSF, TGFB1, IL10, and IFNG and down-regulation of NRAMP1. |
| 707 | 26158463 | Real Time quantitative PCR (RT-qPCR) analysis revealed that both LPS and ConA caused an upregulation (p < 0.05) of GMCSF, TGFB1, IL10, and IFNG and down-regulation of NRAMP1. |
| 708 | 26158463 | TNFA and IL2, and NOS2 were upregulated (p < 0.05) by ConA and LPS, respectively. |
| 709 | 26158463 | TNFA and IL2, and NOS2 were upregulated (p < 0.05) by ConA and LPS, respectively. |
| 710 | 26090673 | The expression of the IL-12 receptor β1 chain on the surface, the phosphorylation of signal transducer and activator of transcription (STAT) 4, and the synthesis of IFN-γ on/in individual CD56 bright NK cells were investigated using flow cytometry. |
| 711 | 26090673 | The IFN-γ secretion from purified CD56 bright NK cells was quantified after stimulation with IL-12 and IL-18. |
| 712 | 26090673 | CD56 bright NK cells displayed reduced levels of the IL-12Rβ1 chain whereas the phosphorylation of STAT4, the key transcription factor for the Ifng gene was not diminished. |
| 713 | 26084024 | E3 Ubiquitin Ligase VHL Regulates Hypoxia-Inducible Factor-1α to Maintain Regulatory T Cell Stability and Suppressive Capacity. |
| 714 | 26084024 | Mice with Foxp3-restricted VHL deletion displayed massive inflammation associated with excessive Treg cell interferon-γ (IFN-γ) production. |
| 715 | 26084024 | Augmented hypoxia-inducible factor 1α (HIF-1α)-induced glycolytic reprogramming was required for IFN-γ production. |
| 716 | 26084024 | Furthermore, HIF-1α bound directly to the Ifng promoter. |
| 717 | 26072430 | Furthermore, DA39 showed higher expression of Ifng and Il12 mRNA at week 8 post-infection while the ratio of its Ifng/Il4 mRNA expressions was higher than other strains. |
| 718 | 26023782 | At low concentrations it clearly contributed to IL-6 and monocyte chemotactic protein 1 (MCP-1) production. |
| 719 | 26023782 | At high concentrations, used alone or in association with the TNF-related apoptosis-inducing ligand, TNF-α also stimulated hUC-MSC IL-6 but, more intensely, MCP-1 production. |
| 720 | 26023782 | Interferon gamma (IFN-γ), tested to stimulate PBMC and tissue activation, amplified IL-6 and MCP-1 production and cell death by, apparently, a different process involving necrosis. |
| 721 | 26020282 | Type I IFNs (IFNA1, IFNB1), type II (IFNG), type III (IFNL1, IFNL2/3), IFNL4 and ISG hepatic expressions were measured by qPCR from in 65 chronic hepatitis C (CHC) patients whose IFNL4-associated rs368234815 and IFNL3-associated rs12989760 genotype were determined. |
| 722 | 26020282 | Type I IFNs (IFNA1, IFNB1), type II (IFNG), type III (IFNL1, IFNL2/3), IFNL4 and ISG hepatic expressions were measured by qPCR from in 65 chronic hepatitis C (CHC) patients whose IFNL4-associated rs368234815 and IFNL3-associated rs12989760 genotype were determined. |
| 723 | 26020282 | Levels of ISGs and IFNL2/3 mRNAs were lower in IFNL3 rs12979860 CC patients compared with non-CC patients, and in treatment responders, compared with nonresponders. |
| 724 | 26020282 | Levels of ISGs and IFNL2/3 mRNAs were lower in IFNL3 rs12979860 CC patients compared with non-CC patients, and in treatment responders, compared with nonresponders. |
| 725 | 26020282 | Hepatic levels of ISGs in CHC are associated with IFNL2/3 and IFNL4 expression, suggesting that IFNLs, not other types of IFNs, drive ISG expression. |
| 726 | 26020282 | Hepatic levels of ISGs in CHC are associated with IFNL2/3 and IFNL4 expression, suggesting that IFNLs, not other types of IFNs, drive ISG expression. |
| 727 | 26020282 | Hepatic IFNL2/3 expression is functionally linked to IFNL4 and IFNL3 polymorphisms, potentially explaining the tight association among ISG expression and treatment response. |
| 728 | 26020282 | Hepatic IFNL2/3 expression is functionally linked to IFNL4 and IFNL3 polymorphisms, potentially explaining the tight association among ISG expression and treatment response. |
| 729 | 25982946 | The production of interleukin 10 (IL-10), tumour necrosis factor alpha (TNF) and interferon gamma (IFNG) cytokines was measured, and the expression of Toll-like receptors (TLR2, TLR4 and TLR9) was done in the blood samples and also in the THP1 cell line. |
| 730 | 25982946 | TLR4 and TLR9 were found to be highly expressed in patients with VL. |
| 731 | 25982946 | L. donovani increases the expression of TLR4 and TLR9 in patients with VL and TLR2 in THP1 cells, suggesting a TLRs relation in induction of a mixed cytokine response. |
| 732 | 25973438 | Epigenetic control of interferon-gamma expression in CD8 T cells. |
| 733 | 25973438 | Epigenetic control of interferon-gamma expression in CD8 T cells. |
| 734 | 25973438 | Epigenetic control of interferon-gamma expression in CD8 T cells. |
| 735 | 25973438 | IFN-γ expression by CD4 T lymphocytes is observed only after T helper (Th) 1 differentiation and there are several studies about the molecular mechanisms that control Ifng expression in these cells. |
| 736 | 25973438 | IFN-γ expression by CD4 T lymphocytes is observed only after T helper (Th) 1 differentiation and there are several studies about the molecular mechanisms that control Ifng expression in these cells. |
| 737 | 25973438 | IFN-γ expression by CD4 T lymphocytes is observed only after T helper (Th) 1 differentiation and there are several studies about the molecular mechanisms that control Ifng expression in these cells. |
| 738 | 25973438 | This review will focus on the chromatin status of Ifng promoter in CD8 T cells and possible influences of epigenetic modifications in Ifng gene and conserved noncoding sequences (CNSs) in regulation of IFN-γ production by CD8 T lymphocytes. |
| 739 | 25973438 | This review will focus on the chromatin status of Ifng promoter in CD8 T cells and possible influences of epigenetic modifications in Ifng gene and conserved noncoding sequences (CNSs) in regulation of IFN-γ production by CD8 T lymphocytes. |
| 740 | 25973438 | This review will focus on the chromatin status of Ifng promoter in CD8 T cells and possible influences of epigenetic modifications in Ifng gene and conserved noncoding sequences (CNSs) in regulation of IFN-γ production by CD8 T lymphocytes. |
| 741 | 25965835 | These included cadherin 13 (Cdh13), colony stimulating factor 1 (Csf1), chemokine C-X-C motif ligand 1 (Cxcl1), endothelial cell-selective adhesion molecule (Esam), and interferon gamma (Ifng). |
| 742 | 25963922 | Here we show that miR-125a is downregulated in peripheral CD4(+) T cells of human autoimmune diseases including systemic lupus erythematosus and Crohn's disease, and relevant autoimmune mouse models. miR-125a stabilizes both the commitment and immunoregulatory capacity of Treg cells. |
| 743 | 25963922 | The genome-wide target analysis reveals that miR-125a suppresses several effector T-cell factors including Stat3, Ifng and Il13. |
| 744 | 25963913 | Human first-trimester decidual cells (FTDCs) chemoattract CXCR3-expressing circulating CD56(bright)CD16(-) natural killer (NK) cells, which increase uteroplacental blood flow by remodeling spiral arteries and arterioles. |
| 745 | 25963913 | This recruitment reflects elevated FTDC expression of NK cell-recruiting induced protein 10 and interferon (IFN)-inducible T-cell-α chemoattractant produced in response to the synergistic effects of tumor necrosis factor α (TNF-α) and IFN-γ stimulation. |
| 746 | 25956299 | The balance between survival agents, including GM-CSF, CSF1, LIF, HB-EGF and IGFII, against apoptosis-inducing factors such as TNFα, TRAIL and IFNg, influence the course of preimplantation development, causing embryos to develop normally, adapt to varying maternal environments, or in some cases to arrest and undergo demise. |
| 747 | 25942601 | A new effect of IL-4 on human γδ T cells: promoting regulatory Vδ1 T cells via IL-10 production and inhibiting function of Vδ2 T cells. |
| 748 | 25942601 | IL-4 promoted the growth of activated γδ T cells and increased the levels of Vδ1 T cells, which in turn inhibited Vδ2 T-cell growth via significant IL-10 secretion. |
| 749 | 25942601 | Vδ1 T cells secreted significantly less interferon gamma (IFNγ) and more IL-10 relative to Vδ2. |
| 750 | 25942601 | Furthermore, Vδ1 T cells showed relatively low levels of Natural Killer Group 2D (NKG2D) expression in the presence of IL-4, suggesting that Vδ1 T cells weaken the γδ T cell-mediated anti-tumor immune response. |
| 751 | 25924700 | To test the hypothesis that MMP expression in luteal cells is regulated by luteolytic factors, we investigated the effects of prostaglandin F2α (PGF), interferon γ (IFNG) and tumor necrosis factor α (TNF) on the mRNA expression of MMPs and TIMPs in cultured luteal cells. |
| 752 | 25924700 | To test the hypothesis that MMP expression in luteal cells is regulated by luteolytic factors, we investigated the effects of prostaglandin F2α (PGF), interferon γ (IFNG) and tumor necrosis factor α (TNF) on the mRNA expression of MMPs and TIMPs in cultured luteal cells. |
| 753 | 25924700 | To test the hypothesis that MMP expression in luteal cells is regulated by luteolytic factors, we investigated the effects of prostaglandin F2α (PGF), interferon γ (IFNG) and tumor necrosis factor α (TNF) on the mRNA expression of MMPs and TIMPs in cultured luteal cells. |
| 754 | 25924700 | To test the hypothesis that MMP expression in luteal cells is regulated by luteolytic factors, we investigated the effects of prostaglandin F2α (PGF), interferon γ (IFNG) and tumor necrosis factor α (TNF) on the mRNA expression of MMPs and TIMPs in cultured luteal cells. |
| 755 | 25924700 | To test the hypothesis that MMP expression in luteal cells is regulated by luteolytic factors, we investigated the effects of prostaglandin F2α (PGF), interferon γ (IFNG) and tumor necrosis factor α (TNF) on the mRNA expression of MMPs and TIMPs in cultured luteal cells. |
| 756 | 25924700 | To test the hypothesis that MMP expression in luteal cells is regulated by luteolytic factors, we investigated the effects of prostaglandin F2α (PGF), interferon γ (IFNG) and tumor necrosis factor α (TNF) on the mRNA expression of MMPs and TIMPs in cultured luteal cells. |
| 757 | 25924700 | To test the hypothesis that MMP expression in luteal cells is regulated by luteolytic factors, we investigated the effects of prostaglandin F2α (PGF), interferon γ (IFNG) and tumor necrosis factor α (TNF) on the mRNA expression of MMPs and TIMPs in cultured luteal cells. |
| 758 | 25924700 | Luteal cells obtained from the CL at the mid-luteal stage (days 8-12 after ovulation) were cultured with PGF (0.01, 0.1, 1 μM), IFNG (0.05, 0.5, 5 nM) and TNF (0.05, 0.5, 0.5 nM) alone or in combination for 24 h. |
| 759 | 25924700 | Luteal cells obtained from the CL at the mid-luteal stage (days 8-12 after ovulation) were cultured with PGF (0.01, 0.1, 1 μM), IFNG (0.05, 0.5, 5 nM) and TNF (0.05, 0.5, 0.5 nM) alone or in combination for 24 h. |
| 760 | 25924700 | Luteal cells obtained from the CL at the mid-luteal stage (days 8-12 after ovulation) were cultured with PGF (0.01, 0.1, 1 μM), IFNG (0.05, 0.5, 5 nM) and TNF (0.05, 0.5, 0.5 nM) alone or in combination for 24 h. |
| 761 | 25924700 | Luteal cells obtained from the CL at the mid-luteal stage (days 8-12 after ovulation) were cultured with PGF (0.01, 0.1, 1 μM), IFNG (0.05, 0.5, 5 nM) and TNF (0.05, 0.5, 0.5 nM) alone or in combination for 24 h. |
| 762 | 25924700 | Luteal cells obtained from the CL at the mid-luteal stage (days 8-12 after ovulation) were cultured with PGF (0.01, 0.1, 1 μM), IFNG (0.05, 0.5, 5 nM) and TNF (0.05, 0.5, 0.5 nM) alone or in combination for 24 h. |
| 763 | 25924700 | Luteal cells obtained from the CL at the mid-luteal stage (days 8-12 after ovulation) were cultured with PGF (0.01, 0.1, 1 μM), IFNG (0.05, 0.5, 5 nM) and TNF (0.05, 0.5, 0.5 nM) alone or in combination for 24 h. |
| 764 | 25924700 | Luteal cells obtained from the CL at the mid-luteal stage (days 8-12 after ovulation) were cultured with PGF (0.01, 0.1, 1 μM), IFNG (0.05, 0.5, 5 nM) and TNF (0.05, 0.5, 0.5 nM) alone or in combination for 24 h. |
| 765 | 25924700 | PGF and IFNG significantly increased the expression of MMP-1 mRNA. |
| 766 | 25924700 | PGF and IFNG significantly increased the expression of MMP-1 mRNA. |
| 767 | 25924700 | PGF and IFNG significantly increased the expression of MMP-1 mRNA. |
| 768 | 25924700 | PGF and IFNG significantly increased the expression of MMP-1 mRNA. |
| 769 | 25924700 | PGF and IFNG significantly increased the expression of MMP-1 mRNA. |
| 770 | 25924700 | PGF and IFNG significantly increased the expression of MMP-1 mRNA. |
| 771 | 25924700 | PGF and IFNG significantly increased the expression of MMP-1 mRNA. |
| 772 | 25924700 | In addition, 1 μM PGF in combination with 5 nM IFNG stimulated MMP-1 and MMP-9 mRNA expression significantly more than either treatment alone. |
| 773 | 25924700 | In addition, 1 μM PGF in combination with 5 nM IFNG stimulated MMP-1 and MMP-9 mRNA expression significantly more than either treatment alone. |
| 774 | 25924700 | In addition, 1 μM PGF in combination with 5 nM IFNG stimulated MMP-1 and MMP-9 mRNA expression significantly more than either treatment alone. |
| 775 | 25924700 | In addition, 1 μM PGF in combination with 5 nM IFNG stimulated MMP-1 and MMP-9 mRNA expression significantly more than either treatment alone. |
| 776 | 25924700 | In addition, 1 μM PGF in combination with 5 nM IFNG stimulated MMP-1 and MMP-9 mRNA expression significantly more than either treatment alone. |
| 777 | 25924700 | In addition, 1 μM PGF in combination with 5 nM IFNG stimulated MMP-1 and MMP-9 mRNA expression significantly more than either treatment alone. |
| 778 | 25924700 | In addition, 1 μM PGF in combination with 5 nM IFNG stimulated MMP-1 and MMP-9 mRNA expression significantly more than either treatment alone. |
| 779 | 25924700 | In contrast, IFNG significantly decreased the level of MMP-14 mRNA. |
| 780 | 25924700 | In contrast, IFNG significantly decreased the level of MMP-14 mRNA. |
| 781 | 25924700 | In contrast, IFNG significantly decreased the level of MMP-14 mRNA. |
| 782 | 25924700 | In contrast, IFNG significantly decreased the level of MMP-14 mRNA. |
| 783 | 25924700 | In contrast, IFNG significantly decreased the level of MMP-14 mRNA. |
| 784 | 25924700 | In contrast, IFNG significantly decreased the level of MMP-14 mRNA. |
| 785 | 25924700 | In contrast, IFNG significantly decreased the level of MMP-14 mRNA. |
| 786 | 25924700 | The mRNA expression of TIMP-1, which preferentially inhibits MMP-1, was suppressed by 5 nM INFG. |
| 787 | 25924700 | The mRNA expression of TIMP-1, which preferentially inhibits MMP-1, was suppressed by 5 nM INFG. |
| 788 | 25924700 | The mRNA expression of TIMP-1, which preferentially inhibits MMP-1, was suppressed by 5 nM INFG. |
| 789 | 25924700 | The mRNA expression of TIMP-1, which preferentially inhibits MMP-1, was suppressed by 5 nM INFG. |
| 790 | 25924700 | The mRNA expression of TIMP-1, which preferentially inhibits MMP-1, was suppressed by 5 nM INFG. |
| 791 | 25924700 | The mRNA expression of TIMP-1, which preferentially inhibits MMP-1, was suppressed by 5 nM INFG. |
| 792 | 25924700 | The mRNA expression of TIMP-1, which preferentially inhibits MMP-1, was suppressed by 5 nM INFG. |
| 793 | 25924700 | One μM PGF and 5 nM IFNG suppressed TIMP-2 mRNA expression. |
| 794 | 25924700 | One μM PGF and 5 nM IFNG suppressed TIMP-2 mRNA expression. |
| 795 | 25924700 | One μM PGF and 5 nM IFNG suppressed TIMP-2 mRNA expression. |
| 796 | 25924700 | One μM PGF and 5 nM IFNG suppressed TIMP-2 mRNA expression. |
| 797 | 25924700 | One μM PGF and 5 nM IFNG suppressed TIMP-2 mRNA expression. |
| 798 | 25924700 | One μM PGF and 5 nM IFNG suppressed TIMP-2 mRNA expression. |
| 799 | 25924700 | One μM PGF and 5 nM IFNG suppressed TIMP-2 mRNA expression. |
| 800 | 25924700 | These results suggest a new role of MMPs: luteal MMPs stimulated by PGF and IFNG break down the extracellular matrix surrounding luteal cells, which accelerates detachment from the CL during luteolysis, providing an essential prerequisite for outflow of luteal cells from the CL to lymphatic vessels. |
| 801 | 25924700 | These results suggest a new role of MMPs: luteal MMPs stimulated by PGF and IFNG break down the extracellular matrix surrounding luteal cells, which accelerates detachment from the CL during luteolysis, providing an essential prerequisite for outflow of luteal cells from the CL to lymphatic vessels. |
| 802 | 25924700 | These results suggest a new role of MMPs: luteal MMPs stimulated by PGF and IFNG break down the extracellular matrix surrounding luteal cells, which accelerates detachment from the CL during luteolysis, providing an essential prerequisite for outflow of luteal cells from the CL to lymphatic vessels. |
| 803 | 25924700 | These results suggest a new role of MMPs: luteal MMPs stimulated by PGF and IFNG break down the extracellular matrix surrounding luteal cells, which accelerates detachment from the CL during luteolysis, providing an essential prerequisite for outflow of luteal cells from the CL to lymphatic vessels. |
| 804 | 25924700 | These results suggest a new role of MMPs: luteal MMPs stimulated by PGF and IFNG break down the extracellular matrix surrounding luteal cells, which accelerates detachment from the CL during luteolysis, providing an essential prerequisite for outflow of luteal cells from the CL to lymphatic vessels. |
| 805 | 25924700 | These results suggest a new role of MMPs: luteal MMPs stimulated by PGF and IFNG break down the extracellular matrix surrounding luteal cells, which accelerates detachment from the CL during luteolysis, providing an essential prerequisite for outflow of luteal cells from the CL to lymphatic vessels. |
| 806 | 25924700 | These results suggest a new role of MMPs: luteal MMPs stimulated by PGF and IFNG break down the extracellular matrix surrounding luteal cells, which accelerates detachment from the CL during luteolysis, providing an essential prerequisite for outflow of luteal cells from the CL to lymphatic vessels. |
| 807 | 25911310 | Trazodone treatment protects neuronal-like cells from inflammatory insult by inhibiting NF-κB, p38 and JNK. |
| 808 | 25911310 | Our results showed that TDZ significantly increased the mRNA expression of both brain-derived nerve factor (BDNF) and cAMP response element-binding protein (CREB) and decreased the cellular release of the pro-inflammatory cytokine interferon gamma (IFN-γ) in neuronal-like cells. |
| 809 | 25911310 | In contrast, neuronal cell treatment with LPS and TNF-α decreased the expression of CREB and BDNF and increased the expression of nuclear factor kappa B (NF-κB), a primary transcription factor that functions in inflammatory response initiation. |
| 810 | 25911310 | Moreover, the two agents induced the release of pro-inflammatory cytokines (i.e., interleukin-6 and IFN-γ) and decreased the production of the anti-inflammatory cytokine interleukin-10. |
| 811 | 25911310 | TDZ pre-treatment completely reversed the decrease in cell viability and counteracted the decrease in BDNF and CREB expression mediated by LPS-TNF-α. |
| 812 | 25911310 | TDZ induced extracellular signal-regulated kinase (ERK) phosphorylation and inhibited constitutive p38 activation. |
| 813 | 25911310 | Moreover, TDZ counteracted the activation of p38 and c-Jun NH2-terminal kinase (JNK) elicited by LPS-TNF-α, suggesting that the neuro-protective role of TDZ could be mediated by p38 and JNK. |
| 814 | 25890879 | In the present study, to find out whether single nucleotide polymorphisms (SNPs) in the pro-inflammatory and anti-inflammatory cytokine genes are associated with dengue disease severity, SNPs in TNF, IFNG, IL1B, IL8, IL0, IL17A and IL17F genes were investigated using polymerase chain reaction based methods in 132 dengue (DEN) cases [87 dengue fever (DF), 45 dengue hemorrhagic fever (DHF) cases] and 108 apparently healthy controls (HC) from Pune, Maharashtra, western India. |
| 815 | 25890879 | The results suggest that heterozygous genotypes of IL8 rs4973 and IL10 rs1800871 are associated with reduced risk of DHF. |
| 816 | 25877879 | Of these, the potential host responses included up-regulation of genes related to immune response (CD14, S100A8, S100A9, LTF, HP and CHCIL3), up-regulation of Th1-polarizing factor (CCL4, CCL5, CXCL9 and CXCL10), down-regulation of genes related to metabolism (ELANE, IGF1, TCF7L2 and MPO) and no significant response of other genes (GADD45a, GPNMB, HMOX1, IFNG and NQO1) in THP-1 cells infected with MAP. |
| 817 | 25837274 | Non-toxic low concentrations of the plant extract and pure Erucin altered the expression of the interleukin (IL)-2 receptor but did not affect further T cell activation, proliferation and the release of the effector molecules interferon (IFN)-gamma and IL-2 of T-lymphocytes. |
| 818 | 25834350 | TNF, IL12B, and IFNG Gene Polymorphisms in Serbian Patients with Psoriasis. |
| 819 | 25815330 | Our aim was to investigate the effects of hyperthermia, ultraviolet A rays (UVA), and ultraviolet C rays (UVC) as well as glucose and ascorbic acid (AA) on the regulation of human β-defensin 1 (DEFB1), cathelicidin (CAMP), and interferon-γ (IFNG) genes in normal human keratinocytes (NHK). |
| 820 | 25815330 | Our aim was to investigate the effects of hyperthermia, ultraviolet A rays (UVA), and ultraviolet C rays (UVC) as well as glucose and ascorbic acid (AA) on the regulation of human β-defensin 1 (DEFB1), cathelicidin (CAMP), and interferon-γ (IFNG) genes in normal human keratinocytes (NHK). |
| 821 | 25815330 | Our aim was to investigate the effects of hyperthermia, ultraviolet A rays (UVA), and ultraviolet C rays (UVC) as well as glucose and ascorbic acid (AA) on the regulation of human β-defensin 1 (DEFB1), cathelicidin (CAMP), and interferon-γ (IFNG) genes in normal human keratinocytes (NHK). |
| 822 | 25815330 | We found that AA is a more potent APE for DEFB1 than glucose in NHK. |
| 823 | 25815330 | We found that AA is a more potent APE for DEFB1 than glucose in NHK. |
| 824 | 25815330 | We found that AA is a more potent APE for DEFB1 than glucose in NHK. |
| 825 | 25815330 | Glucose but not AA is an APE for CAMP. |
| 826 | 25815330 | Glucose but not AA is an APE for CAMP. |
| 827 | 25815330 | Glucose but not AA is an APE for CAMP. |
| 828 | 25815330 | AA-dependent DEFB1 upregulation below 20 mM predicts in vitro antimicrobial activity as well as glucose- and AA-dependent CAMP and IFNG upregulation. |
| 829 | 25815330 | AA-dependent DEFB1 upregulation below 20 mM predicts in vitro antimicrobial activity as well as glucose- and AA-dependent CAMP and IFNG upregulation. |
| 830 | 25815330 | AA-dependent DEFB1 upregulation below 20 mM predicts in vitro antimicrobial activity as well as glucose- and AA-dependent CAMP and IFNG upregulation. |
| 831 | 25815330 | UVC upregulates CAMP and DEFB1 genes but UVA only upregulates the DEFB1 gene. |
| 832 | 25815330 | UVC upregulates CAMP and DEFB1 genes but UVA only upregulates the DEFB1 gene. |
| 833 | 25815330 | UVC upregulates CAMP and DEFB1 genes but UVA only upregulates the DEFB1 gene. |
| 834 | 25815330 | Our results suggest that glucose upregulates CAMP in an IFN-γ-independent manner. |
| 835 | 25815330 | Our results suggest that glucose upregulates CAMP in an IFN-γ-independent manner. |
| 836 | 25815330 | Our results suggest that glucose upregulates CAMP in an IFN-γ-independent manner. |
| 837 | 25792853 | Data elucidate the role of VSC in patients with immunologic diseases and the role of a semiquantitative chairside test, like the VSC indicator presented here, in correlation to IFNg and IL-10 sensitization in peripheral blood mononuclear cells. |
| 838 | 25792853 | Data elucidate the role of VSC in patients with immunologic diseases and the role of a semiquantitative chairside test, like the VSC indicator presented here, in correlation to IFNg and IL-10 sensitization in peripheral blood mononuclear cells. |
| 839 | 25792853 | The association between ex vivo-stimulated cytokines and endodontically derived sulfur components is supported by the fact that the number of interferon gamma- and/or interleukin-10-positive sensitized patients declined significantly 3-8 months after extraction of the corresponding teeth. |
| 840 | 25792853 | The association between ex vivo-stimulated cytokines and endodontically derived sulfur components is supported by the fact that the number of interferon gamma- and/or interleukin-10-positive sensitized patients declined significantly 3-8 months after extraction of the corresponding teeth. |
| 841 | 25787894 | In cultured cells, the transcripts strongly associated with ABMR were expressed in endothelial cells, e.g. cadherins CDH5 and CDH13; IFNG-treated endothelial cells, e.g. phospholipase PLA1A and chemokine CXCL11; or NK cells, e.g. cytotoxicity molecules granulysin (GNLY) and FGFBP2. |
| 842 | 25787894 | Duffy chemokine receptor (DARC) or decreased e.g. sclerostin (SOST). |
| 843 | 25774595 | Risk model incorporating donor IL6 and IFNG genotype and gastrointestinal GVHD can discriminate patients at high risk of steroid refractory acute GVHD. |
| 844 | 25774455 | Genes that were significantly regulated between VRs and VNRs were CREB3L4, HIST1H3A, HIST1H3H, IFNA1, IFNA4, IFNA5, IFNA6, IFNA8, IFNA14, IFNG, IFNAR1, IL6, IRF9, MAPK4, MAPK5, MAPK14, NET1, and PIK3C2A in the IFN array. |
| 845 | 25774455 | In the TLR array, only LBP and MAPK8 were found to be differentially regulated. |
| 846 | 25774455 | In the antigen processing array, HLA-A, HLA-C, HLA-DMA, HLA-DMB, HLA-F, PSMA5, PSMB8, and PSMB9 were differentially downregulated. |
| 847 | 25732728 | Type I IFNs and IL-18 regulate the antiviral response of primary human γδ T cells against dendritic cells infected with Dengue virus. |
| 848 | 25732728 | Type I IFNs and IL-18 regulate the antiviral response of primary human γδ T cells against dendritic cells infected with Dengue virus. |
| 849 | 25732728 | The anti-DV IFN-γ response is regulated by type I IFN and IL-18 in a TCR-independent manner, and IFN-γ secreting γδ T cells predominantly expressed IL-18Rα. |
| 850 | 25732728 | The anti-DV IFN-γ response is regulated by type I IFN and IL-18 in a TCR-independent manner, and IFN-γ secreting γδ T cells predominantly expressed IL-18Rα. |
| 851 | 25726583 | T-bet expression was then identified by FACS after infection of CD4+ primary T cells from T-bet knockout mouse with recombinant retrovirus. |
| 852 | 25726583 | To determine if exogenous expressing T-bet has normal function, we checked the expression level of T-bet target gene, Ifng. |
| 853 | 25720254 | Proinflammatory cytokines TNF, IFNG and ILl7 play an important role in eruption of psoriasis. |
| 854 | 25720254 | Proinflammatory cytokines TNF, IFNG and ILl7 play an important role in eruption of psoriasis. |
| 855 | 25720254 | Proinflammatory cytokines TNF, IFNG and ILl7 play an important role in eruption of psoriasis. |
| 856 | 25720254 | Proinflammatory cytokines TNF, IFNG and ILl7 play an important role in eruption of psoriasis. |
| 857 | 25720254 | The aim of this study was to evaluate changes in gene expression and the proliferation rates in cultured HaCaT cells treated with TNF, IFNG and IL17. |
| 858 | 25720254 | The aim of this study was to evaluate changes in gene expression and the proliferation rates in cultured HaCaT cells treated with TNF, IFNG and IL17. |
| 859 | 25720254 | The aim of this study was to evaluate changes in gene expression and the proliferation rates in cultured HaCaT cells treated with TNF, IFNG and IL17. |
| 860 | 25720254 | The aim of this study was to evaluate changes in gene expression and the proliferation rates in cultured HaCaT cells treated with TNF, IFNG and IL17. |
| 861 | 25720254 | We found that HaCaT cells decrease their proliferation rate in response to either IL17 or a combination TNF and IF-NG. |
| 862 | 25720254 | We found that HaCaT cells decrease their proliferation rate in response to either IL17 or a combination TNF and IF-NG. |
| 863 | 25720254 | We found that HaCaT cells decrease their proliferation rate in response to either IL17 or a combination TNF and IF-NG. |
| 864 | 25720254 | We found that HaCaT cells decrease their proliferation rate in response to either IL17 or a combination TNF and IF-NG. |
| 865 | 25720254 | We conclude that HaCaT cells have a sufficient limitation as a cellular model of psoriasis due to their treatment with proinflammatory cytokines, namely TNF, IFNG and IL17 does not increase their proliferation rate. |
| 866 | 25720254 | We conclude that HaCaT cells have a sufficient limitation as a cellular model of psoriasis due to their treatment with proinflammatory cytokines, namely TNF, IFNG and IL17 does not increase their proliferation rate. |
| 867 | 25720254 | We conclude that HaCaT cells have a sufficient limitation as a cellular model of psoriasis due to their treatment with proinflammatory cytokines, namely TNF, IFNG and IL17 does not increase their proliferation rate. |
| 868 | 25720254 | We conclude that HaCaT cells have a sufficient limitation as a cellular model of psoriasis due to their treatment with proinflammatory cytokines, namely TNF, IFNG and IL17 does not increase their proliferation rate. |
| 869 | 25711680 | Ifng expression was increased in MLN and Foxp3 expression was decreased in the jejunum of LEW.1AR1-iddm rats; Ifng/Il4 was decreased in jejunum of LEW.1AR1-iddm rats fed HC. |
| 870 | 25673564 | IL10, TGF beta1, and IFN gamma modulate intracellular signaling pathways and cytokine production to control Toxoplasma gondii infection in BeWo trophoblast cells. |
| 871 | 25673564 | IL10, TGF beta1, and IFN gamma modulate intracellular signaling pathways and cytokine production to control Toxoplasma gondii infection in BeWo trophoblast cells. |
| 872 | 25673564 | IL10, TGF beta1, and IFN gamma modulate intracellular signaling pathways and cytokine production to control Toxoplasma gondii infection in BeWo trophoblast cells. |
| 873 | 25673564 | IL10, TGF beta1, and IFN gamma modulate intracellular signaling pathways and cytokine production to control Toxoplasma gondii infection in BeWo trophoblast cells. |
| 874 | 25673564 | IL10, TGF beta1, and IFN gamma modulate intracellular signaling pathways and cytokine production to control Toxoplasma gondii infection in BeWo trophoblast cells. |
| 875 | 25673564 | IL10, TGF beta1, and IFN gamma modulate intracellular signaling pathways and cytokine production to control Toxoplasma gondii infection in BeWo trophoblast cells. |
| 876 | 25673564 | Considering that interleukin 10 (IL10), transforming growth factor beta1 (TGFB1), and interferon gamma (IFNG) are involved in the susceptibility of BeWo trophoblast cells to Toxoplasma gondii infection, the aim of the present study was to investigate the effector mechanisms triggered by these cytokines in the control of T. gondii in BeWo cells. |
| 877 | 25673564 | Considering that interleukin 10 (IL10), transforming growth factor beta1 (TGFB1), and interferon gamma (IFNG) are involved in the susceptibility of BeWo trophoblast cells to Toxoplasma gondii infection, the aim of the present study was to investigate the effector mechanisms triggered by these cytokines in the control of T. gondii in BeWo cells. |
| 878 | 25673564 | Considering that interleukin 10 (IL10), transforming growth factor beta1 (TGFB1), and interferon gamma (IFNG) are involved in the susceptibility of BeWo trophoblast cells to Toxoplasma gondii infection, the aim of the present study was to investigate the effector mechanisms triggered by these cytokines in the control of T. gondii in BeWo cells. |
| 879 | 25673564 | Considering that interleukin 10 (IL10), transforming growth factor beta1 (TGFB1), and interferon gamma (IFNG) are involved in the susceptibility of BeWo trophoblast cells to Toxoplasma gondii infection, the aim of the present study was to investigate the effector mechanisms triggered by these cytokines in the control of T. gondii in BeWo cells. |
| 880 | 25673564 | Considering that interleukin 10 (IL10), transforming growth factor beta1 (TGFB1), and interferon gamma (IFNG) are involved in the susceptibility of BeWo trophoblast cells to Toxoplasma gondii infection, the aim of the present study was to investigate the effector mechanisms triggered by these cytokines in the control of T. gondii in BeWo cells. |
| 881 | 25673564 | Considering that interleukin 10 (IL10), transforming growth factor beta1 (TGFB1), and interferon gamma (IFNG) are involved in the susceptibility of BeWo trophoblast cells to Toxoplasma gondii infection, the aim of the present study was to investigate the effector mechanisms triggered by these cytokines in the control of T. gondii in BeWo cells. |
| 882 | 25673564 | For this purpose, infected/uninfected BeWo cells were treated with IL10, TGFB1 (50 ng/ml), and IFNG (20 or 100 ng/ml) in order to verify the phosphorylation of signal transducers and activators of transcription 1 (STAT1), STAT3, and Smad2, parasite intracellular proliferation, as well as the Th1/Th2/IL17A cytokine production. |
| 883 | 25673564 | For this purpose, infected/uninfected BeWo cells were treated with IL10, TGFB1 (50 ng/ml), and IFNG (20 or 100 ng/ml) in order to verify the phosphorylation of signal transducers and activators of transcription 1 (STAT1), STAT3, and Smad2, parasite intracellular proliferation, as well as the Th1/Th2/IL17A cytokine production. |
| 884 | 25673564 | For this purpose, infected/uninfected BeWo cells were treated with IL10, TGFB1 (50 ng/ml), and IFNG (20 or 100 ng/ml) in order to verify the phosphorylation of signal transducers and activators of transcription 1 (STAT1), STAT3, and Smad2, parasite intracellular proliferation, as well as the Th1/Th2/IL17A cytokine production. |
| 885 | 25673564 | For this purpose, infected/uninfected BeWo cells were treated with IL10, TGFB1 (50 ng/ml), and IFNG (20 or 100 ng/ml) in order to verify the phosphorylation of signal transducers and activators of transcription 1 (STAT1), STAT3, and Smad2, parasite intracellular proliferation, as well as the Th1/Th2/IL17A cytokine production. |
| 886 | 25673564 | For this purpose, infected/uninfected BeWo cells were treated with IL10, TGFB1 (50 ng/ml), and IFNG (20 or 100 ng/ml) in order to verify the phosphorylation of signal transducers and activators of transcription 1 (STAT1), STAT3, and Smad2, parasite intracellular proliferation, as well as the Th1/Th2/IL17A cytokine production. |
| 887 | 25673564 | For this purpose, infected/uninfected BeWo cells were treated with IL10, TGFB1 (50 ng/ml), and IFNG (20 or 100 ng/ml) in order to verify the phosphorylation of signal transducers and activators of transcription 1 (STAT1), STAT3, and Smad2, parasite intracellular proliferation, as well as the Th1/Th2/IL17A cytokine production. |
| 888 | 25673564 | The treatment of BeWo cells with IL10 and TGFB1 favored T. gondii proliferation, and these findings were associated with STAT3 and Smad2 phosphorylation, respectively (P < 0.05). |
| 889 | 25673564 | The treatment of BeWo cells with IL10 and TGFB1 favored T. gondii proliferation, and these findings were associated with STAT3 and Smad2 phosphorylation, respectively (P < 0.05). |
| 890 | 25673564 | The treatment of BeWo cells with IL10 and TGFB1 favored T. gondii proliferation, and these findings were associated with STAT3 and Smad2 phosphorylation, respectively (P < 0.05). |
| 891 | 25673564 | The treatment of BeWo cells with IL10 and TGFB1 favored T. gondii proliferation, and these findings were associated with STAT3 and Smad2 phosphorylation, respectively (P < 0.05). |
| 892 | 25673564 | The treatment of BeWo cells with IL10 and TGFB1 favored T. gondii proliferation, and these findings were associated with STAT3 and Smad2 phosphorylation, respectively (P < 0.05). |
| 893 | 25673564 | The treatment of BeWo cells with IL10 and TGFB1 favored T. gondii proliferation, and these findings were associated with STAT3 and Smad2 phosphorylation, respectively (P < 0.05). |
| 894 | 25673564 | Also, these cytokine treatments were able to down-modulate TNF alpha (TNFA) and IL6 production (P < 0.05). |
| 895 | 25673564 | Also, these cytokine treatments were able to down-modulate TNF alpha (TNFA) and IL6 production (P < 0.05). |
| 896 | 25673564 | Also, these cytokine treatments were able to down-modulate TNF alpha (TNFA) and IL6 production (P < 0.05). |
| 897 | 25673564 | Also, these cytokine treatments were able to down-modulate TNF alpha (TNFA) and IL6 production (P < 0.05). |
| 898 | 25673564 | Also, these cytokine treatments were able to down-modulate TNF alpha (TNFA) and IL6 production (P < 0.05). |
| 899 | 25673564 | Also, these cytokine treatments were able to down-modulate TNF alpha (TNFA) and IL6 production (P < 0.05). |
| 900 | 25673564 | Low concentration of IFNG was unable to control T. gondii infection but was able to trigger STAT1 phosphorylation and up-regulate IL6 and IL17A production; whereas a high concentration of IFNG was unable to activate STAT1 but down-modulated IL6 and TNFA and increased T. gondii proliferation (P < 0.05). |
| 901 | 25673564 | Low concentration of IFNG was unable to control T. gondii infection but was able to trigger STAT1 phosphorylation and up-regulate IL6 and IL17A production; whereas a high concentration of IFNG was unable to activate STAT1 but down-modulated IL6 and TNFA and increased T. gondii proliferation (P < 0.05). |
| 902 | 25673564 | Low concentration of IFNG was unable to control T. gondii infection but was able to trigger STAT1 phosphorylation and up-regulate IL6 and IL17A production; whereas a high concentration of IFNG was unable to activate STAT1 but down-modulated IL6 and TNFA and increased T. gondii proliferation (P < 0.05). |
| 903 | 25673564 | Low concentration of IFNG was unable to control T. gondii infection but was able to trigger STAT1 phosphorylation and up-regulate IL6 and IL17A production; whereas a high concentration of IFNG was unable to activate STAT1 but down-modulated IL6 and TNFA and increased T. gondii proliferation (P < 0.05). |
| 904 | 25673564 | Low concentration of IFNG was unable to control T. gondii infection but was able to trigger STAT1 phosphorylation and up-regulate IL6 and IL17A production; whereas a high concentration of IFNG was unable to activate STAT1 but down-modulated IL6 and TNFA and increased T. gondii proliferation (P < 0.05). |
| 905 | 25673564 | Low concentration of IFNG was unable to control T. gondii infection but was able to trigger STAT1 phosphorylation and up-regulate IL6 and IL17A production; whereas a high concentration of IFNG was unable to activate STAT1 but down-modulated IL6 and TNFA and increased T. gondii proliferation (P < 0.05). |
| 906 | 25673564 | IL10, TGFB1, and IFNG regulate a differential T. gondii proliferation in BeWo cells because they distinctly trigger intracellular signaling pathways and cytokine production, especially IL6 and TNFA. |
| 907 | 25673564 | IL10, TGFB1, and IFNG regulate a differential T. gondii proliferation in BeWo cells because they distinctly trigger intracellular signaling pathways and cytokine production, especially IL6 and TNFA. |
| 908 | 25673564 | IL10, TGFB1, and IFNG regulate a differential T. gondii proliferation in BeWo cells because they distinctly trigger intracellular signaling pathways and cytokine production, especially IL6 and TNFA. |
| 909 | 25673564 | IL10, TGFB1, and IFNG regulate a differential T. gondii proliferation in BeWo cells because they distinctly trigger intracellular signaling pathways and cytokine production, especially IL6 and TNFA. |
| 910 | 25673564 | IL10, TGFB1, and IFNG regulate a differential T. gondii proliferation in BeWo cells because they distinctly trigger intracellular signaling pathways and cytokine production, especially IL6 and TNFA. |
| 911 | 25673564 | IL10, TGFB1, and IFNG regulate a differential T. gondii proliferation in BeWo cells because they distinctly trigger intracellular signaling pathways and cytokine production, especially IL6 and TNFA. |
| 912 | 25673564 | Our data open new windows to understand the mechanisms triggered by IL10, TGFB1, and IFNG at the maternal-fetal interface in the presence of T. gondii, contributing to recognizing the importance of these effector mechanisms involved in the vertical transmission of this parasite. |
| 913 | 25673564 | Our data open new windows to understand the mechanisms triggered by IL10, TGFB1, and IFNG at the maternal-fetal interface in the presence of T. gondii, contributing to recognizing the importance of these effector mechanisms involved in the vertical transmission of this parasite. |
| 914 | 25673564 | Our data open new windows to understand the mechanisms triggered by IL10, TGFB1, and IFNG at the maternal-fetal interface in the presence of T. gondii, contributing to recognizing the importance of these effector mechanisms involved in the vertical transmission of this parasite. |
| 915 | 25673564 | Our data open new windows to understand the mechanisms triggered by IL10, TGFB1, and IFNG at the maternal-fetal interface in the presence of T. gondii, contributing to recognizing the importance of these effector mechanisms involved in the vertical transmission of this parasite. |
| 916 | 25673564 | Our data open new windows to understand the mechanisms triggered by IL10, TGFB1, and IFNG at the maternal-fetal interface in the presence of T. gondii, contributing to recognizing the importance of these effector mechanisms involved in the vertical transmission of this parasite. |
| 917 | 25673564 | Our data open new windows to understand the mechanisms triggered by IL10, TGFB1, and IFNG at the maternal-fetal interface in the presence of T. gondii, contributing to recognizing the importance of these effector mechanisms involved in the vertical transmission of this parasite. |
| 918 | 25648131 | This cross-sectional study analyzes factors associated with the development of CMV-specific CD8+ response, measured by IFNg production after cytomegalovirus (CMV) peptide stimulation, in CMV-seropositive solid organ transplantation candidates. |
| 919 | 25619828 | IFNg-induced Irgm1 promotes tumorigenesis of melanoma via dual regulation of apoptosis and Bif-1-dependent autophagy. |
| 920 | 25619828 | IFNg-induced Irgm1 promotes tumorigenesis of melanoma via dual regulation of apoptosis and Bif-1-dependent autophagy. |
| 921 | 25619828 | IFNg-induced Irgm1 promotes tumorigenesis of melanoma via dual regulation of apoptosis and Bif-1-dependent autophagy. |
| 922 | 25619828 | IFNg-induced Irgm1 promotes tumorigenesis of melanoma via dual regulation of apoptosis and Bif-1-dependent autophagy. |
| 923 | 25619828 | IFNg-induced Irgm1 promotes tumorigenesis of melanoma via dual regulation of apoptosis and Bif-1-dependent autophagy. |
| 924 | 25619828 | IFNg-induced Irgm1 promotes tumorigenesis of melanoma via dual regulation of apoptosis and Bif-1-dependent autophagy. |
| 925 | 25619828 | In the current study, we showed that immunity-related GTPase family member 1 (mouse: Irgm1; human: IRGM) is essential for IFNg-mediated regulation of tumor cell growth in melanoma. |
| 926 | 25619828 | In the current study, we showed that immunity-related GTPase family member 1 (mouse: Irgm1; human: IRGM) is essential for IFNg-mediated regulation of tumor cell growth in melanoma. |
| 927 | 25619828 | In the current study, we showed that immunity-related GTPase family member 1 (mouse: Irgm1; human: IRGM) is essential for IFNg-mediated regulation of tumor cell growth in melanoma. |
| 928 | 25619828 | In the current study, we showed that immunity-related GTPase family member 1 (mouse: Irgm1; human: IRGM) is essential for IFNg-mediated regulation of tumor cell growth in melanoma. |
| 929 | 25619828 | In the current study, we showed that immunity-related GTPase family member 1 (mouse: Irgm1; human: IRGM) is essential for IFNg-mediated regulation of tumor cell growth in melanoma. |
| 930 | 25619828 | In the current study, we showed that immunity-related GTPase family member 1 (mouse: Irgm1; human: IRGM) is essential for IFNg-mediated regulation of tumor cell growth in melanoma. |
| 931 | 25619828 | IFNg and starvation synergistically induced Irgm1 expression in melanoma B16 cells. |
| 932 | 25619828 | IFNg and starvation synergistically induced Irgm1 expression in melanoma B16 cells. |
| 933 | 25619828 | IFNg and starvation synergistically induced Irgm1 expression in melanoma B16 cells. |
| 934 | 25619828 | IFNg and starvation synergistically induced Irgm1 expression in melanoma B16 cells. |
| 935 | 25619828 | IFNg and starvation synergistically induced Irgm1 expression in melanoma B16 cells. |
| 936 | 25619828 | IFNg and starvation synergistically induced Irgm1 expression in melanoma B16 cells. |
| 937 | 25619828 | In vitro, knockdown endogenous or IFNg-induced Irgm1 significantly decreases the proliferation and increases apoptosis of B16 cells. |
| 938 | 25619828 | In vitro, knockdown endogenous or IFNg-induced Irgm1 significantly decreases the proliferation and increases apoptosis of B16 cells. |
| 939 | 25619828 | In vitro, knockdown endogenous or IFNg-induced Irgm1 significantly decreases the proliferation and increases apoptosis of B16 cells. |
| 940 | 25619828 | In vitro, knockdown endogenous or IFNg-induced Irgm1 significantly decreases the proliferation and increases apoptosis of B16 cells. |
| 941 | 25619828 | In vitro, knockdown endogenous or IFNg-induced Irgm1 significantly decreases the proliferation and increases apoptosis of B16 cells. |
| 942 | 25619828 | In vitro, knockdown endogenous or IFNg-induced Irgm1 significantly decreases the proliferation and increases apoptosis of B16 cells. |
| 943 | 25619828 | In addition, suppressing Irgm1 decreased the IFNg/starvation-induced autophagy, while overexpressing Irgm1 significantly increased autophagy and rescued starvation-challenged cells. |
| 944 | 25619828 | In addition, suppressing Irgm1 decreased the IFNg/starvation-induced autophagy, while overexpressing Irgm1 significantly increased autophagy and rescued starvation-challenged cells. |
| 945 | 25619828 | In addition, suppressing Irgm1 decreased the IFNg/starvation-induced autophagy, while overexpressing Irgm1 significantly increased autophagy and rescued starvation-challenged cells. |
| 946 | 25619828 | In addition, suppressing Irgm1 decreased the IFNg/starvation-induced autophagy, while overexpressing Irgm1 significantly increased autophagy and rescued starvation-challenged cells. |
| 947 | 25619828 | In addition, suppressing Irgm1 decreased the IFNg/starvation-induced autophagy, while overexpressing Irgm1 significantly increased autophagy and rescued starvation-challenged cells. |
| 948 | 25619828 | In addition, suppressing Irgm1 decreased the IFNg/starvation-induced autophagy, while overexpressing Irgm1 significantly increased autophagy and rescued starvation-challenged cells. |
| 949 | 25619828 | Moreover, IFNg and starvation-induced the co-localization of Irgm1 with Bax-interacting factor 1 (Bif-1). |
| 950 | 25619828 | Moreover, IFNg and starvation-induced the co-localization of Irgm1 with Bax-interacting factor 1 (Bif-1). |
| 951 | 25619828 | Moreover, IFNg and starvation-induced the co-localization of Irgm1 with Bax-interacting factor 1 (Bif-1). |
| 952 | 25619828 | Moreover, IFNg and starvation-induced the co-localization of Irgm1 with Bax-interacting factor 1 (Bif-1). |
| 953 | 25619828 | Moreover, IFNg and starvation-induced the co-localization of Irgm1 with Bax-interacting factor 1 (Bif-1). |
| 954 | 25619828 | Moreover, IFNg and starvation-induced the co-localization of Irgm1 with Bax-interacting factor 1 (Bif-1). |
| 955 | 25556651 | Induced expression of FcγRIIIa (CD16a) on CD4+ T cells triggers generation of IFN-γhigh subset. |
| 956 | 25556651 | The ligation of FcγRIIIa by immune complexes (ICs) in human CD4(+) T-cells produced co-stimulatory signal like CD28 that triggered IFN-γ production. |
| 957 | 25535857 | Plasma cytokines were analyzed, and genotyping was conducted for 15 candidate genes involved in cytokine signaling: interferon-gamma (IFNG), IFNG receptor 1 (IFNGR1), interleukins (IL1R2, IL2, IL4, IL6, IL8, IL10, IL13, IL17A), nuclear factor of kappa light polypeptide gene enhancer in B cells (NFKB1 and NFKB2), and tumor necrosis factor alpha (TNFA). |
| 958 | 25535857 | After adjusting for genomic estimates of ancestry, self-reported race/ethnicity and viral load, SOI was associated with higher IL-13 plasma levels and with six single nucleotide polymorphisms (SNPs): IL1B rs1143642 and rs1143623, IL6 rs4719714, IL13 rs1295686, NFKB1 rs4648110, and TNFA rs2857602. |
| 959 | 25496030 | This phase I/II study assessed the safety, immunity and clinical response to 6 or 12 bi-weekly intradermal ImMucin vaccines, co-administered with human granulocyte-macrophage colony-stimulating factor to 15 MUC1-positive multiple myeloma (MM) patients, with residual or biochemically progressive disease following autologous stem cell transplantation. |
| 960 | 25496030 | ImMucin vaccination induced a robust increase in γ-interferon (IFN-γ-producing CD4+ and CD8+ T-cells (≤80-fold), a pronounced population of ImMucin multimer CD8+ T-cells (>2%), a 9·4-fold increase in peripheral blood mononuclear cells proliferation and 6·8-fold increase in anti-ImMucin antibodies, accompanied with T-cell and antibody-dependent cell-mediated cytotoxicity. |
| 961 | 25466928 | Insights into the possible role of IFNG and IFNGR1 in Kala-azar and Post Kala-azar Dermal Leishmaniasis in Sudanese patients. |
| 962 | 25458316 | FAS/FASL-mediated cell death in the bovine endometrium. |
| 963 | 25458316 | FAS/FASL-mediated cell death in the bovine endometrium. |
| 964 | 25458316 | We examined (1) the cyclic expressions of apoptosis-related factors, FAS, DcR3, BCL2 and BAX, in the bovine endometrium and (2) the effect of death ligands on the viability of, and FAS mRNA expression in, cultured bovine endometrial epithelial and stromal cells. |
| 965 | 25458316 | We examined (1) the cyclic expressions of apoptosis-related factors, FAS, DcR3, BCL2 and BAX, in the bovine endometrium and (2) the effect of death ligands on the viability of, and FAS mRNA expression in, cultured bovine endometrial epithelial and stromal cells. |
| 966 | 25458316 | FAS expression did not change during the estrous cycle, whereas DcR3 expression was higher at the mid and late luteal stages than at the early luteal and follicular stages. |
| 967 | 25458316 | FAS expression did not change during the estrous cycle, whereas DcR3 expression was higher at the mid and late luteal stages than at the early luteal and follicular stages. |
| 968 | 25458316 | BCL2 expression was higher at the late luteal stage than at the early luteal and follicular stages, and the BAX/BCL2 ratio was higher at the early luteal stage than at the late luteal stage. |
| 969 | 25458316 | BCL2 expression was higher at the late luteal stage than at the early luteal and follicular stages, and the BAX/BCL2 ratio was higher at the early luteal stage than at the late luteal stage. |
| 970 | 25458316 | Treatment or pretreatment with tumor necrosis factor-α (TNF)+interferon γ (IFNG) in combination with FAS ligand significantly reduced the viability of both epithelial and stromal cells. |
| 971 | 25458316 | Treatment or pretreatment with tumor necrosis factor-α (TNF)+interferon γ (IFNG) in combination with FAS ligand significantly reduced the viability of both epithelial and stromal cells. |
| 972 | 25458316 | Furthermore, TNF+IFNG treatment significantly increased the expression of FAS mRNA in both types of endometrial cells. |
| 973 | 25458316 | Furthermore, TNF+IFNG treatment significantly increased the expression of FAS mRNA in both types of endometrial cells. |
| 974 | 25457680 | The present study was undertaken to evaluate (1) apoptosis measured as the proportions of early apoptotic, late apoptotic, and viable cells; (2) expression of factors involved in the extrinsic (TNFA/TNFα, TNFRSF1A/TNFR1, TNFRSF1B/TNFR2, FAS/Fas, and FASLG/FasL) and intrinsic (CASP3/Casp3, TP53/p-53, BAX/Bax, and BCL2/Bcl-2) apoptotic pathways, with two components of the activating protein-1 complex, i.e., FOS/Fos and JUN/Jun and IFNG/IFNγ; and (3) concentrations of luteal and blood plasma progesterone (P4) throughout the luteal phase of the estrous cycle and early pregnancy. |
| 975 | 25457680 | The present study was undertaken to evaluate (1) apoptosis measured as the proportions of early apoptotic, late apoptotic, and viable cells; (2) expression of factors involved in the extrinsic (TNFA/TNFα, TNFRSF1A/TNFR1, TNFRSF1B/TNFR2, FAS/Fas, and FASLG/FasL) and intrinsic (CASP3/Casp3, TP53/p-53, BAX/Bax, and BCL2/Bcl-2) apoptotic pathways, with two components of the activating protein-1 complex, i.e., FOS/Fos and JUN/Jun and IFNG/IFNγ; and (3) concentrations of luteal and blood plasma progesterone (P4) throughout the luteal phase of the estrous cycle and early pregnancy. |
| 976 | 25457680 | The present study was undertaken to evaluate (1) apoptosis measured as the proportions of early apoptotic, late apoptotic, and viable cells; (2) expression of factors involved in the extrinsic (TNFA/TNFα, TNFRSF1A/TNFR1, TNFRSF1B/TNFR2, FAS/Fas, and FASLG/FasL) and intrinsic (CASP3/Casp3, TP53/p-53, BAX/Bax, and BCL2/Bcl-2) apoptotic pathways, with two components of the activating protein-1 complex, i.e., FOS/Fos and JUN/Jun and IFNG/IFNγ; and (3) concentrations of luteal and blood plasma progesterone (P4) throughout the luteal phase of the estrous cycle and early pregnancy. |
| 977 | 25457680 | Increase (P < 0.05) of TNFA messenger RNA (mRNA) level coincided with that of IFNG on Day 12 of the estrous cycle but not on the corresponding day of pregnancy. |
| 978 | 25457680 | Increase (P < 0.05) of TNFA messenger RNA (mRNA) level coincided with that of IFNG on Day 12 of the estrous cycle but not on the corresponding day of pregnancy. |
| 979 | 25457680 | Increase (P < 0.05) of TNFA messenger RNA (mRNA) level coincided with that of IFNG on Day 12 of the estrous cycle but not on the corresponding day of pregnancy. |
| 980 | 25457680 | The mRNA expression of CASP3, BCL-2 and BAX was unchanged in cyclic and pregnant CL, while level of TP53 increased (P < 0.05) on Day 12 of the estrous cycle versus Day 8. |
| 981 | 25457680 | The mRNA expression of CASP3, BCL-2 and BAX was unchanged in cyclic and pregnant CL, while level of TP53 increased (P < 0.05) on Day 12 of the estrous cycle versus Day 8. |
| 982 | 25457680 | The mRNA expression of CASP3, BCL-2 and BAX was unchanged in cyclic and pregnant CL, while level of TP53 increased (P < 0.05) on Day 12 of the estrous cycle versus Day 8. |
| 983 | 25457680 | The level of FOS and JUN mRNA increased (P < 0.05) on Day 14 of the estrous cycle versus the remaining days. |
| 984 | 25457680 | The level of FOS and JUN mRNA increased (P < 0.05) on Day 14 of the estrous cycle versus the remaining days. |
| 985 | 25457680 | The level of FOS and JUN mRNA increased (P < 0.05) on Day 14 of the estrous cycle versus the remaining days. |
| 986 | 25457680 | The level of FOS and JUN mRNA was significantly higher (P < 0.001 and P < 0.05, respectively) on Day 14 of the estrous cycle than that on the corresponding day of pregnancy. |
| 987 | 25457680 | The level of FOS and JUN mRNA was significantly higher (P < 0.001 and P < 0.05, respectively) on Day 14 of the estrous cycle than that on the corresponding day of pregnancy. |
| 988 | 25457680 | The level of FOS and JUN mRNA was significantly higher (P < 0.001 and P < 0.05, respectively) on Day 14 of the estrous cycle than that on the corresponding day of pregnancy. |
| 989 | 25457680 | In summary, the simultaneous increase of TNFA and IFNG transcript in cyclic CL suggests the crucial role of both cytokines in sensitization of porcine CL to further luteolytic action of PGF2α. |
| 990 | 25457680 | In summary, the simultaneous increase of TNFA and IFNG transcript in cyclic CL suggests the crucial role of both cytokines in sensitization of porcine CL to further luteolytic action of PGF2α. |
| 991 | 25457680 | In summary, the simultaneous increase of TNFA and IFNG transcript in cyclic CL suggests the crucial role of both cytokines in sensitization of porcine CL to further luteolytic action of PGF2α. |
| 992 | 25457680 | The upregulated expression of FAS, FOS, and JUN mRNA in the late luteal phase in cyclic CL can indicate their involvement in structural luteolysis. |
| 993 | 25457680 | The upregulated expression of FAS, FOS, and JUN mRNA in the late luteal phase in cyclic CL can indicate their involvement in structural luteolysis. |
| 994 | 25457680 | The upregulated expression of FAS, FOS, and JUN mRNA in the late luteal phase in cyclic CL can indicate their involvement in structural luteolysis. |
| 995 | 25453950 | Then, we designed scaffolds for bone regeneration based on modifications of decellularized bone for a short release of interferon-gamma (IFNg) to promote the M1 phenotype, followed by a more sustained release of interleukin-4 (IL4) to promote the M2 phenotype. |
| 996 | 25453950 | Then, we designed scaffolds for bone regeneration based on modifications of decellularized bone for a short release of interferon-gamma (IFNg) to promote the M1 phenotype, followed by a more sustained release of interleukin-4 (IL4) to promote the M2 phenotype. |
| 997 | 25453950 | Then, we designed scaffolds for bone regeneration based on modifications of decellularized bone for a short release of interferon-gamma (IFNg) to promote the M1 phenotype, followed by a more sustained release of interleukin-4 (IL4) to promote the M2 phenotype. |
| 998 | 25453950 | To achieve this sequential release profile, IFNg was physically adsorbed onto the scaffolds, while IL4 was attached via biotin-streptavidin binding. |
| 999 | 25453950 | To achieve this sequential release profile, IFNg was physically adsorbed onto the scaffolds, while IL4 was attached via biotin-streptavidin binding. |
| 1000 | 25453950 | To achieve this sequential release profile, IFNg was physically adsorbed onto the scaffolds, while IL4 was attached via biotin-streptavidin binding. |
| 1001 | 25453950 | These scaffolds promoted sequential M1 and M2 polarization of primary human macrophages as measured by gene expression of ten M1 and M2 markers and secretion of four cytokines, although the overlapping phases of IFNg and IL4 release tempered polarization to some extent. |
| 1002 | 25453950 | These scaffolds promoted sequential M1 and M2 polarization of primary human macrophages as measured by gene expression of ten M1 and M2 markers and secretion of four cytokines, although the overlapping phases of IFNg and IL4 release tempered polarization to some extent. |
| 1003 | 25453950 | These scaffolds promoted sequential M1 and M2 polarization of primary human macrophages as measured by gene expression of ten M1 and M2 markers and secretion of four cytokines, although the overlapping phases of IFNg and IL4 release tempered polarization to some extent. |
| 1004 | 25445652 | Interferon-γ (IFNG) microsatellite repeat and single nucleotide polymorphism haplotypes of IFN-α receptor (IFNAR1) associated with enhanced malaria susceptibility in Indian populations. |
| 1005 | 25445652 | One SNP each from the IFNA8 and IFNA17 of IFNA gene cluster had a protective effect in the non-endemic region but not in the endemic region. |
| 1006 | 25411767 | The results showed that PE patients exhibited significantly increased expression levels of the B‑cell receptor genes LYN, CD22, SYK, BTK, PTPRC and NFAM1, whereas expression levels of FYN, FCRL4 and LAX1 were significantly decreased compared to those of the control group. |
| 1007 | 25411767 | Expression levels of T‑cell‑dependent B‑cell‑activation genes, including EMR2, TNFSF9, CD86, ICOSLG, CD37 and CD97, were significantly upregulated in PE patients, whereas SPN mRNA expression was significantly downregulated compared with those of the control group. |
| 1008 | 25411767 | LILRA1 and TLR9 T cell‑independent B‑cell activation mRNAs were significantly upregulated in PE patients compared with those of the control group. |
| 1009 | 25411767 | In addition, the expression levels of B‑cell‑activation regulator genes, including CR1, LILRB4 and VAV1, were significantly increased, whereas SLAMF7 expression levels were significantly decreased in PE patients compared with those of the control group. |
| 1010 | 25411767 | Furthermore, the expression levels of B‑cell‑activation‑associated cytokine genes demonstrated a significant upregulation of LTA and IL10 and downregulation of L1A, IFNA5, IFNA6, IFNA8, IFNA14, IL2, IL13 and IFNG in PE patients compared to those of the control group. |
| 1011 | 25409241 | The aim of the present study was to assess the serum levels of interferon (IFN)-γ and interleukin (IL)-6 and to examine the association of IFN-γ+874 T/A and IL-6-174 G/C cytokine gene polymorphisms. |
| 1012 | 25398328 | Moreover, C/EBPα binds to the Ifng gene and inhibits T-bet-driven Ifng transcription in a DNA binding-dependent manner. |
| 1013 | 25387892 | Combination of 4-1BB agonist and PD-1 antagonist promotes antitumor effector/memory CD8 T cells in a poorly immunogenic tumor model. |
| 1014 | 25387892 | The activity of the anti-4-1BB/anti-PD-1 combination was dependent on IFNγ and CD8(+) T cells. |
| 1015 | 25387892 | Both 4-1BB and PD-1 proteins were elevated on the surface of CD8(+) T cells by anti-4-1BB/anti-PD-1 cotreatment. |
| 1016 | 25387892 | In the tumor microenvironment, an effective antitumor immune response was induced as indicated by the increased CD8(+)/Treg ratio and the enrichment of genes such as Cd3e, Cd8a, Ifng, and Eomes. |
| 1017 | 25366747 | Four candidate genes of the cytokine family (IL2, IL4, IL13, and IFNG) were selected to identify Single Nucleotide Polymorphisms (SNPs) that might be associated with resistance to gastrointestinal endoparasites in goats. |
| 1018 | 25346938 | Depression is a common side-effect of interferon (IFN)-alpha treatment of hepatitis C virus (HCV) infection and melanoma. |
| 1019 | 25346938 | Disturbances of tryptophan (TRP) metabolism might contribute to development of IFN-alpha-associated depression due to IFN-alpha-induced activation of indoleamine 2,3-dioxygenase (IDO), a rate-limiting enzyme of TRP-kynurenine (KYN) metabolism. |
| 1020 | 25346938 | The present study assessed KYN/TRP ratio (KTR) as a marker of IDO activity in American Caucasian HCV patients awaiting IFN-alpha treatment. |
| 1021 | 25346938 | Up-regulation of IDO might be an additional risk factor of IFN-alpha-associated depression. |
| 1022 | 25346938 | Future studies shall explore the causes of elevated serum TRP in relation to IFN-alpha-associated depression. |
| 1023 | 25329659 | In the present study, we demonstrated that only NKG2Chi NK cells expanded in human CMV (HCMV) seropositive individuals underwent epigenetic remodeling of the IFNG conserved non-coding sequence (CNS) 1, similar to memory CD8(+) T cells or T(H)1 cells. |
| 1024 | 25329659 | The accessibility of the CNS1 was required to enhance IFN-γ transcriptional activity in response to NKG2C and 2B4 engagement, which led to consistent IFN-γ production in NKG2C(hi) NK cells. |
| 1025 | 25273529 | BESCs expressed functional IFNG receptors (IFNGR) 1 and 2 but not IFNG ligand. |
| 1026 | 25273529 | BESCs expressed functional IFNG receptors (IFNGR) 1 and 2 but not IFNG ligand. |
| 1027 | 25273529 | BESCs transfected with a new reporter construct made by cloning the bovine indoleamine 2, 3-dioxygenase 1 (IDO1) promoter in front of the luciferase reporter gene responded to exogenous IFNG treatment. |
| 1028 | 25273529 | BESCs transfected with a new reporter construct made by cloning the bovine indoleamine 2, 3-dioxygenase 1 (IDO1) promoter in front of the luciferase reporter gene responded to exogenous IFNG treatment. |
| 1029 | 25266649 | Expression levels of forkhead box protein 3 (FOXP3), interleukin 10 (IL10), interleukin 4 (IL4) and interferon gamma (IFNG) mRNA in lesional and tumour-distant samples from ES-affected horses, as well as in dermal samples of healthy control horses were measured using quantitative reverse transcription polymerase chain reaction (PCR). |
| 1030 | 25266649 | Expression levels of forkhead box protein 3 (FOXP3), interleukin 10 (IL10), interleukin 4 (IL4) and interferon gamma (IFNG) mRNA in lesional and tumour-distant samples from ES-affected horses, as well as in dermal samples of healthy control horses were measured using quantitative reverse transcription polymerase chain reaction (PCR). |
| 1031 | 25266649 | Expression levels of FOXP3, IL10 and IFNG mRNA and BPV-1 E5 copy numbers were significantly increased in lesional compared to tumour-distant samples. |
| 1032 | 25266649 | Expression levels of FOXP3, IL10 and IFNG mRNA and BPV-1 E5 copy numbers were significantly increased in lesional compared to tumour-distant samples. |
| 1033 | 25257094 | Patients who had a platelet response to eradication of the bacteria had higher pre-treatment serum levels of γ-interferon (IFNG, IFN-γ), transforming growth factor-β (TGFB1, TGF-β) and interleukin 17 (IL17A, IL-17) than patients who did not respond, but only higher pre-treatment TGFB1 levels was independently associated with platelet response. |
| 1034 | 25253772 | Hot-spot WAS mutations Thr45Met and Arg86Cys, which result in XLT-to-WAS disease progression, impair recruitment of hBRM- but not BRG1-enriched BAF complexes to IFNG and TBX21 promoters. |
| 1035 | 25248876 | Polymorphisms in TNF and IFNG are associated with clinical characteristics of aplastic anemia in Argentinean population. |
| 1036 | 25248876 | Polymorphisms in TNF and IFNG are associated with clinical characteristics of aplastic anemia in Argentinean population. |
| 1037 | 25248876 | The higher producing IFNG 12 CA-repeat allele showed strong linkage disequilibrium with the + 874T allele, and was associated with a lower hemoglobin level (p = 0.0351). |
| 1038 | 25248876 | The higher producing IFNG 12 CA-repeat allele showed strong linkage disequilibrium with the + 874T allele, and was associated with a lower hemoglobin level (p = 0.0351). |
| 1039 | 25239251 | In the present study we focused on SNPs in cytokine and inflammatory mediator genes: tumor necrosis factor (TNF) -308G>A (rs1800629), interleukin-10 (IL10) -819C>T (rs1800871), interferon-gamma (IFNG) +874T>A (rs2430561), and leukotriene A4 hydrolase (LTA4H) rs1978331, rs17525495 and rs2660898 in a case-control study involving 102 pulmonary tuberculosis patients and 456 controls from Mozambique. |
| 1040 | 25239251 | In the present study we focused on SNPs in cytokine and inflammatory mediator genes: tumor necrosis factor (TNF) -308G>A (rs1800629), interleukin-10 (IL10) -819C>T (rs1800871), interferon-gamma (IFNG) +874T>A (rs2430561), and leukotriene A4 hydrolase (LTA4H) rs1978331, rs17525495 and rs2660898 in a case-control study involving 102 pulmonary tuberculosis patients and 456 controls from Mozambique. |
| 1041 | 25239251 | LTA4H, IL10 and IFNG SNPs showed no associations with pulmonary tuberculosis. |
| 1042 | 25239251 | LTA4H, IL10 and IFNG SNPs showed no associations with pulmonary tuberculosis. |
| 1043 | 25225903 | Expression and DNA methylation of TNF, IFNG and FOXP3 in colorectal cancer and their prognostic significance. |
| 1044 | 25219326 | Molecular landscape of T cell-mediated rejection in human kidney transplants: prominence of CTLA4 and PD ligands. |
| 1045 | 25219326 | Molecular landscape of T cell-mediated rejection in human kidney transplants: prominence of CTLA4 and PD ligands. |
| 1046 | 25219326 | CTLA4, CD28, IFNG), macrophages (e.g. |
| 1047 | 25219326 | CTLA4, CD28, IFNG), macrophages (e.g. |
| 1048 | 25219326 | PDL1, CD86, SLAMF8, ADAMDEC1), B cells (e.g. |
| 1049 | 25219326 | PDL1, CD86, SLAMF8, ADAMDEC1), B cells (e.g. |
| 1050 | 25219326 | CD72, BTLA) and IFNG-treated macrophages (e.g. |
| 1051 | 25219326 | CD72, BTLA) and IFNG-treated macrophages (e.g. |
| 1052 | 25219326 | ANKRD22, AIM2). |
| 1053 | 25219326 | ANKRD22, AIM2). |
| 1054 | 25219326 | In pathway analysis, the top pathways included T cell receptor signaling and CTLA4 costimulation. |
| 1055 | 25219326 | In pathway analysis, the top pathways included T cell receptor signaling and CTLA4 costimulation. |
| 1056 | 25219326 | The prominence of inhibitors like CTLA4 and PDL1 raises the possibility of active negative controls within the rejecting tissue. |
| 1057 | 25219326 | The prominence of inhibitors like CTLA4 and PDL1 raises the possibility of active negative controls within the rejecting tissue. |
| 1058 | 25217635 | A20 regulates atherogenic interferon (IFN)-γ signaling in vascular cells by modulating basal IFNβ levels. |
| 1059 | 25217635 | In gain- and loss-of-function studies, A20 inversely regulated expression of IFNγ-induced atherogenic genes in human EC and SMC by modulating STAT1 transcription. |
| 1060 | 25217635 | Transcriptome analysis of the aortic media from A20 heterozygote versus wild-type mice revealed increased basal Ifnβ signaling as the likely cause for higher Stat1 transcription. |
| 1061 | 25217635 | We confirmed higher basal IFNβ levels in A20-silenced human SMC and showed that neutralization or knockdown of IFNβ abrogates heightened STAT1 levels in these cells. |
| 1062 | 25217635 | Upstream of IFNβ, A20-silenced EC and SMC demonstrated higher levels of phosphorylated/activated TANK-binding kinase-1 (TBK1), a regulator of IFNβ transcription. |
| 1063 | 25217635 | This suggested that A20 knockdown increased STAT1 transcription by enhancing TBK1 activation and subsequently basal IFNβ levels. |
| 1064 | 25217635 | Altogether, these results uncover A20 as a key physiologic regulator of atherogenic IFNγ/STAT1 signaling. |
| 1065 | 25196646 | Inhibition of HO-1 via SnMP in cytomegalovirus (CMV)pp65-peptide-pulsed peripheral blood mononuclear cells (PBMCs) led to increased anti-viral T cell activation and the generation of a higher proportion of effector memory T cells (CD45RA(-) CD62L(-)) with increased capability to secrete interferon (IFN)-γ and granzyme B. |
| 1066 | 25196646 | Compared to control, SnMP treatment resulted in higher cell counts and purity without negative impact on quality and effector function [CD107a, IFN-γ and tumour necrosis factor (TNF)-α levels were stable]. |
| 1067 | 25138705 | The cytokines that were found to fluctuate over the course of the oestrous cycle were colony-stimulating factor (CSF)1, CSF2, interferon gamma (IFNG) and tumour necrosis factor alpha (TNFA), all of which were significantly elevated at oestrus compared with other phases. |
| 1068 | 25138705 | The cytokines that were found to fluctuate over the course of the oestrous cycle were colony-stimulating factor (CSF)1, CSF2, interferon gamma (IFNG) and tumour necrosis factor alpha (TNFA), all of which were significantly elevated at oestrus compared with other phases. |
| 1069 | 25138705 | The cytokines that were found to fluctuate over the course of the oestrous cycle were colony-stimulating factor (CSF)1, CSF2, interferon gamma (IFNG) and tumour necrosis factor alpha (TNFA), all of which were significantly elevated at oestrus compared with other phases. |
| 1070 | 25138705 | The cytokines that were found to fluctuate over the course of the oestrous cycle were colony-stimulating factor (CSF)1, CSF2, interferon gamma (IFNG) and tumour necrosis factor alpha (TNFA), all of which were significantly elevated at oestrus compared with other phases. |
| 1071 | 25138705 | The concentration of serum progesterone during the oestrus phase negatively correlated with the abundance of cytokines CSF3, IL12p40, IFNG and leukaemia inhibitory factor (LIF). |
| 1072 | 25138705 | The concentration of serum progesterone during the oestrus phase negatively correlated with the abundance of cytokines CSF3, IL12p40, IFNG and leukaemia inhibitory factor (LIF). |
| 1073 | 25138705 | The concentration of serum progesterone during the oestrus phase negatively correlated with the abundance of cytokines CSF3, IL12p40, IFNG and leukaemia inhibitory factor (LIF). |
| 1074 | 25138705 | The concentration of serum progesterone during the oestrus phase negatively correlated with the abundance of cytokines CSF3, IL12p40, IFNG and leukaemia inhibitory factor (LIF). |
| 1075 | 25138705 | In ovariectomised mice, exogenous oestradiol administration increased mammary gland CSF1, CSF2, IFNG and LIF, compared with ovariectomised control mice. |
| 1076 | 25138705 | In ovariectomised mice, exogenous oestradiol administration increased mammary gland CSF1, CSF2, IFNG and LIF, compared with ovariectomised control mice. |
| 1077 | 25138705 | In ovariectomised mice, exogenous oestradiol administration increased mammary gland CSF1, CSF2, IFNG and LIF, compared with ovariectomised control mice. |
| 1078 | 25138705 | In ovariectomised mice, exogenous oestradiol administration increased mammary gland CSF1, CSF2, IFNG and LIF, compared with ovariectomised control mice. |
| 1079 | 25138705 | Progesterone administration together with oestradiol resulted in reduced CSF1, CSF3 and IFNG compared with oestradiol administration alone. |
| 1080 | 25138705 | Progesterone administration together with oestradiol resulted in reduced CSF1, CSF3 and IFNG compared with oestradiol administration alone. |
| 1081 | 25138705 | Progesterone administration together with oestradiol resulted in reduced CSF1, CSF3 and IFNG compared with oestradiol administration alone. |
| 1082 | 25138705 | Progesterone administration together with oestradiol resulted in reduced CSF1, CSF3 and IFNG compared with oestradiol administration alone. |
| 1083 | 25060131 | Interleukin-18 and interferon gamma levels in preeclampsia: a systematic review and meta-analysis. |
| 1084 | 25055749 | Serum was analysed for circulating cytokines TNF (tumour necrosis factor), IL-6 (interleukin 6, IFNG (interferon gamma), IL1R1 (interleukin-1 receptor-1). |
| 1085 | 25055749 | Serum was analysed for circulating cytokines TNF (tumour necrosis factor), IL-6 (interleukin 6, IFNG (interferon gamma), IL1R1 (interleukin-1 receptor-1). |
| 1086 | 25055749 | Serum was analysed for circulating cytokines TNF (tumour necrosis factor), IL-6 (interleukin 6, IFNG (interferon gamma), IL1R1 (interleukin-1 receptor-1). |
| 1087 | 25055749 | Expression of VDR (vitamin D receptor) [fold change (FC) 0.52, standard error for fold change (SE) ± 0.08, p = 0.01] and IFNG mRNA (FC 0.31; SE ± 0.19, p = 0.01) were lower in those with higher lean mass. |
| 1088 | 25055749 | Expression of VDR (vitamin D receptor) [fold change (FC) 0.52, standard error for fold change (SE) ± 0.08, p = 0.01] and IFNG mRNA (FC 0.31; SE ± 0.19, p = 0.01) were lower in those with higher lean mass. |
| 1089 | 25055749 | Expression of VDR (vitamin D receptor) [fold change (FC) 0.52, standard error for fold change (SE) ± 0.08, p = 0.01] and IFNG mRNA (FC 0.31; SE ± 0.19, p = 0.01) were lower in those with higher lean mass. |
| 1090 | 25055749 | Expression of IL-6 (FC 0.43; SE ± 0.13, p = 0.02), TNF (FC 0.52; SE ± 0.10, p = 0.02), IL1R1 (FC 0.63; SE ± 0.09, p = 0.04) and MSTN (myostatin) (FC 0.64; SE ± 0.11, p = 0.04) were lower in those with higher grip strength. |
| 1091 | 25055749 | Expression of IL-6 (FC 0.43; SE ± 0.13, p = 0.02), TNF (FC 0.52; SE ± 0.10, p = 0.02), IL1R1 (FC 0.63; SE ± 0.09, p = 0.04) and MSTN (myostatin) (FC 0.64; SE ± 0.11, p = 0.04) were lower in those with higher grip strength. |
| 1092 | 25055749 | Expression of IL-6 (FC 0.43; SE ± 0.13, p = 0.02), TNF (FC 0.52; SE ± 0.10, p = 0.02), IL1R1 (FC 0.63; SE ± 0.09, p = 0.04) and MSTN (myostatin) (FC 0.64; SE ± 0.11, p = 0.04) were lower in those with higher grip strength. |
| 1093 | 25055749 | Significant negative correlations between serum IL-6 (R = -0.29, p = 0.005), TNF (R = -0.24, p = 0.017) and grip strength were demonstrated. |
| 1094 | 25055749 | Significant negative correlations between serum IL-6 (R = -0.29, p = 0.005), TNF (R = -0.24, p = 0.017) and grip strength were demonstrated. |
| 1095 | 25055749 | Significant negative correlations between serum IL-6 (R = -0.29, p = 0.005), TNF (R = -0.24, p = 0.017) and grip strength were demonstrated. |
| 1096 | 25055749 | This novel skeletal muscle gene expression study carried out within a well-characterized epidemiological birth cohort has demonstrated that lower expression of VDR and IFNG is associated with higher lean mass, and lower expression of IL-6, TNF, IL1R1 and myostatin is associated with higher grip strength. |
| 1097 | 25055749 | This novel skeletal muscle gene expression study carried out within a well-characterized epidemiological birth cohort has demonstrated that lower expression of VDR and IFNG is associated with higher lean mass, and lower expression of IL-6, TNF, IL1R1 and myostatin is associated with higher grip strength. |
| 1098 | 25055749 | This novel skeletal muscle gene expression study carried out within a well-characterized epidemiological birth cohort has demonstrated that lower expression of VDR and IFNG is associated with higher lean mass, and lower expression of IL-6, TNF, IL1R1 and myostatin is associated with higher grip strength. |
| 1099 | 25052849 | We found that preexisting levels of transforming growth factor beta (TGF-β) had an inverse correlation with in vivo and in vitro immunologic responses to the AE37 vaccine which were measured as delayed-type hypersensitivity (DTH) and interferon gamma (IFN-γ) production in response to the native HER-2(776-790) (or AE36) peptide, respectively. |
| 1100 | 25045661 | We identified the correlation of miR-9-3p, miR-155-5p, miR-150-3p, and miR-378-3p expression with that of genes involved in immune/inflammatory response (e.g., IFNG and IL17F), apoptosis (e.g., PDCD4 and PTEN), and cell proliferation (e.g., NKX3-1 and GADD45A). |
| 1101 | 25041739 | Dengue virus up-regulates expression of notch ligands Dll1 and Dll4 through interferon-β signalling pathway. |
| 1102 | 25041739 | The real-time PCR data showed that Notch ligand Dll1 was significantly induced in DENV-infected monocytes; and receptor Notch4, ligands Dll1 and Dll4, and target Hes1 were dramatically enhanced in DENV-infected macrophages and dendritic cells. |
| 1103 | 25041739 | In macrophages, induction of Dll1 and Dll4 mediated by DENV2 was increased by treatment with interferon-β (IFN-β), and was impaired by neutralization of IFN-β. |
| 1104 | 25041739 | The DENV-induced Dll1 and Dll4 expression level was decreased by silencing key innate immune molecules, including Toll-like receptor 3 (TLR3), MyD88, RIG-I and IPS-I. |
| 1105 | 25041739 | In IFN-receptor-depleted macrophages, the Dll1 and Dll4 induction was significantly alleviated. |
| 1106 | 25041739 | Functionally, activation of Notch signalling by Dll1 in CD4(+) T cells enhanced the expression of a T helper type 1 (Th1) cytokine IFN-γ, while Notch activation in macrophages had no direct effect on replication of DENV. |
| 1107 | 25038949 | Effect of arginine or glutamine supplementation on production, organ weights, interferon gamma, interleukin 6 and antibody titre of broilers. |
| 1108 | 25038949 | Effect of arginine or glutamine supplementation on production, organ weights, interferon gamma, interleukin 6 and antibody titre of broilers. |
| 1109 | 25038949 | Effect of arginine or glutamine supplementation on production, organ weights, interferon gamma, interleukin 6 and antibody titre of broilers. |
| 1110 | 25038949 | Ten and 21 days after immunisation blood samples were collected to determine the anti-albumin IgY titre, interleukin 6 (IL6) and interferon gamma (IFNG) and to measure the weight of the liver, spleen, bursa of Fabricius and thymus. |
| 1111 | 25038949 | Ten and 21 days after immunisation blood samples were collected to determine the anti-albumin IgY titre, interleukin 6 (IL6) and interferon gamma (IFNG) and to measure the weight of the liver, spleen, bursa of Fabricius and thymus. |
| 1112 | 25038949 | Ten and 21 days after immunisation blood samples were collected to determine the anti-albumin IgY titre, interleukin 6 (IL6) and interferon gamma (IFNG) and to measure the weight of the liver, spleen, bursa of Fabricius and thymus. |
| 1113 | 25038949 | Supplementations with Arg and Gln did not influence the IL6 and IFNG level of the blood; however, on day 10 after immunisation these two parameters showed a negative correlation with each other. |
| 1114 | 25038949 | Supplementations with Arg and Gln did not influence the IL6 and IFNG level of the blood; however, on day 10 after immunisation these two parameters showed a negative correlation with each other. |
| 1115 | 25038949 | Supplementations with Arg and Gln did not influence the IL6 and IFNG level of the blood; however, on day 10 after immunisation these two parameters showed a negative correlation with each other. |
| 1116 | 25022448 | Polymorphisms in cytokine genes IL6, TNF, IL10, IL17A and IFNG influence susceptibility to complicated skin and skin structure infections. |
| 1117 | 25022448 | Polymorphisms in cytokine genes IL6, TNF, IL10, IL17A and IFNG influence susceptibility to complicated skin and skin structure infections. |
| 1118 | 25022448 | Polymorphisms in cytokine genes IL6, TNF, IL10, IL17A and IFNG influence susceptibility to complicated skin and skin structure infections. |
| 1119 | 25022448 | For the association study, 318 patients with cSSSI and 328 healthy controls were genotyped for single nucleotide polymorphisms (SNPs) in cytokine genes IL1A, IL1B, IL1RN, TNF, IL10, IL17A, IL17F and IFNG. |
| 1120 | 25022448 | For the association study, 318 patients with cSSSI and 328 healthy controls were genotyped for single nucleotide polymorphisms (SNPs) in cytokine genes IL1A, IL1B, IL1RN, TNF, IL10, IL17A, IL17F and IFNG. |
| 1121 | 25022448 | For the association study, 318 patients with cSSSI and 328 healthy controls were genotyped for single nucleotide polymorphisms (SNPs) in cytokine genes IL1A, IL1B, IL1RN, TNF, IL10, IL17A, IL17F and IFNG. |
| 1122 | 25022448 | Polymorphisms IL6 rs1800797, TNF rs1800629, IL10 rs1800871, IL17A rs8193036 and IFNG rs2069705 influenced susceptibility to cSSSIs. |
| 1123 | 25022448 | Polymorphisms IL6 rs1800797, TNF rs1800629, IL10 rs1800871, IL17A rs8193036 and IFNG rs2069705 influenced susceptibility to cSSSIs. |
| 1124 | 25022448 | Polymorphisms IL6 rs1800797, TNF rs1800629, IL10 rs1800871, IL17A rs8193036 and IFNG rs2069705 influenced susceptibility to cSSSIs. |
| 1125 | 25022448 | No association with cSSSIs was observed for polymorphisms IL1A rs17561 and rs1800587, IL1B rs16944 and rs1143627, IL1RN rs4251961, TNF rs361525, IL10 rs1800896, IL17A rs2275913 and IL17F rs763780. |
| 1126 | 25022448 | No association with cSSSIs was observed for polymorphisms IL1A rs17561 and rs1800587, IL1B rs16944 and rs1143627, IL1RN rs4251961, TNF rs361525, IL10 rs1800896, IL17A rs2275913 and IL17F rs763780. |
| 1127 | 25022448 | No association with cSSSIs was observed for polymorphisms IL1A rs17561 and rs1800587, IL1B rs16944 and rs1143627, IL1RN rs4251961, TNF rs361525, IL10 rs1800896, IL17A rs2275913 and IL17F rs763780. |
| 1128 | 25022448 | In conclusion, polymorphisms in IL6, TNF, IL10, IL17A and IFNG are associated with susceptibility to cSSSIs. |
| 1129 | 25022448 | In conclusion, polymorphisms in IL6, TNF, IL10, IL17A and IFNG are associated with susceptibility to cSSSIs. |
| 1130 | 25022448 | In conclusion, polymorphisms in IL6, TNF, IL10, IL17A and IFNG are associated with susceptibility to cSSSIs. |
| 1131 | 24951427 | The epigenetic silencing of cytokine genes is associated with the repressive H3K27 trimethylation mark, mediated by the Ezh2 or Ezh1 methyltransferase components of the polycomb repressive complex 2 (PRC2). |
| 1132 | 24951427 | The epigenetic silencing of cytokine genes is associated with the repressive H3K27 trimethylation mark, mediated by the Ezh2 or Ezh1 methyltransferase components of the polycomb repressive complex 2 (PRC2). |
| 1133 | 24951427 | Here we show that silencing of the Ifng, Gata3, and Il10 loci in naïve CD4(+) T cells is dependent on Ezh2. |
| 1134 | 24951427 | Here we show that silencing of the Ifng, Gata3, and Il10 loci in naïve CD4(+) T cells is dependent on Ezh2. |
| 1135 | 24951427 | Naïve CD4(+) T cells lacking Ezh2 were epigenetically primed for overproduction of IFN-γ in Th2 and iTreg and IL-10 in Th2 cells. |
| 1136 | 24951427 | Naïve CD4(+) T cells lacking Ezh2 were epigenetically primed for overproduction of IFN-γ in Th2 and iTreg and IL-10 in Th2 cells. |
| 1137 | 24951427 | In addition, deficiency of Ezh2 accelerated effector Th cell death via death receptor-mediated extrinsic and intrinsic apoptotic pathways, confirmed in vivo for Ezh2-null IFN-γ-producing CD4(+) and CD8(+) T cells responding to Listeria monocytogenes infection. |
| 1138 | 24951427 | In addition, deficiency of Ezh2 accelerated effector Th cell death via death receptor-mediated extrinsic and intrinsic apoptotic pathways, confirmed in vivo for Ezh2-null IFN-γ-producing CD4(+) and CD8(+) T cells responding to Listeria monocytogenes infection. |
| 1139 | 24935968 | MAPKAP kinase 3 suppresses Ifng gene expression and attenuates NK cell cytotoxicity and Th1 CD4 T-cell development upon influenza A virus infection. |
| 1140 | 24935968 | MAPKAP kinase 3 suppresses Ifng gene expression and attenuates NK cell cytotoxicity and Th1 CD4 T-cell development upon influenza A virus infection. |
| 1141 | 24935968 | MAPKAP kinase 3 suppresses Ifng gene expression and attenuates NK cell cytotoxicity and Th1 CD4 T-cell development upon influenza A virus infection. |
| 1142 | 24935968 | MK2 and MK3 are downstream targets of p38 and ERK1/2. |
| 1143 | 24935968 | MK2 and MK3 are downstream targets of p38 and ERK1/2. |
| 1144 | 24935968 | MK2 and MK3 are downstream targets of p38 and ERK1/2. |
| 1145 | 24935968 | Using Mk-deficient and wild-type (WT) mice, we demonstrated an inhibitory effect of MK3, but not of MK2, on interferon (IFN)-γ expression in T and NK lymphocytes. |
| 1146 | 24935968 | Using Mk-deficient and wild-type (WT) mice, we demonstrated an inhibitory effect of MK3, but not of MK2, on interferon (IFN)-γ expression in T and NK lymphocytes. |
| 1147 | 24935968 | Using Mk-deficient and wild-type (WT) mice, we demonstrated an inhibitory effect of MK3, but not of MK2, on interferon (IFN)-γ expression in T and NK lymphocytes. |
| 1148 | 24935968 | The results provided evidence that the inhibitory effect of MK3 is based on negative feedback phosphorylation of p38 and ERK1/2, which causes decreased binding of Stat4 to the IFN-γ promoter and reduced expression of IFN-γ mRNA and protein. |
| 1149 | 24935968 | The results provided evidence that the inhibitory effect of MK3 is based on negative feedback phosphorylation of p38 and ERK1/2, which causes decreased binding of Stat4 to the IFN-γ promoter and reduced expression of IFN-γ mRNA and protein. |
| 1150 | 24935968 | The results provided evidence that the inhibitory effect of MK3 is based on negative feedback phosphorylation of p38 and ERK1/2, which causes decreased binding of Stat4 to the IFN-γ promoter and reduced expression of IFN-γ mRNA and protein. |
| 1151 | 24935968 | The reduced disease severity in the Mk3(-/-) mice was accompanied by a >10-fold reduction in viral lung titer and an increase in the number of activated NK cells and enhanced Th1 activation of CD4 T cells. |
| 1152 | 24935968 | The reduced disease severity in the Mk3(-/-) mice was accompanied by a >10-fold reduction in viral lung titer and an increase in the number of activated NK cells and enhanced Th1 activation of CD4 T cells. |
| 1153 | 24935968 | The reduced disease severity in the Mk3(-/-) mice was accompanied by a >10-fold reduction in viral lung titer and an increase in the number of activated NK cells and enhanced Th1 activation of CD4 T cells. |
| 1154 | 24911453 | B-cell-activating factor, a proliferation inducing ligand and co-stimulatory molecules in the pathogenesis of immune thrombocytopenia in childhood. |
| 1155 | 24911453 | The aim of this study was to measure the levels of B-cell-activating factor (BAFF), a proliferation-inducing ligand (APRIL), and co-stimulatory molecules in immune thrombocytopenia (ITP) of childhood to investigate the interaction between T and B lymphocytes and the impact of proliferation of B lymphocytes in the pathogenesis. |
| 1156 | 24911453 | Hemogram, BAFF, APRIL, interleukin-4, and interferon (IFN)-γ levels in sera and expressions of CD19, CD 3, CD21, CD40, and CD 154 on leukocytes were measured by ELISA and flow cytometry. |
| 1157 | 24911453 | APRIL, interleukin-4, and IFN-γ in newly diagnosed ITP group and BAFF, APRIL, interleukin-4, and IFN-γ in chronic ITP group were similar before and after treatment. |
| 1158 | 24911453 | There was no statistical difference for expressions of CD 19 and CD3 on lymphocytes, CD40 on leukocytes, CD154 on T cells, and for percentages of CD21/CD40, CD21/CD40, CD21/CD40 B cells, and CD19/CD3 lymphocytes for pretreatment and posttreatment levels in both ITP groups. |
| 1159 | 24901046 | Apolipoprotein L1 and apolipoprotein L6 have been recently described as novel pro-death BH3-only proteins that are also capable of regulating autophagy. |
| 1160 | 24901046 | Apolipoprotein L1 and apolipoprotein L6 have been recently described as novel pro-death BH3-only proteins that are also capable of regulating autophagy. |
| 1161 | 24901046 | In an in-silico screening to discover novel putative BH3-only proteins, we identified yet another member of the apolipoprotein L family, apolipoprotein L2 (ApoL2), as a BH3 motif-containing protein. |
| 1162 | 24901046 | In an in-silico screening to discover novel putative BH3-only proteins, we identified yet another member of the apolipoprotein L family, apolipoprotein L2 (ApoL2), as a BH3 motif-containing protein. |
| 1163 | 24901046 | ApoL2 has been suggested to behave as a BH3-only protein and mediate cell death induced by interferon-gamma or viral infection. |
| 1164 | 24901046 | ApoL2 has been suggested to behave as a BH3-only protein and mediate cell death induced by interferon-gamma or viral infection. |
| 1165 | 24901046 | As previously described, we observed that ApoL2 protein was induced by interferon-gamma. |
| 1166 | 24901046 | As previously described, we observed that ApoL2 protein was induced by interferon-gamma. |
| 1167 | 24901046 | ApoL2 did not sensitize or protect cells from overexpression of the BH3-only proteins Bmf or Noxa. |
| 1168 | 24901046 | ApoL2 did not sensitize or protect cells from overexpression of the BH3-only proteins Bmf or Noxa. |
| 1169 | 24901046 | We could, however, detect a weak interaction between ApoL2 and Bcl-2 by immunoprecipitation of the former, suggesting a role of ApoL2 in a Bcl-2-regulated process like autophagy. |
| 1170 | 24901046 | We could, however, detect a weak interaction between ApoL2 and Bcl-2 by immunoprecipitation of the former, suggesting a role of ApoL2 in a Bcl-2-regulated process like autophagy. |
| 1171 | 24901046 | However, in contrast to what has been described about its homologs ApoL1 and ApoL6, ApoL2 did not regulate autophagy. |
| 1172 | 24901046 | However, in contrast to what has been described about its homologs ApoL1 and ApoL6, ApoL2 did not regulate autophagy. |
| 1173 | 24876666 | Interaction with mesenchymal stem cells provokes natural killer cells for enhanced IL-12/IL-18-induced interferon-gamma secretion. |
| 1174 | 24876666 | Interaction with mesenchymal stem cells provokes natural killer cells for enhanced IL-12/IL-18-induced interferon-gamma secretion. |
| 1175 | 24876666 | After stimulation with interleukin- (IL-) 12 and IL-18 natural killer (NK) cells secrete the proinflammatory cytokine interferon- (IFN-) γ. |
| 1176 | 24876666 | After stimulation with interleukin- (IL-) 12 and IL-18 natural killer (NK) cells secrete the proinflammatory cytokine interferon- (IFN-) γ. |
| 1177 | 24876666 | MSC enhanced the ability of IL-12/IL-18-stimulated NK cells to secrete IFN- γ in a dose-dependent manner. |
| 1178 | 24876666 | MSC enhanced the ability of IL-12/IL-18-stimulated NK cells to secrete IFN- γ in a dose-dependent manner. |
| 1179 | 24876666 | Alterations in the IL-12 signaling pathway including an increased expression of the IL-12β1 receptor subunit and an increased phosphorylation of signal transducer and activator of transcription 4 (STAT4) could be observed. |
| 1180 | 24876666 | Alterations in the IL-12 signaling pathway including an increased expression of the IL-12β1 receptor subunit and an increased phosphorylation of signal transducer and activator of transcription 4 (STAT4) could be observed. |
| 1181 | 24872192 | Accordingly, an isolated deficiency of nuclear-WASp is sufficient to impair the transcriptional reprogramming of TBX21 and IFNG promoters in TH1-skewed cells, whereas an isolated deficiency of cytosolic-WASp does not impair this process. |
| 1182 | 24872192 | In contrast, nuclear presence of WASp in TH2-skewed cells is small, and its loss does not impair transcriptional reprogramming of GATA3 and IL4 promoters. |
| 1183 | 24872192 | Our study unveils an ARP2/3:VCA-independent function of nuclear-WASp in TH1 gene activation that is uncoupled from its cytoplasmic role in actin polymerization. |
| 1184 | 24850427 | SIRT1, a class III NAD+-dependent deacetylase, regulates negatively the expression of various proteins involved in the control of immune-inflammatory pathways, such as Stat3, Smad7, and NF-κB. |
| 1185 | 24850427 | SIRT1 expression was downregulated in control LPMC by tumor necrosis factor (TNF)-α and interleukin (IL)-21, and upregulated in IBD LPMC by neutralizing TNF-α and IL-21antibodies. |
| 1186 | 24850427 | Treatment of IBD LPMC with Cay10591, a specific SIRT1 activator, reduced NF-κB activation and inhibited inflammatory cytokine synthesis, whereas Ex527, an inhibitor of SIRT1, increased interferon (IFN)-γ in control LPMC. |
| 1187 | 24829028 | Analysis of intracellular cytokines indicated that midcycle luteal cells increased the proportion of γδ(+) cells containing interleukin 10 (P < 0.05), but reduced the proportion of γδ(+) cells containing interferon gamma (IFNG; P < 0.05). |
| 1188 | 24829028 | There were no changes in the proportions of γδ(+) cells synthesizing interleukin 4 or tumor necrosis factor. |
| 1189 | 24812901 | [Effect of Qiju Dihuang Pill on serum levels of IFN-gamma and IL-4 in pregnant women of Gan-Shen yin deficiency syndrome]. |
| 1190 | 24808182 | Myelin oligodendrocyte glycoprotein-specific T cells in culture exhibited an increased expression of Il17a, Ifng, Rorc, and Tbet after treatment with recombinant LCN2 protein. |
| 1191 | 24808182 | Moreover, LCN2-treated glial cells expressed higher levels of proinflammatory cytokines, chemokines, and MMP-9. |
| 1192 | 24778443 | IFN-γ-producing CD4+ T cells promote generation of protective germinal center-derived IgM+ B cell memory against Salmonella Typhi. |
| 1193 | 24778443 | Genetic ablation of individual cytokine receptors revealed that both IFN-γ and IL-17 are required for optimal germinal center reactions and production of porin-specific memory IgM(+) B cells. |
| 1194 | 24776844 | Nineteen functional polymorphisms that alter the NFκB-mediated inflammatory response (TLR2 (rs3804099, rs11938228, rs1816702, rs4696480), TLR4 (rs5030728, rs1554973), TLR9 (rs187084, rs352139), LY96 (MD-2) (rs11465996), CD14 (rs2569190), MAP3K14 (NIK) (rs7222094)), TNF-α signaling (TNFA (TNF-α) (rs361525), TNFRSF1A (TNFR1) (rs4149570), TNFAIP3(A20) (rs6927172)) and other cytokines regulated by NFκB (IL1B (rs4848306), IL1RN (rs4251961), IL6 (rs10499563), IL17A (rs2275913), IFNG (rs2430561)) were associated with response to anti-TNF therapy among patients with CD, UC or both CD and UC (P ⩽ 0.05). |
| 1195 | 24776844 | In addition, the cytokines IL-1β, IL-6 and IFN-γ may be potential targets for treating patients with IBD who do not respond to anti-TNF therapy. |
| 1196 | 24752800 | Conversely, acquisition of IFN-γ-competence in CD4(+) T helper cells requires a differentiation process from naïve toward type 1 (Th1) cells, which is associated with epigenetic remodeling at the IFNG locus. |
| 1197 | 24752800 | Conversely, acquisition of IFN-γ-competence in CD4(+) T helper cells requires a differentiation process from naïve toward type 1 (Th1) cells, which is associated with epigenetic remodeling at the IFNG locus. |
| 1198 | 24752800 | Conversely, acquisition of IFN-γ-competence in CD4(+) T helper cells requires a differentiation process from naïve toward type 1 (Th1) cells, which is associated with epigenetic remodeling at the IFNG locus. |
| 1199 | 24752800 | Moreover, during the differentiation process NK cells gradually display increasing expression of IFNG and TBX21 (encoding T-bet) transcripts and demethylation at the IFNG promoter. |
| 1200 | 24752800 | Moreover, during the differentiation process NK cells gradually display increasing expression of IFNG and TBX21 (encoding T-bet) transcripts and demethylation at the IFNG promoter. |
| 1201 | 24752800 | Moreover, during the differentiation process NK cells gradually display increasing expression of IFNG and TBX21 (encoding T-bet) transcripts and demethylation at the IFNG promoter. |
| 1202 | 24752800 | Thus, we propose that in order to efficiently produce IFN-γ in response to infected or transformed cells, NK cells gain Th1-like features, such as higher IFN-γ competence and epigenetic remodeling of the IFNG promoter, during their terminal differentiation. |
| 1203 | 24752800 | Thus, we propose that in order to efficiently produce IFN-γ in response to infected or transformed cells, NK cells gain Th1-like features, such as higher IFN-γ competence and epigenetic remodeling of the IFNG promoter, during their terminal differentiation. |
| 1204 | 24752800 | Thus, we propose that in order to efficiently produce IFN-γ in response to infected or transformed cells, NK cells gain Th1-like features, such as higher IFN-γ competence and epigenetic remodeling of the IFNG promoter, during their terminal differentiation. |
| 1205 | 24751285 | IFNG, TLR1), or by sampling exons from genes spaced evenly across chromosomes. |
| 1206 | 24748505 | Serum APRIL, interleukin-17 (IL-17), IL-4 and interferon gamma (IFN-γ) levels were measured in forty patients with SLE and 30 healthy controls. |
| 1207 | 24748505 | Significant positive correlations between serum levels of APRIL and IL-17 and IFN-γ and a negative correlation between serum levels of APRIL and IL-4 were found. |
| 1208 | 24680779 | Genetic polymorphisms of IFNG and IFNGR1 in association with the risk of pulmonary tuberculosis. |
| 1209 | 24657288 | Blood hematocrit and iron, footpad size, parasite load and concentration of IFNG, IL4 and IL10 by ELISA were measured in the treated and untreated mice. |
| 1210 | 24657288 | Moreover, lower levels of IL4 and IL10 and higher ratios of IFNG/IL4 or IFNG/IL10 were shown in the treated, compared to the untreated mice. |
| 1211 | 24632226 | Plasma cytokines were analyzed, and genotyping was conducted for 15 candidate genes involved in cytokine signaling: interferon-gamma (IFNG), IFNG receptor 1 (IFNGR1), interleukins (IL), nuclear factor of kappa light polypeptide gene enhancer in B cells (NFKB-1 and -2), and tumor necrosis factor alpha (TNFA). |
| 1212 | 24632226 | Controlling for genomic estimates of ancestry and self-reported race/ethnicity and gender, the high fatigue pattern was associated with five single nucleotide polymorphisms (SNPs): IL1B rs1071676 and rs1143627, IL4 rs2243274, and TNFA rs1800683 and rs1041981. |
| 1213 | 24632226 | The IL1B and TNFA polymorphisms were not associated with plasma levels of IL-1β or TNFα, respectively. |
| 1214 | 24578067 | When isolating splenic CD4(+) T cells from mice infected with the parasitic helminth Schistosoma mansoni, we observed a defined population of IFN-γ/IL-4 double-positive cells. |
| 1215 | 24578067 | These IFN-γ(+) IL-4(+) cells showed differences in DNA methylation at the Ifng and Il4 loci when compared with IFN-γ(+) IL-4(-) (Th1) and IFN-γ(-) IL-4(+) (Th2) cells, demonstrating that they represent a distinct effector cell population. |
| 1216 | 24578067 | IFN-γ(+) IL-4(+) cells also displayed a discrete DNA methylation pattern at a CpG island within the body of the Gata3 gene, which encodes the master regulator of Th2 identity. |
| 1217 | 24530058 | T helper 17 (Th17) cells can give rise to interleukin-17A (IL-17A)- and interferon (IFN)-γ-double-producing cells that are implicated in development of autoimmune diseases. |
| 1218 | 24530058 | T helper 17 (Th17) cells can give rise to interleukin-17A (IL-17A)- and interferon (IFN)-γ-double-producing cells that are implicated in development of autoimmune diseases. |
| 1219 | 24530058 | T helper 17 (Th17) cells can give rise to interleukin-17A (IL-17A)- and interferon (IFN)-γ-double-producing cells that are implicated in development of autoimmune diseases. |
| 1220 | 24530058 | T helper 17 (Th17) cells can give rise to interleukin-17A (IL-17A)- and interferon (IFN)-γ-double-producing cells that are implicated in development of autoimmune diseases. |
| 1221 | 24530058 | T helper 17 (Th17) cells can give rise to interleukin-17A (IL-17A)- and interferon (IFN)-γ-double-producing cells that are implicated in development of autoimmune diseases. |
| 1222 | 24530058 | We found that coexpression of the Th1 and Th17 cell master transcription factors, T-bet and retinoid-related orphan receptor gamma-t (RORγt), respectively, did not generate Th cells with robust IL-17 and IFN-γ expression. |
| 1223 | 24530058 | We found that coexpression of the Th1 and Th17 cell master transcription factors, T-bet and retinoid-related orphan receptor gamma-t (RORγt), respectively, did not generate Th cells with robust IL-17 and IFN-γ expression. |
| 1224 | 24530058 | We found that coexpression of the Th1 and Th17 cell master transcription factors, T-bet and retinoid-related orphan receptor gamma-t (RORγt), respectively, did not generate Th cells with robust IL-17 and IFN-γ expression. |
| 1225 | 24530058 | We found that coexpression of the Th1 and Th17 cell master transcription factors, T-bet and retinoid-related orphan receptor gamma-t (RORγt), respectively, did not generate Th cells with robust IL-17 and IFN-γ expression. |
| 1226 | 24530058 | We found that coexpression of the Th1 and Th17 cell master transcription factors, T-bet and retinoid-related orphan receptor gamma-t (RORγt), respectively, did not generate Th cells with robust IL-17 and IFN-γ expression. |
| 1227 | 24530058 | Instead, development of IFN-γ-producing Th17 cells required T-bet and Runx1 or Runx3. |
| 1228 | 24530058 | Instead, development of IFN-γ-producing Th17 cells required T-bet and Runx1 or Runx3. |
| 1229 | 24530058 | Instead, development of IFN-γ-producing Th17 cells required T-bet and Runx1 or Runx3. |
| 1230 | 24530058 | Instead, development of IFN-γ-producing Th17 cells required T-bet and Runx1 or Runx3. |
| 1231 | 24530058 | Instead, development of IFN-γ-producing Th17 cells required T-bet and Runx1 or Runx3. |
| 1232 | 24530058 | IL-12-stimulated Th17 cells upregulated Runx1, which bound to the Ifng locus in a T-bet-dependent manner. |
| 1233 | 24530058 | IL-12-stimulated Th17 cells upregulated Runx1, which bound to the Ifng locus in a T-bet-dependent manner. |
| 1234 | 24530058 | IL-12-stimulated Th17 cells upregulated Runx1, which bound to the Ifng locus in a T-bet-dependent manner. |
| 1235 | 24530058 | IL-12-stimulated Th17 cells upregulated Runx1, which bound to the Ifng locus in a T-bet-dependent manner. |
| 1236 | 24530058 | IL-12-stimulated Th17 cells upregulated Runx1, which bound to the Ifng locus in a T-bet-dependent manner. |
| 1237 | 24530058 | Reciprocally, T-bet or Runx1 deficiency or inhibition of Runx transcriptional activity impaired the development of IFN-γ-producing Th17 cells during experimental autoimmune encephalomyelitis, which correlated with substantially ameliorated disease course. |
| 1238 | 24530058 | Reciprocally, T-bet or Runx1 deficiency or inhibition of Runx transcriptional activity impaired the development of IFN-γ-producing Th17 cells during experimental autoimmune encephalomyelitis, which correlated with substantially ameliorated disease course. |
| 1239 | 24530058 | Reciprocally, T-bet or Runx1 deficiency or inhibition of Runx transcriptional activity impaired the development of IFN-γ-producing Th17 cells during experimental autoimmune encephalomyelitis, which correlated with substantially ameliorated disease course. |
| 1240 | 24530058 | Reciprocally, T-bet or Runx1 deficiency or inhibition of Runx transcriptional activity impaired the development of IFN-γ-producing Th17 cells during experimental autoimmune encephalomyelitis, which correlated with substantially ameliorated disease course. |
| 1241 | 24530058 | Reciprocally, T-bet or Runx1 deficiency or inhibition of Runx transcriptional activity impaired the development of IFN-γ-producing Th17 cells during experimental autoimmune encephalomyelitis, which correlated with substantially ameliorated disease course. |
| 1242 | 24530058 | Thus, our studies identify a critical role for T-bet and Runx transcription factors in the generation of pathogenic IFN-γ-producing Th17 cells. |
| 1243 | 24530058 | Thus, our studies identify a critical role for T-bet and Runx transcription factors in the generation of pathogenic IFN-γ-producing Th17 cells. |
| 1244 | 24530058 | Thus, our studies identify a critical role for T-bet and Runx transcription factors in the generation of pathogenic IFN-γ-producing Th17 cells. |
| 1245 | 24530058 | Thus, our studies identify a critical role for T-bet and Runx transcription factors in the generation of pathogenic IFN-γ-producing Th17 cells. |
| 1246 | 24530058 | Thus, our studies identify a critical role for T-bet and Runx transcription factors in the generation of pathogenic IFN-γ-producing Th17 cells. |
| 1247 | 24527586 | [The over-expression of STAT1 and IFN-gamma in lesions of human oral lichen planus]. |
| 1248 | 24505407 | The induction of a balanced Th1 and Th17 response, together with expression of effector cytokines, such as IFNG, IL2, IL17, IL21 and IL22, could be used as correlates of a protective host response. |
| 1249 | 24478392 | Synergistic effect of interferon-gamma and tumor necrosis factor-alpha on coxsackievirus and adenovirus receptor expression: an explanation of cell sloughing during testicular inflammation in mice. |
| 1250 | 24478392 | Synergistic effect of interferon-gamma and tumor necrosis factor-alpha on coxsackievirus and adenovirus receptor expression: an explanation of cell sloughing during testicular inflammation in mice. |
| 1251 | 24478392 | Synergistic effect of interferon-gamma and tumor necrosis factor-alpha on coxsackievirus and adenovirus receptor expression: an explanation of cell sloughing during testicular inflammation in mice. |
| 1252 | 24478392 | Synergistic effect of interferon-gamma and tumor necrosis factor-alpha on coxsackievirus and adenovirus receptor expression: an explanation of cell sloughing during testicular inflammation in mice. |
| 1253 | 24478392 | Synergistic effect of interferon-gamma and tumor necrosis factor-alpha on coxsackievirus and adenovirus receptor expression: an explanation of cell sloughing during testicular inflammation in mice. |
| 1254 | 24478392 | Synergistic effect of interferon-gamma and tumor necrosis factor-alpha on coxsackievirus and adenovirus receptor expression: an explanation of cell sloughing during testicular inflammation in mice. |
| 1255 | 24478392 | Synergistic effect of interferon-gamma and tumor necrosis factor-alpha on coxsackievirus and adenovirus receptor expression: an explanation of cell sloughing during testicular inflammation in mice. |
| 1256 | 24478392 | Synergistic effect of interferon-gamma and tumor necrosis factor-alpha on coxsackievirus and adenovirus receptor expression: an explanation of cell sloughing during testicular inflammation in mice. |
| 1257 | 24478392 | Synergistic effect of interferon-gamma and tumor necrosis factor-alpha on coxsackievirus and adenovirus receptor expression: an explanation of cell sloughing during testicular inflammation in mice. |
| 1258 | 24478392 | Synergistic effect of interferon-gamma and tumor necrosis factor-alpha on coxsackievirus and adenovirus receptor expression: an explanation of cell sloughing during testicular inflammation in mice. |
| 1259 | 24478392 | Interferon-gamma (IFNG) and tumor necrosis factor alpha (TNF) are two major cytokines that are elevated during testicular inflammation and cause reduced fertility. |
| 1260 | 24478392 | Interferon-gamma (IFNG) and tumor necrosis factor alpha (TNF) are two major cytokines that are elevated during testicular inflammation and cause reduced fertility. |
| 1261 | 24478392 | Interferon-gamma (IFNG) and tumor necrosis factor alpha (TNF) are two major cytokines that are elevated during testicular inflammation and cause reduced fertility. |
| 1262 | 24478392 | Interferon-gamma (IFNG) and tumor necrosis factor alpha (TNF) are two major cytokines that are elevated during testicular inflammation and cause reduced fertility. |
| 1263 | 24478392 | Interferon-gamma (IFNG) and tumor necrosis factor alpha (TNF) are two major cytokines that are elevated during testicular inflammation and cause reduced fertility. |
| 1264 | 24478392 | Interferon-gamma (IFNG) and tumor necrosis factor alpha (TNF) are two major cytokines that are elevated during testicular inflammation and cause reduced fertility. |
| 1265 | 24478392 | Interferon-gamma (IFNG) and tumor necrosis factor alpha (TNF) are two major cytokines that are elevated during testicular inflammation and cause reduced fertility. |
| 1266 | 24478392 | Interferon-gamma (IFNG) and tumor necrosis factor alpha (TNF) are two major cytokines that are elevated during testicular inflammation and cause reduced fertility. |
| 1267 | 24478392 | Interferon-gamma (IFNG) and tumor necrosis factor alpha (TNF) are two major cytokines that are elevated during testicular inflammation and cause reduced fertility. |
| 1268 | 24478392 | Interferon-gamma (IFNG) and tumor necrosis factor alpha (TNF) are two major cytokines that are elevated during testicular inflammation and cause reduced fertility. |
| 1269 | 24478392 | We investigated the mechanism by which IFNG and TNF exert their disruptive effects on testicular cell adhesion. |
| 1270 | 24478392 | We investigated the mechanism by which IFNG and TNF exert their disruptive effects on testicular cell adhesion. |
| 1271 | 24478392 | We investigated the mechanism by which IFNG and TNF exert their disruptive effects on testicular cell adhesion. |
| 1272 | 24478392 | We investigated the mechanism by which IFNG and TNF exert their disruptive effects on testicular cell adhesion. |
| 1273 | 24478392 | We investigated the mechanism by which IFNG and TNF exert their disruptive effects on testicular cell adhesion. |
| 1274 | 24478392 | We investigated the mechanism by which IFNG and TNF exert their disruptive effects on testicular cell adhesion. |
| 1275 | 24478392 | We investigated the mechanism by which IFNG and TNF exert their disruptive effects on testicular cell adhesion. |
| 1276 | 24478392 | We investigated the mechanism by which IFNG and TNF exert their disruptive effects on testicular cell adhesion. |
| 1277 | 24478392 | We investigated the mechanism by which IFNG and TNF exert their disruptive effects on testicular cell adhesion. |
| 1278 | 24478392 | We investigated the mechanism by which IFNG and TNF exert their disruptive effects on testicular cell adhesion. |
| 1279 | 24478392 | We have demonstrated that combined treatment with IFNG and TNF (IFNG+TNF) exerts a synergistic effect by downregulating CAR mRNA and protein levels. |
| 1280 | 24478392 | We have demonstrated that combined treatment with IFNG and TNF (IFNG+TNF) exerts a synergistic effect by downregulating CAR mRNA and protein levels. |
| 1281 | 24478392 | We have demonstrated that combined treatment with IFNG and TNF (IFNG+TNF) exerts a synergistic effect by downregulating CAR mRNA and protein levels. |
| 1282 | 24478392 | We have demonstrated that combined treatment with IFNG and TNF (IFNG+TNF) exerts a synergistic effect by downregulating CAR mRNA and protein levels. |
| 1283 | 24478392 | We have demonstrated that combined treatment with IFNG and TNF (IFNG+TNF) exerts a synergistic effect by downregulating CAR mRNA and protein levels. |
| 1284 | 24478392 | We have demonstrated that combined treatment with IFNG and TNF (IFNG+TNF) exerts a synergistic effect by downregulating CAR mRNA and protein levels. |
| 1285 | 24478392 | We have demonstrated that combined treatment with IFNG and TNF (IFNG+TNF) exerts a synergistic effect by downregulating CAR mRNA and protein levels. |
| 1286 | 24478392 | We have demonstrated that combined treatment with IFNG and TNF (IFNG+TNF) exerts a synergistic effect by downregulating CAR mRNA and protein levels. |
| 1287 | 24478392 | We have demonstrated that combined treatment with IFNG and TNF (IFNG+TNF) exerts a synergistic effect by downregulating CAR mRNA and protein levels. |
| 1288 | 24478392 | We have demonstrated that combined treatment with IFNG and TNF (IFNG+TNF) exerts a synergistic effect by downregulating CAR mRNA and protein levels. |
| 1289 | 24478392 | Immunofluorescence staining revealed that IFNG+TNF treatment effectively removes CAR from the site of cell-cell contact. |
| 1290 | 24478392 | Immunofluorescence staining revealed that IFNG+TNF treatment effectively removes CAR from the site of cell-cell contact. |
| 1291 | 24478392 | Immunofluorescence staining revealed that IFNG+TNF treatment effectively removes CAR from the site of cell-cell contact. |
| 1292 | 24478392 | Immunofluorescence staining revealed that IFNG+TNF treatment effectively removes CAR from the site of cell-cell contact. |
| 1293 | 24478392 | Immunofluorescence staining revealed that IFNG+TNF treatment effectively removes CAR from the site of cell-cell contact. |
| 1294 | 24478392 | Immunofluorescence staining revealed that IFNG+TNF treatment effectively removes CAR from the site of cell-cell contact. |
| 1295 | 24478392 | Immunofluorescence staining revealed that IFNG+TNF treatment effectively removes CAR from the site of cell-cell contact. |
| 1296 | 24478392 | Immunofluorescence staining revealed that IFNG+TNF treatment effectively removes CAR from the site of cell-cell contact. |
| 1297 | 24478392 | Immunofluorescence staining revealed that IFNG+TNF treatment effectively removes CAR from the site of cell-cell contact. |
| 1298 | 24478392 | Immunofluorescence staining revealed that IFNG+TNF treatment effectively removes CAR from the site of cell-cell contact. |
| 1299 | 24478392 | Using inhibitor and co-immunoprecipitation, we confirmed that IFNG+TNF mediates CAR protein degradation via ubiquitin-proteasome and NFKB pathways. |
| 1300 | 24478392 | Using inhibitor and co-immunoprecipitation, we confirmed that IFNG+TNF mediates CAR protein degradation via ubiquitin-proteasome and NFKB pathways. |
| 1301 | 24478392 | Using inhibitor and co-immunoprecipitation, we confirmed that IFNG+TNF mediates CAR protein degradation via ubiquitin-proteasome and NFKB pathways. |
| 1302 | 24478392 | Using inhibitor and co-immunoprecipitation, we confirmed that IFNG+TNF mediates CAR protein degradation via ubiquitin-proteasome and NFKB pathways. |
| 1303 | 24478392 | Using inhibitor and co-immunoprecipitation, we confirmed that IFNG+TNF mediates CAR protein degradation via ubiquitin-proteasome and NFKB pathways. |
| 1304 | 24478392 | Using inhibitor and co-immunoprecipitation, we confirmed that IFNG+TNF mediates CAR protein degradation via ubiquitin-proteasome and NFKB pathways. |
| 1305 | 24478392 | Using inhibitor and co-immunoprecipitation, we confirmed that IFNG+TNF mediates CAR protein degradation via ubiquitin-proteasome and NFKB pathways. |
| 1306 | 24478392 | Using inhibitor and co-immunoprecipitation, we confirmed that IFNG+TNF mediates CAR protein degradation via ubiquitin-proteasome and NFKB pathways. |
| 1307 | 24478392 | Using inhibitor and co-immunoprecipitation, we confirmed that IFNG+TNF mediates CAR protein degradation via ubiquitin-proteasome and NFKB pathways. |
| 1308 | 24478392 | Using inhibitor and co-immunoprecipitation, we confirmed that IFNG+TNF mediates CAR protein degradation via ubiquitin-proteasome and NFKB pathways. |
| 1309 | 24478392 | Blockage of ubiquitin-proteasome pathway significantly inhibits CAR degradation, as indicated by the reappearance of CAR at the site of cell-cell contact. |
| 1310 | 24478392 | Blockage of ubiquitin-proteasome pathway significantly inhibits CAR degradation, as indicated by the reappearance of CAR at the site of cell-cell contact. |
| 1311 | 24478392 | Blockage of ubiquitin-proteasome pathway significantly inhibits CAR degradation, as indicated by the reappearance of CAR at the site of cell-cell contact. |
| 1312 | 24478392 | Blockage of ubiquitin-proteasome pathway significantly inhibits CAR degradation, as indicated by the reappearance of CAR at the site of cell-cell contact. |
| 1313 | 24478392 | Blockage of ubiquitin-proteasome pathway significantly inhibits CAR degradation, as indicated by the reappearance of CAR at the site of cell-cell contact. |
| 1314 | 24478392 | Blockage of ubiquitin-proteasome pathway significantly inhibits CAR degradation, as indicated by the reappearance of CAR at the site of cell-cell contact. |
| 1315 | 24478392 | Blockage of ubiquitin-proteasome pathway significantly inhibits CAR degradation, as indicated by the reappearance of CAR at the site of cell-cell contact. |
| 1316 | 24478392 | Blockage of ubiquitin-proteasome pathway significantly inhibits CAR degradation, as indicated by the reappearance of CAR at the site of cell-cell contact. |
| 1317 | 24478392 | Blockage of ubiquitin-proteasome pathway significantly inhibits CAR degradation, as indicated by the reappearance of CAR at the site of cell-cell contact. |
| 1318 | 24478392 | Blockage of ubiquitin-proteasome pathway significantly inhibits CAR degradation, as indicated by the reappearance of CAR at the site of cell-cell contact. |
| 1319 | 24478392 | Additionally, IFNG+TNF reduces CAR mRNA via transcriptional regulation. |
| 1320 | 24478392 | Additionally, IFNG+TNF reduces CAR mRNA via transcriptional regulation. |
| 1321 | 24478392 | Additionally, IFNG+TNF reduces CAR mRNA via transcriptional regulation. |
| 1322 | 24478392 | Additionally, IFNG+TNF reduces CAR mRNA via transcriptional regulation. |
| 1323 | 24478392 | Additionally, IFNG+TNF reduces CAR mRNA via transcriptional regulation. |
| 1324 | 24478392 | Additionally, IFNG+TNF reduces CAR mRNA via transcriptional regulation. |
| 1325 | 24478392 | Additionally, IFNG+TNF reduces CAR mRNA via transcriptional regulation. |
| 1326 | 24478392 | Additionally, IFNG+TNF reduces CAR mRNA via transcriptional regulation. |
| 1327 | 24478392 | Additionally, IFNG+TNF reduces CAR mRNA via transcriptional regulation. |
| 1328 | 24478392 | Additionally, IFNG+TNF reduces CAR mRNA via transcriptional regulation. |
| 1329 | 24478392 | Mutational studies have shown that IFNG+TNF-induced CAR repression is achieved by suppression of the basal transcription. |
| 1330 | 24478392 | Mutational studies have shown that IFNG+TNF-induced CAR repression is achieved by suppression of the basal transcription. |
| 1331 | 24478392 | Mutational studies have shown that IFNG+TNF-induced CAR repression is achieved by suppression of the basal transcription. |
| 1332 | 24478392 | Mutational studies have shown that IFNG+TNF-induced CAR repression is achieved by suppression of the basal transcription. |
| 1333 | 24478392 | Mutational studies have shown that IFNG+TNF-induced CAR repression is achieved by suppression of the basal transcription. |
| 1334 | 24478392 | Mutational studies have shown that IFNG+TNF-induced CAR repression is achieved by suppression of the basal transcription. |
| 1335 | 24478392 | Mutational studies have shown that IFNG+TNF-induced CAR repression is achieved by suppression of the basal transcription. |
| 1336 | 24478392 | Mutational studies have shown that IFNG+TNF-induced CAR repression is achieved by suppression of the basal transcription. |
| 1337 | 24478392 | Mutational studies have shown that IFNG+TNF-induced CAR repression is achieved by suppression of the basal transcription. |
| 1338 | 24478392 | Mutational studies have shown that IFNG+TNF-induced CAR repression is achieved by suppression of the basal transcription. |
| 1339 | 24478392 | Electrophoretic mobility shift assay and chromatin immunoprecipitation assays further confirmed that IFNG+TNF treament not only inhibits binding of the basal transcription factors but also promotes binding of NFKB subunits and Sp1 (negative regulators) to the CAR promoter region. |
| 1340 | 24478392 | Electrophoretic mobility shift assay and chromatin immunoprecipitation assays further confirmed that IFNG+TNF treament not only inhibits binding of the basal transcription factors but also promotes binding of NFKB subunits and Sp1 (negative regulators) to the CAR promoter region. |
| 1341 | 24478392 | Electrophoretic mobility shift assay and chromatin immunoprecipitation assays further confirmed that IFNG+TNF treament not only inhibits binding of the basal transcription factors but also promotes binding of NFKB subunits and Sp1 (negative regulators) to the CAR promoter region. |
| 1342 | 24478392 | Electrophoretic mobility shift assay and chromatin immunoprecipitation assays further confirmed that IFNG+TNF treament not only inhibits binding of the basal transcription factors but also promotes binding of NFKB subunits and Sp1 (negative regulators) to the CAR promoter region. |
| 1343 | 24478392 | Electrophoretic mobility shift assay and chromatin immunoprecipitation assays further confirmed that IFNG+TNF treament not only inhibits binding of the basal transcription factors but also promotes binding of NFKB subunits and Sp1 (negative regulators) to the CAR promoter region. |
| 1344 | 24478392 | Electrophoretic mobility shift assay and chromatin immunoprecipitation assays further confirmed that IFNG+TNF treament not only inhibits binding of the basal transcription factors but also promotes binding of NFKB subunits and Sp1 (negative regulators) to the CAR promoter region. |
| 1345 | 24478392 | Electrophoretic mobility shift assay and chromatin immunoprecipitation assays further confirmed that IFNG+TNF treament not only inhibits binding of the basal transcription factors but also promotes binding of NFKB subunits and Sp1 (negative regulators) to the CAR promoter region. |
| 1346 | 24478392 | Electrophoretic mobility shift assay and chromatin immunoprecipitation assays further confirmed that IFNG+TNF treament not only inhibits binding of the basal transcription factors but also promotes binding of NFKB subunits and Sp1 (negative regulators) to the CAR promoter region. |
| 1347 | 24478392 | Electrophoretic mobility shift assay and chromatin immunoprecipitation assays further confirmed that IFNG+TNF treament not only inhibits binding of the basal transcription factors but also promotes binding of NFKB subunits and Sp1 (negative regulators) to the CAR promoter region. |
| 1348 | 24478392 | Electrophoretic mobility shift assay and chromatin immunoprecipitation assays further confirmed that IFNG+TNF treament not only inhibits binding of the basal transcription factors but also promotes binding of NFKB subunits and Sp1 (negative regulators) to the CAR promoter region. |
| 1349 | 24478392 | Taken together, IFNG+TNF treatment significantly downregulates CAR expression, which provides an explanation of how cell sloughing in the epithelium mediates, by loss of CAR-based cell adhesion, during testicular inflammation. |
| 1350 | 24478392 | Taken together, IFNG+TNF treatment significantly downregulates CAR expression, which provides an explanation of how cell sloughing in the epithelium mediates, by loss of CAR-based cell adhesion, during testicular inflammation. |
| 1351 | 24478392 | Taken together, IFNG+TNF treatment significantly downregulates CAR expression, which provides an explanation of how cell sloughing in the epithelium mediates, by loss of CAR-based cell adhesion, during testicular inflammation. |
| 1352 | 24478392 | Taken together, IFNG+TNF treatment significantly downregulates CAR expression, which provides an explanation of how cell sloughing in the epithelium mediates, by loss of CAR-based cell adhesion, during testicular inflammation. |
| 1353 | 24478392 | Taken together, IFNG+TNF treatment significantly downregulates CAR expression, which provides an explanation of how cell sloughing in the epithelium mediates, by loss of CAR-based cell adhesion, during testicular inflammation. |
| 1354 | 24478392 | Taken together, IFNG+TNF treatment significantly downregulates CAR expression, which provides an explanation of how cell sloughing in the epithelium mediates, by loss of CAR-based cell adhesion, during testicular inflammation. |
| 1355 | 24478392 | Taken together, IFNG+TNF treatment significantly downregulates CAR expression, which provides an explanation of how cell sloughing in the epithelium mediates, by loss of CAR-based cell adhesion, during testicular inflammation. |
| 1356 | 24478392 | Taken together, IFNG+TNF treatment significantly downregulates CAR expression, which provides an explanation of how cell sloughing in the epithelium mediates, by loss of CAR-based cell adhesion, during testicular inflammation. |
| 1357 | 24478392 | Taken together, IFNG+TNF treatment significantly downregulates CAR expression, which provides an explanation of how cell sloughing in the epithelium mediates, by loss of CAR-based cell adhesion, during testicular inflammation. |
| 1358 | 24478392 | Taken together, IFNG+TNF treatment significantly downregulates CAR expression, which provides an explanation of how cell sloughing in the epithelium mediates, by loss of CAR-based cell adhesion, during testicular inflammation. |
| 1359 | 24477887 | IGRA-positive patients and interferon-gamma/interleukin-2 signatures: can the Fluorospot assay provide further information? |
| 1360 | 24477887 | IGRA-positive patients and interferon-gamma/interleukin-2 signatures: can the Fluorospot assay provide further information? |
| 1361 | 24477887 | IGRA-positive patients and interferon-gamma/interleukin-2 signatures: can the Fluorospot assay provide further information? |
| 1362 | 24477887 | Determination of the interferon-gamma and interleukin-2 T cell signature might provide an additional and rapid tool to evaluate treatment necessity and clinical management of a patient. |
| 1363 | 24477887 | Determination of the interferon-gamma and interleukin-2 T cell signature might provide an additional and rapid tool to evaluate treatment necessity and clinical management of a patient. |
| 1364 | 24477887 | Determination of the interferon-gamma and interleukin-2 T cell signature might provide an additional and rapid tool to evaluate treatment necessity and clinical management of a patient. |
| 1365 | 24477887 | Here, we present three cases of interferon-gamma release assay-positive patients with differing interferon-gamma and interleukin-2 signatures when analyzed by the Fluorospot assay. |
| 1366 | 24477887 | Here, we present three cases of interferon-gamma release assay-positive patients with differing interferon-gamma and interleukin-2 signatures when analyzed by the Fluorospot assay. |
| 1367 | 24477887 | Here, we present three cases of interferon-gamma release assay-positive patients with differing interferon-gamma and interleukin-2 signatures when analyzed by the Fluorospot assay. |
| 1368 | 24469722 | The aim of the study was to find association of bovine brucellosis with 20 SNPs pertaining to bovine cytokine (IFNG, IFNGR1, IFNGR2, TNFA) and innate immunity (SLC11A1, TLR1, TLR4, and TLR9) genes using PCR-RFLP genotyping technique and it was observed that SLC11A1 (+1066 C/G), TLR1 (+1446 C/A), TLR1 (+1380 G/A), TLR4 (+10 C/T) and TLR4 (+399 C/T) loci were significantly (P≤0.05) associated with bovine brucellosis. |
| 1369 | 24455190 | Treatment of the three-dimensional model with either interleukin 17 or a combination of tumor necrosis factor and interferon γ was shown to produce morphological changes, which were similar to acanthosis in psoriatic skin. |
| 1370 | 24455190 | Notably, changes caused by interleukin 17 were less evident than those caused by the combination of interferon γ and tumor necrosis factor. |
| 1371 | 24455190 | On the contrary, HaCaT cells exhibited no significant changes in the expression of fosl1 and had decreased levels of mki67 after being treated with a combination of TNF and IFNG. |
| 1372 | 24446517 | However, an inability to generate Th1 cells because of Stat4, Ifngr, and Ifng deficiencies did not prevent diabetes. |
| 1373 | 24434371 | Interleukin-2 (IL-2) and interferon gamma (IFNg) cytokine secretions were measured by multi-cytokine luminex technology. |
| 1374 | 24434371 | Interleukin-2 (IL-2) and interferon gamma (IFNg) cytokine secretions were measured by multi-cytokine luminex technology. |
| 1375 | 24434371 | Interleukin-2 (IL-2) and interferon gamma (IFNg) cytokine secretions were measured by multi-cytokine luminex technology. |
| 1376 | 24434371 | EchNWA mediated a strong dose-dependent enhancement of high-density T-cell production of IL-2 and IFNg response to PMA+I. |
| 1377 | 24434371 | EchNWA mediated a strong dose-dependent enhancement of high-density T-cell production of IL-2 and IFNg response to PMA+I. |
| 1378 | 24434371 | EchNWA mediated a strong dose-dependent enhancement of high-density T-cell production of IL-2 and IFNg response to PMA+I. |
| 1379 | 24434371 | Conversely EchNWA mediated modest but significant suppression of IFNg response and reduced the percentage of CD25+ T-cells under low-density conditions. |
| 1380 | 24434371 | Conversely EchNWA mediated modest but significant suppression of IFNg response and reduced the percentage of CD25+ T-cells under low-density conditions. |
| 1381 | 24434371 | Conversely EchNWA mediated modest but significant suppression of IFNg response and reduced the percentage of CD25+ T-cells under low-density conditions. |
| 1382 | 24415943 | We previously identified a cis-regulatory element located 22 kb upstream of the Ifng gene (Conserved Non-coding Sequence -22, or CNS-22) that is a site for recruitment of the transcription factors T-bet, Runx3, NF-κB and STAT4, which act to regulate transcription of the Ifng gene in Th1 cells. |
| 1383 | 24415943 | We previously identified a cis-regulatory element located 22 kb upstream of the Ifng gene (Conserved Non-coding Sequence -22, or CNS-22) that is a site for recruitment of the transcription factors T-bet, Runx3, NF-κB and STAT4, which act to regulate transcription of the Ifng gene in Th1 cells. |
| 1384 | 24415943 | We previously identified a cis-regulatory element located 22 kb upstream of the Ifng gene (Conserved Non-coding Sequence -22, or CNS-22) that is a site for recruitment of the transcription factors T-bet, Runx3, NF-κB and STAT4, which act to regulate transcription of the Ifng gene in Th1 cells. |
| 1385 | 24415943 | Deletion of CNS-22 led to a defect in induction of Ifng by the cytokines IL-12 and IL-18, with a more modest effect on induction via T-cell receptor activation. |
| 1386 | 24415943 | Deletion of CNS-22 led to a defect in induction of Ifng by the cytokines IL-12 and IL-18, with a more modest effect on induction via T-cell receptor activation. |
| 1387 | 24415943 | Deletion of CNS-22 led to a defect in induction of Ifng by the cytokines IL-12 and IL-18, with a more modest effect on induction via T-cell receptor activation. |
| 1388 | 24415943 | Finally, we show that impairment in IL-12+IL-18 dependent induction of Ifng stems from the importance of CNS-22 in coordinating locus-wide levels of histone acetylation in response to these cytokines. |
| 1389 | 24415943 | Finally, we show that impairment in IL-12+IL-18 dependent induction of Ifng stems from the importance of CNS-22 in coordinating locus-wide levels of histone acetylation in response to these cytokines. |
| 1390 | 24415943 | Finally, we show that impairment in IL-12+IL-18 dependent induction of Ifng stems from the importance of CNS-22 in coordinating locus-wide levels of histone acetylation in response to these cytokines. |
| 1391 | 24403550 | In particular, profilin induced the expressions of macrophage chemotactic protein 1 (MCP1), interleukin 12 (IL12), and interferon gamma (IFNG) through nuclear factor KB (NFKB) activation. |
| 1392 | 24403550 | In particular, profilin induced the expressions of macrophage chemotactic protein 1 (MCP1), interleukin 12 (IL12), and interferon gamma (IFNG) through nuclear factor KB (NFKB) activation. |
| 1393 | 24403550 | UPEC induced the expressions of MCP1, IL12, and IFNG, as well as tumor necrosis factor alpha (TNFA), IL6, and IFNB, through the activation of NFKB, IFN regulatory factor 3, and mitogen-activated protein kinases. |
| 1394 | 24403550 | UPEC induced the expressions of MCP1, IL12, and IFNG, as well as tumor necrosis factor alpha (TNFA), IL6, and IFNB, through the activation of NFKB, IFN regulatory factor 3, and mitogen-activated protein kinases. |
| 1395 | 24376880 | Further improvements in the limit of detection of an ICT for IFNg, and possibly combination of IFNg with other biomarkers such as adenosine deaminase, are necessary for such a test to be of value in the evaluation of pleural tuberculosis. |
| 1396 | 24368122 | These stimuli can also induce IFN-γ-pretreated neutrophils to release reactive oxygen species (ROS), such as superoxide anion, hydrogen peroxide and hypochlorous acid, as well as granule lysosomal enzymes and the pro-inflammatory cytokines TNF-α and IL-6. |
| 1397 | 24368122 | The enhancing effect of IFN-γ on the respiratory burst was found to be associated with up-regulation of the gp91(phox) and p47(phox) subunits of NADPH oxidase, as measured by their mRNA levels. |
| 1398 | 24363024 | Peripheral blood mononuclear cells of healthy donors and post-transplant lymphoma patients were stimulated with or without lunasin in the presence of IL-12 or IL-2. |
| 1399 | 24363024 | Adding lunasin to IL-12- or IL-2-stimulated NK cells demonstrated synergistic effects in the induction of IFNG and GZMB involved in cytotoxicity. |
| 1400 | 24363024 | The combination of lunasin and cytokines (IL-12 plus IL-2) was capable of restoring IFNγ production by NK cells from post-transplant lymphoma patients. |
| 1401 | 24313359 | Peripheral and site-specific CD4(+) CD28(null) T cells from rheumatoid arthritis patients show distinct characteristics. |
| 1402 | 24313359 | Peripheral and site-specific CD4(+) CD28(null) T cells from rheumatoid arthritis patients show distinct characteristics. |
| 1403 | 24313359 | Proinflammatory CD4(+) CD28(null) T cells are frequently found in the circulation of patients with rheumatoid arthritis (RA), but are less common in the rheumatic joint. |
| 1404 | 24313359 | Proinflammatory CD4(+) CD28(null) T cells are frequently found in the circulation of patients with rheumatoid arthritis (RA), but are less common in the rheumatic joint. |
| 1405 | 24313359 | In the present study, we sought to identify functional differences between CD4(+) CD28(null) T cells from blood and synovial fluid in comparison with conventional CD28-expressing CD4(+) T cells. |
| 1406 | 24313359 | In the present study, we sought to identify functional differences between CD4(+) CD28(null) T cells from blood and synovial fluid in comparison with conventional CD28-expressing CD4(+) T cells. |
| 1407 | 24313359 | Forty-four patients with RA, displaying a distinct CD4(+) CD28(null) T cell population in blood, were recruited for this study; the methylation status of the IFNG locus was examined in isolated T cell subsets, and intracellular cytokine production (IFN-γ, TNF, IL-17) and chemokine receptor expression (CXCR3, CCR6 and CCR7) were assessed by flow cytometry on T cells from the two compartments. |
| 1408 | 24313359 | Forty-four patients with RA, displaying a distinct CD4(+) CD28(null) T cell population in blood, were recruited for this study; the methylation status of the IFNG locus was examined in isolated T cell subsets, and intracellular cytokine production (IFN-γ, TNF, IL-17) and chemokine receptor expression (CXCR3, CCR6 and CCR7) were assessed by flow cytometry on T cells from the two compartments. |
| 1409 | 24313359 | Circulating CD4(+) CD28(null) T cells were significantly more hypomethylated in the CNS-1 region of the IFNG locus than conventional CD4(+) CD28(+) T cells and produced higher levels of both IFN-γ and TNF after TCR cross-linking. |
| 1410 | 24313359 | Circulating CD4(+) CD28(null) T cells were significantly more hypomethylated in the CNS-1 region of the IFNG locus than conventional CD4(+) CD28(+) T cells and produced higher levels of both IFN-γ and TNF after TCR cross-linking. |
| 1411 | 24313359 | CD4(+) CD28(null) T cells from the site of inflammation expressed significantly more CXCR3 and CCR6 compared to their counterparts in blood. |
| 1412 | 24313359 | CD4(+) CD28(null) T cells from the site of inflammation expressed significantly more CXCR3 and CCR6 compared to their counterparts in blood. |
| 1413 | 24313359 | While IL-17A production could hardly be detected in CD4(+) CD28(null) cells from the blood, a significant production was observed in CD4(+) CD28(null) T cells from synovial fluid. |
| 1414 | 24313359 | While IL-17A production could hardly be detected in CD4(+) CD28(null) cells from the blood, a significant production was observed in CD4(+) CD28(null) T cells from synovial fluid. |
| 1415 | 24313359 | CD4(+) CD28(null) T cells were not only found to differ from conventional CD4(+) CD28(+) T cells in the circulation, but we could also demonstrate that synovial CD4(+) CD28(null) T cells showed additional effector functions (IL-17 coproduction) as compared to the same subset in peripheral blood, suggesting an active role for these cells in the perpetuation of inflammation in the subset of patients having a CD28(null) population. |
| 1416 | 24313359 | CD4(+) CD28(null) T cells were not only found to differ from conventional CD4(+) CD28(+) T cells in the circulation, but we could also demonstrate that synovial CD4(+) CD28(null) T cells showed additional effector functions (IL-17 coproduction) as compared to the same subset in peripheral blood, suggesting an active role for these cells in the perpetuation of inflammation in the subset of patients having a CD28(null) population. |
| 1417 | 24286163 | To better understand possible causes, an analysis was conducted of gene expression of a set of transcripts related to maternal recognition and establishment of rabbit pregnancy (uteroglobin, SCGB1A1; integrin α1, ITGA1; interferon-γ, IFNG; vascular endothelial growth factor, VEGF) in oviduct and uterine tissue at 16, 72 or 144 h post-ovulation and insemination. |
| 1418 | 24273896 | Cytokine gene polymorphisms of TNFα, IL-6, IL-10, TGFβ and IFNγ in the Saudi population. |
| 1419 | 24273896 | In the present work the authors examine polymorphisms in the genes encoding interleukin-6 (IL-6), IL-10, interferon-gamma (IFNgamma), tumour necrosis factor-alpha (TNFalpha) and transforming growth factor-beta (TGFbeta1) using the polymerase chain reaction sequence-specific primer (PCR-SSP) method in 150 healthy unrelated Saudis, and results compared with those from other studied populations. |
| 1420 | 24266365 | The present review focuses on a small subset of iTregs that produces IFNg, comprises only 0.04% of all CD4(+) T lymphocytes in the blood of healthy individuals, and increases strongly during an immune response. |
| 1421 | 24266365 | The present review focuses on a small subset of iTregs that produces IFNg, comprises only 0.04% of all CD4(+) T lymphocytes in the blood of healthy individuals, and increases strongly during an immune response. |
| 1422 | 24266365 | IFNg(+) Tregs are induced by IFNg and IL12, making them sensors for inflammatory cytokines. |
| 1423 | 24266365 | IFNg(+) Tregs are induced by IFNg and IL12, making them sensors for inflammatory cytokines. |
| 1424 | 24264476 | Levels of inflammatory cytokines including interleukin 1 beta, IL-4, IL-6, and interferon gamma (INF-γ) were measured after the infection of M. leprae in the peripheral blood mononuclear cell (PBMC) of subjects with different genotypes of rs13361189. |
| 1425 | 24244422 | Downregulation of IFNG in CD4(+) T cells in lung cancer through hypermethylation: a possible mechanism of tumor-induced immunosuppression. |
| 1426 | 24244422 | Downregulation of IFNG in CD4(+) T cells in lung cancer through hypermethylation: a possible mechanism of tumor-induced immunosuppression. |
| 1427 | 24244422 | Downregulation of IFNG in CD4(+) T cells in lung cancer through hypermethylation: a possible mechanism of tumor-induced immunosuppression. |
| 1428 | 24244422 | Downregulation of IFNG in CD4(+) T cells in lung cancer through hypermethylation: a possible mechanism of tumor-induced immunosuppression. |
| 1429 | 24244422 | Downregulation of IFNG in CD4(+) T cells in lung cancer through hypermethylation: a possible mechanism of tumor-induced immunosuppression. |
| 1430 | 24244422 | Hypermethylation of the IFNG promoter in CD4(+) T cells and plasma IFNG was negatively correlated. |
| 1431 | 24244422 | Hypermethylation of the IFNG promoter in CD4(+) T cells and plasma IFNG was negatively correlated. |
| 1432 | 24244422 | Hypermethylation of the IFNG promoter in CD4(+) T cells and plasma IFNG was negatively correlated. |
| 1433 | 24244422 | Hypermethylation of the IFNG promoter in CD4(+) T cells and plasma IFNG was negatively correlated. |
| 1434 | 24244422 | Hypermethylation of the IFNG promoter in CD4(+) T cells and plasma IFNG was negatively correlated. |
| 1435 | 24244422 | CD4(+) T cells from healthy individuals co-cultured with SPC-A1 cells generated lower levels of IFNG after activation, elevated expression of DNA methyltransferases (DNMTs), and exhibited hypermethylation of the IFNG promoter. |
| 1436 | 24244422 | CD4(+) T cells from healthy individuals co-cultured with SPC-A1 cells generated lower levels of IFNG after activation, elevated expression of DNA methyltransferases (DNMTs), and exhibited hypermethylation of the IFNG promoter. |
| 1437 | 24244422 | CD4(+) T cells from healthy individuals co-cultured with SPC-A1 cells generated lower levels of IFNG after activation, elevated expression of DNA methyltransferases (DNMTs), and exhibited hypermethylation of the IFNG promoter. |
| 1438 | 24244422 | CD4(+) T cells from healthy individuals co-cultured with SPC-A1 cells generated lower levels of IFNG after activation, elevated expression of DNA methyltransferases (DNMTs), and exhibited hypermethylation of the IFNG promoter. |
| 1439 | 24244422 | CD4(+) T cells from healthy individuals co-cultured with SPC-A1 cells generated lower levels of IFNG after activation, elevated expression of DNA methyltransferases (DNMTs), and exhibited hypermethylation of the IFNG promoter. |
| 1440 | 24244422 | In conclusion, decreased IFNG expression of CD4(+) T cells co-cultured with lung cancer cell is associated with IFNG promoter hypermethylation. |
| 1441 | 24244422 | In conclusion, decreased IFNG expression of CD4(+) T cells co-cultured with lung cancer cell is associated with IFNG promoter hypermethylation. |
| 1442 | 24244422 | In conclusion, decreased IFNG expression of CD4(+) T cells co-cultured with lung cancer cell is associated with IFNG promoter hypermethylation. |
| 1443 | 24244422 | In conclusion, decreased IFNG expression of CD4(+) T cells co-cultured with lung cancer cell is associated with IFNG promoter hypermethylation. |
| 1444 | 24244422 | In conclusion, decreased IFNG expression of CD4(+) T cells co-cultured with lung cancer cell is associated with IFNG promoter hypermethylation. |
| 1445 | 24244422 | Our study suggests that interaction between lung cancer cells and CD4(+) T cells induces DNMT expression and IFNG promoter hypermethylation in CD4(+) T cell, which may serve as an important mechanism of tumor-induced immunosuppression. |
| 1446 | 24244422 | Our study suggests that interaction between lung cancer cells and CD4(+) T cells induces DNMT expression and IFNG promoter hypermethylation in CD4(+) T cell, which may serve as an important mechanism of tumor-induced immunosuppression. |
| 1447 | 24244422 | Our study suggests that interaction between lung cancer cells and CD4(+) T cells induces DNMT expression and IFNG promoter hypermethylation in CD4(+) T cell, which may serve as an important mechanism of tumor-induced immunosuppression. |
| 1448 | 24244422 | Our study suggests that interaction between lung cancer cells and CD4(+) T cells induces DNMT expression and IFNG promoter hypermethylation in CD4(+) T cell, which may serve as an important mechanism of tumor-induced immunosuppression. |
| 1449 | 24244422 | Our study suggests that interaction between lung cancer cells and CD4(+) T cells induces DNMT expression and IFNG promoter hypermethylation in CD4(+) T cell, which may serve as an important mechanism of tumor-induced immunosuppression. |
| 1450 | 24218883 | [Association research between polymorphism of IFN-gamma and IL-10, environmental risk factors, and susceptibility to esophageal cancer]. |
| 1451 | 24216234 | Rosette pre-depletion of blood was also investigated for detecting CD4+ or CD8+ T-cell responses using the IFN-g ELISPOT assay. |
| 1452 | 24216234 | Rosette pre-depletion of whole blood proved to be effective in detecting CD4+ or CD8+ T-cell responses similarly to flow cytometry. |
| 1453 | 24216234 | Taken together, the following recommendations are suggested to optimize the CMV-ELISPOT for transplantation settings: (1) use PMA/iono as positive control; (2) whole virus particle should be used to avoid peptide-related false negative responses; (3) a rosette pre-depletion step may be useful to detect CD4+ or CD8+ T-cell responses. |
| 1454 | 24204576 | Samples were analysed by immunofluorescence to identify the presence and abundance of B-B7 (B-cells), CD4 (LTh), CD8 (LTc), γδT cell receptor (TCR) and CD335/NKp46 (NK cells) -positive immune cells. |
| 1455 | 24204576 | Samples were analysed by immunofluorescence to identify the presence and abundance of B-B7 (B-cells), CD4 (LTh), CD8 (LTc), γδT cell receptor (TCR) and CD335/NKp46 (NK cells) -positive immune cells. |
| 1456 | 24204576 | Quantitative real time PCR (QPCR) was carried out to analyse mRNA relative abundance of FOXP3 (a marker of regulatory T (Treg) cells) and a panel of immune factors, including MHC-I, LIF, Interleukins 1, 2, 6, 8, 10, 11,12A, IFNa and IFNG. |
| 1457 | 24204576 | Quantitative real time PCR (QPCR) was carried out to analyse mRNA relative abundance of FOXP3 (a marker of regulatory T (Treg) cells) and a panel of immune factors, including MHC-I, LIF, Interleukins 1, 2, 6, 8, 10, 11,12A, IFNa and IFNG. |
| 1458 | 24204576 | Results indicate that B-B7+ cells are quite populous in bovine endometrial tissue, CD4+ and CD8+ -cells are present in moderate numbers and γδTCR+ and CD335+ cells are present in low numbers. |
| 1459 | 24204576 | Results indicate that B-B7+ cells are quite populous in bovine endometrial tissue, CD4+ and CD8+ -cells are present in moderate numbers and γδTCR+ and CD335+ cells are present in low numbers. |
| 1460 | 24204576 | Neither B lymphocytes nor T lymphocyte subsets were regulated temporally during the oestrous cycle or by pregnancy prior to implantation. mRNA transcript abundance of the immune factors LIF, IL1b, IL8 and IL12A, IFNa and IFNG, expression was regulated temporally during the estrous cycle and LIF, IL1b, IL-10, IL11, IL12A were also temporally regulated during pregnancy. |
| 1461 | 24204576 | Neither B lymphocytes nor T lymphocyte subsets were regulated temporally during the oestrous cycle or by pregnancy prior to implantation. mRNA transcript abundance of the immune factors LIF, IL1b, IL8 and IL12A, IFNa and IFNG, expression was regulated temporally during the estrous cycle and LIF, IL1b, IL-10, IL11, IL12A were also temporally regulated during pregnancy. |
| 1462 | 24200694 | JUNB/AP-1 controls IFN-γ during inflammatory liver disease. |
| 1463 | 24200694 | In hepatocytes, the dimeric transcription factor c-JUN/AP-1 is a major mediator of cell survival during hepatitis, although functions for other JUN proteins in liver disease are less defined. |
| 1464 | 24200694 | The absence of JUNB in immune cells decreased IFN-γ expression and secretion from NK and NKT cells, leading to reduced STAT1 pathway activation. |
| 1465 | 24200694 | Systemic IFN-γ treatment or adenovirus-based IRF1 delivery to Junb-deficient mice restored hepatotoxicity, and we demonstrate that Ifng is a direct transcriptional target of JUNB. |
| 1466 | 24200694 | These findings demonstrate that JUNB/AP-1 promotes cell death during acute hepatitis by regulating IFN-γ production in NK and NKT cells and thus functionally antagonizes the hepatoprotective function of c-JUN/AP-1 in hepatocytes. |
| 1467 | 24176007 | Potential association of pulmonary tuberculosis with genetic polymorphisms of toll-like receptor 9 and interferon-gamma in a Chinese population. |
| 1468 | 24167151 | IL10 rs1800896, IFNG rs2430561, and IL18 rs1872387 polymorphims and their associations with asthma and allergy were studied in 135 preschool-aged children hospitalized for bronchiolitis at age 0-6 months. |
| 1469 | 24163409 | Aggregates of activated IFN-γ- and IL-17A-secreting CD4(+) T cells as well as B cells surrounded the airways. |
| 1470 | 24163409 | Lung pathology was similar in Ifng(-/-) and Il17a(-/-) mice, indicating that either cytokine is sufficient to establish chronic disease. |
| 1471 | 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. |
| 1472 | 24134186 | Galectin-7 administration upregulated apoptosis and inhibited the expression of interleukin-2 (IL2) and interferon-γ (IFNG) mRNA in Jurkat cells. |
| 1473 | 24121019 | We, therefore, established human myxovirus resistance protein A and human guanylate-binding protein-1 as markers for the differential detection of IFN-α- and IFN-γ-driven tumor micromilieus, respectively. |
| 1474 | 24120504 | In biofunction assays, recombinant gCCL4 was found to induce chemotactic activity in the peripheral blood leukocytes of groupers and up-regulate the gene expressions of grouper TNFA1 (TNF-α1), TNFA2 (TNF-α2), IFNG (IFN-γ), MX, TBX21 (T-bet), CD8 (α and β chain). |
| 1475 | 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. |
| 1476 | 24096714 | The BiPN grade was associated with phytohemagglutinin-induced IL2, IFNG and TNFSF2, as well as with lipopolysaccharide-induced IL6 levels. |
| 1477 | 24084096 | The gene expression of cytokines/chemokines in skin biopsies from the CL group showed higher transcript levels of modulatory (IL10 and TGFB1), anti-inflammatory (IL4), and pro-inflammatory (TNF, IFNG, IL12B, CCL2, CCL3, CCL5, CXCL10) biomarkers in recent lesions than in late lesions. |
| 1478 | 24065520 | Genetic variants in transforming growth factor-β gene (TGFB1) affect susceptibility to schizophrenia. |
| 1479 | 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). |
| 1480 | 24058673 | Hedgehog/GLI signaling activates suppressor of cytokine signaling 1 (SOCS1) in epidermal and neural tumor cells. |
| 1481 | 24058673 | Here we show that SOCS1 is a direct target of Hh/GLI signaling in human keratinocytes and medulloblastoma cells. |
| 1482 | 24058673 | SOCS1 is a potent inhibitor of interferon gamma (IFN-y)/STAT1 signaling. |
| 1483 | 24058673 | The transcription factors GLI1 and GLI2 activate the SOCS1 promoter, which contains five putative GLI binding sites, and GLI2 binding to the promoter was shown by chromatin immunoprecipitation. |
| 1484 | 24058673 | Consistent with a role of GLI in SOCS1 regulation, STAT1 phosphorylation is reduced in cells with active Hh/GLI signaling and IFN-у/STAT1 target gene activation is decreased. |
| 1485 | 24058673 | Here, we identify SOCS1 as a novel Hh/GLI target gene, indicating a negative role of Hh/GLI pathway in IFN-y/STAT1 signaling. |
| 1486 | 24055710 | Selective modulation of MHC class II chaperons by a novel IFN-γ-inducible class II transactivator variant in lung adenocarcinoma A549 cells. |
| 1487 | 24055710 | Class II transactivator (CIITA) plays a critical role in controlling major histocompatibility complex (MHC) class II gene expression. |
| 1488 | 24055710 | In this study, two novel alternatively spliced variants of human interferon (IFN)-γ-inducible CIITA, one missing exon 7 (CIITAΔE7), the other with TAG inserted at exon 4/5 junction (CIITA-TAG), were identified and characterized. |
| 1489 | 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. |
| 1490 | 24010824 | Hypoxia-inducible factor 1α (HIF-1α) has been well established as a protective factor for intestinal barrier function in intestinal epithelial cells. |
| 1491 | 24010824 | We proposed that lymphocyte-derived interferon-gamma (IFN-γ) might be responsible for the intestinal barrier dysfunction caused by increased HIF-1α. |
| 1492 | 23995235 | Two distinct subsets of γδ T cells that produce interleukin 17 (IL-17) (CD27(-) γδ T cells) or interferon-γ (IFN-γ) (CD27(+) γδ T cells) develop in the mouse thymus, but the molecular determinants of their functional potential in the periphery remain unknown. |
| 1493 | 23995235 | Two distinct subsets of γδ T cells that produce interleukin 17 (IL-17) (CD27(-) γδ T cells) or interferon-γ (IFN-γ) (CD27(+) γδ T cells) develop in the mouse thymus, but the molecular determinants of their functional potential in the periphery remain unknown. |
| 1494 | 23995235 | Here we conducted a genome-wide characterization of the methylation patterns of histone H3, along with analysis of mRNA encoding transcription factors, to identify the regulatory networks of peripheral IFN-γ-producing or IL-17-producing γδ T cell subsets in vivo. |
| 1495 | 23995235 | Here we conducted a genome-wide characterization of the methylation patterns of histone H3, along with analysis of mRNA encoding transcription factors, to identify the regulatory networks of peripheral IFN-γ-producing or IL-17-producing γδ T cell subsets in vivo. |
| 1496 | 23995235 | We found that CD27(+) γδ T cells were committed to the expression of Ifng but not Il17, whereas CD27(-) γδ T cells displayed permissive chromatin configurations at loci encoding both cytokines and their regulatory transcription factors and differentiated into cells that produced both IL-17 and IFN-γ in a tumor microenvironment. |
| 1497 | 23995235 | We found that CD27(+) γδ T cells were committed to the expression of Ifng but not Il17, whereas CD27(-) γδ T cells displayed permissive chromatin configurations at loci encoding both cytokines and their regulatory transcription factors and differentiated into cells that produced both IL-17 and IFN-γ in a tumor microenvironment. |
| 1498 | 23982206 | Activation of the transcriptional function of the NF-κB protein c-Rel by O-GlcNAc glycosylation. |
| 1499 | 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. |
| 1500 | 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. |
| 1501 | 23941776 | Role of tumor necrosis factor-α, interferon-γ and Fas-ligand on in vitro nitric oxide activity in the corpus luteum. |
| 1502 | 23941776 | Role of tumor necrosis factor-α, interferon-γ and Fas-ligand on in vitro nitric oxide activity in the corpus luteum. |
| 1503 | 23941776 | Role of tumor necrosis factor-α, interferon-γ and Fas-ligand on in vitro nitric oxide activity in the corpus luteum. |
| 1504 | 23941776 | Moreover, TNF, IFNG and FASL were shown to regulate equine CL establishment and regression. |
| 1505 | 23941776 | Moreover, TNF, IFNG and FASL were shown to regulate equine CL establishment and regression. |
| 1506 | 23941776 | Moreover, TNF, IFNG and FASL were shown to regulate equine CL establishment and regression. |
| 1507 | 23941776 | TNF increased eNOS mRNA level and NO metabolite (nitrite) production during CL growth. |
| 1508 | 23941776 | TNF increased eNOS mRNA level and NO metabolite (nitrite) production during CL growth. |
| 1509 | 23941776 | TNF increased eNOS mRNA level and NO metabolite (nitrite) production during CL growth. |
| 1510 | 23941776 | Cytokines combined action (TNF+IFNG+FASL) promoted eNOS protein upregulation in mid-CL and nitrite production in mid and late-CL. |
| 1511 | 23941776 | Cytokines combined action (TNF+IFNG+FASL) promoted eNOS protein upregulation in mid-CL and nitrite production in mid and late-CL. |
| 1512 | 23941776 | Cytokines combined action (TNF+IFNG+FASL) promoted eNOS protein upregulation in mid-CL and nitrite production in mid and late-CL. |
| 1513 | 23941776 | These results indicate that in equine CL, cytokines TNF, IFNG and FASL regulate NO activity, via eNOS expression modulation. |
| 1514 | 23941776 | These results indicate that in equine CL, cytokines TNF, IFNG and FASL regulate NO activity, via eNOS expression modulation. |
| 1515 | 23941776 | These results indicate that in equine CL, cytokines TNF, IFNG and FASL regulate NO activity, via eNOS expression modulation. |
| 1516 | 23939944 | Here we show that human umbilical cord blood (UCB)-derived CD34+CD38-/low hematopoietic stem cells can be successfully differentiated into functional, antigen-specific cytotoxic CD8+ T cells without direct stromal coculture or retroviral TCR transfection. |
| 1517 | 23939944 | Surface-immobilized Notch ligands (DLL1) and stromal cell conditioned medium successfully induced the development of CD1a+CD7+ and CD4+CD8+ early T cells. |
| 1518 | 23939944 | These cells, upon continued culture with cytomegalovirus (CMV) or influenza-A virus M1 (GIL) epitope-loaded human leukocyte antigen (HLA)-A*0201 tetramers, resulted in the generation of a polyclonal population of CMV-specific or GIL-specific CD8+ T cells, respectively. |
| 1519 | 23939944 | Upon further activation with antigen-loaded target cells, these antigen-specific, stem cell-derived T cells exhibited cytolytic functionality, specifically CD107a surface mobilization, interferon gamma (IFNg) production, and Granzyme B secretion. |
| 1520 | 23918204 | In this study we investigated ROS production in human astrocytes stimulated with interleukin (IL)-1β and interferon (IFN)-γ and its potential harmful effects. |
| 1521 | 23918204 | One of the sources of ROS in IL-1β-activated astrocytes was from increased superoxide production in mitochondria accompanied by enhanced manganese superoxide dismutase and inhibited catalase expression. |
| 1522 | 23918204 | NADPH oxidase (NOX) may also contribute to ROS production as astrocytes express NOX isoforms. |
| 1523 | 23884468 | NCR3/NKp30 is a natural killer (NK)-specific activating receptor regulating the cross talk between NK and dendritic cells and type II IFN secretion. |
| 1524 | 23884468 | We also demonstrated that circulating levels of NCR3/NKp30 were significantly increased among pSS patients compared with controls and correlated with higher NCR3/NKp30 but not CD16-dependent IFN-γ secretion by NK cells. |
| 1525 | 23840095 | Using the mare CL as a model, reports on locally produced cytokines, such as tumor necrosis factor α (TNF), interferon gamma (IFNG), or Fas ligand (FASL), pointed out their role on angiogenic activity modulation throughout the luteal phase. |
| 1526 | 23831616 | Arg1 deficiency did not affect the allergic response in lungs and large-airway resistance, but it improved peripheral lung function (tissue elastance and resistance) and attenuated adaptive increases in mRNA expression of arginine-catabolizing enzymes Arg2 and Nos2, arginine transporters Slc7a1 and Slc7a7, chemokines Ccl2 and Ccl11, cytokines Tnfa and Ifng, mucus-associated epithelial markers Clca3 and Muc5ac, and lung content of IL-13 and CCL11. |
| 1527 | 23831616 | However, expression of Il4, Il5, Il10, and Il13 mRNA; lung content of IL-4, IL-5, IL-10, TNF-α, and IFN-γ protein; and lung pathology were not affected. |
| 1528 | 23808390 | Interleukin-26 (IL26) is a member of the IL10 cytokine family. |
| 1529 | 23808390 | The IL26 gene is located between two other well-known cytokines genes of this family encoding interferon-gamma (IFNG) and IL22 in an evolutionary conserved gene cluster. |
| 1530 | 23798565 | Suppression is associated with development of a regulatory population of donor CD4(+) CD25(+)T-cells that express high levels of cytotoxic T-lymphocyte antigen 4 (CTLA-4). |
| 1531 | 23798565 | CTLA-4 is a negative regulator of T-cell responses and is associated with the induction of tolerogenic dendritic cells (DCs) that produce indoleamine 2,3-dioxygenase (IDO). |
| 1532 | 23798565 | Here, we show that despite increased expression of Ifng, Irf3, Irf7, Ido1, and Ido2 in the lymph nodes of TCDD-treated host mice, inhibition of IDO enzyme activity by 1-methyl-tryptophan was unable to relieve TCDD-mediated suppression of the GVH response. |
| 1533 | 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. |
| 1534 | 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. |
| 1535 | 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. |
| 1536 | 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. |
| 1537 | 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. |
| 1538 | 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. |
| 1539 | 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. |
| 1540 | 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. |
| 1541 | 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. |
| 1542 | 23777204 | Involvement of interferon-gamma genetic variants and intercellular adhesion molecule-1 in onset and progression of generalized vitiligo. |
| 1543 | 23777204 | Involvement of interferon-gamma genetic variants and intercellular adhesion molecule-1 in onset and progression of generalized vitiligo. |
| 1544 | 23777204 | Involvement of interferon-gamma genetic variants and intercellular adhesion molecule-1 in onset and progression of generalized vitiligo. |
| 1545 | 23777204 | The aim of present study was to determine whether intron 1 +874A/T (rs2430561) and CA microsatellite (rs3138557) polymorphisms in IFNG are associated with generalized vitiligo (GV) susceptibility and expression of IFNG and intercellular adhesion molecule-1 (ICAM1) affects the disease onset and progression. |
| 1546 | 23777204 | The aim of present study was to determine whether intron 1 +874A/T (rs2430561) and CA microsatellite (rs3138557) polymorphisms in IFNG are associated with generalized vitiligo (GV) susceptibility and expression of IFNG and intercellular adhesion molecule-1 (ICAM1) affects the disease onset and progression. |
| 1547 | 23777204 | The aim of present study was to determine whether intron 1 +874A/T (rs2430561) and CA microsatellite (rs3138557) polymorphisms in IFNG are associated with generalized vitiligo (GV) susceptibility and expression of IFNG and intercellular adhesion molecule-1 (ICAM1) affects the disease onset and progression. |
| 1548 | 23777204 | Patients with the early age of onset showed higher IFNG expression and female GV patients showed higher IFNG and ICAM1 expression implicating gender biasness and involvement of IFN-γ in early onset of the disease. |
| 1549 | 23777204 | Patients with the early age of onset showed higher IFNG expression and female GV patients showed higher IFNG and ICAM1 expression implicating gender biasness and involvement of IFN-γ in early onset of the disease. |
| 1550 | 23777204 | Patients with the early age of onset showed higher IFNG expression and female GV patients showed higher IFNG and ICAM1 expression implicating gender biasness and involvement of IFN-γ in early onset of the disease. |
| 1551 | 23764468 | Firstly, epigenetic enzyme gene expression (histone deacetylase (HDAC) and DNA methyltransferase (DNMT)) was measured after LPS stimulation. |
| 1552 | 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. |
| 1553 | 23761633 | STAT4 and T-bet are required for the plasticity of IFN-γ expression across Th2 ontogeny and influence changes in Ifng promoter DNA methylation. |
| 1554 | 23761633 | STAT4 and T-bet are required for the plasticity of IFN-γ expression across Th2 ontogeny and influence changes in Ifng promoter DNA methylation. |
| 1555 | 23761633 | STAT4 and T-bet are required for the plasticity of IFN-γ expression across Th2 ontogeny and influence changes in Ifng promoter DNA methylation. |
| 1556 | 23761633 | CD4(+) T cells developing toward a Th2 fate express IL-4, IL-5, and IL-13 while inhibiting production of cytokines associated with other Th types, such as the Th1 cytokine IFN- γ. |
| 1557 | 23761633 | CD4(+) T cells developing toward a Th2 fate express IL-4, IL-5, and IL-13 while inhibiting production of cytokines associated with other Th types, such as the Th1 cytokine IFN- γ. |
| 1558 | 23761633 | CD4(+) T cells developing toward a Th2 fate express IL-4, IL-5, and IL-13 while inhibiting production of cytokines associated with other Th types, such as the Th1 cytokine IFN- γ. |
| 1559 | 23761633 | We now show that this flexibility ("plasticity") of cytokine expression is preceded by a loss of the repressive DNA methylation of the Ifng promoter acquired during Th2 polarization yet requires STAT4 along with T-box expressed in T cells. |
| 1560 | 23761633 | We now show that this flexibility ("plasticity") of cytokine expression is preceded by a loss of the repressive DNA methylation of the Ifng promoter acquired during Th2 polarization yet requires STAT4 along with T-box expressed in T cells. |
| 1561 | 23761633 | We now show that this flexibility ("plasticity") of cytokine expression is preceded by a loss of the repressive DNA methylation of the Ifng promoter acquired during Th2 polarization yet requires STAT4 along with T-box expressed in T cells. |
| 1562 | 23761633 | Surprisingly, loss of either STAT4 or T-box expressed in T cells increased Ifng promoter CpG methylation in both effector and memory Th2 cells. |
| 1563 | 23761633 | Surprisingly, loss of either STAT4 or T-box expressed in T cells increased Ifng promoter CpG methylation in both effector and memory Th2 cells. |
| 1564 | 23761633 | Surprisingly, loss of either STAT4 or T-box expressed in T cells increased Ifng promoter CpG methylation in both effector and memory Th2 cells. |
| 1565 | 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. |
| 1566 | 23668260 | However, CD4 T cells of the untreated and C. difficile-infected mice expressed similar levels of CD69 and CD25. |
| 1567 | 23668260 | Neither tissue had up-regulated levels of Tbx21, Gata3 or Rorc. |
| 1568 | 23668260 | They also displayed significantly higher phosphorylation of AKT and signal transducer and activator of transcription 3 (STAT3), an indication of pro-survival signalling. |
| 1569 | 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. |
| 1570 | 23634300 | Therefore, the aim of this study was to verify if IFNG, IL12B, TNF, IL17A, IL10, and TGFB1 gene polymorphisms influence the immune response of Brazilian patients with pulmonary tuberculosis (PTB) at different time points of antituberculosis treatment (T1, T2, and T3). |
| 1571 | 23634300 | Therefore, the aim of this study was to verify if IFNG, IL12B, TNF, IL17A, IL10, and TGFB1 gene polymorphisms influence the immune response of Brazilian patients with pulmonary tuberculosis (PTB) at different time points of antituberculosis treatment (T1, T2, and T3). |
| 1572 | 23634300 | Therefore, the aim of this study was to verify if IFNG, IL12B, TNF, IL17A, IL10, and TGFB1 gene polymorphisms influence the immune response of Brazilian patients with pulmonary tuberculosis (PTB) at different time points of antituberculosis treatment (T1, T2, and T3). |
| 1573 | 23634300 | Our results showed the following associations: IFNG +874 T allele and IFNG +2109 A allele with higher IFN- γ levels; IL12B +1188 C allele with higher IL-12 levels; TNF -308 A allele with higher TNF- α plasma levels in controls and mRNA levels in PTB patients at T1; IL17A A allele at rs7747909 with higher IL-17 levels; IL10 -819 T allele with higher IL-10 levels; and TGFB1 +29 CC genotype higher TGF- β plasma levels in PTB patients at T2. |
| 1574 | 23634300 | Our results showed the following associations: IFNG +874 T allele and IFNG +2109 A allele with higher IFN- γ levels; IL12B +1188 C allele with higher IL-12 levels; TNF -308 A allele with higher TNF- α plasma levels in controls and mRNA levels in PTB patients at T1; IL17A A allele at rs7747909 with higher IL-17 levels; IL10 -819 T allele with higher IL-10 levels; and TGFB1 +29 CC genotype higher TGF- β plasma levels in PTB patients at T2. |
| 1575 | 23634300 | Our results showed the following associations: IFNG +874 T allele and IFNG +2109 A allele with higher IFN- γ levels; IL12B +1188 C allele with higher IL-12 levels; TNF -308 A allele with higher TNF- α plasma levels in controls and mRNA levels in PTB patients at T1; IL17A A allele at rs7747909 with higher IL-17 levels; IL10 -819 T allele with higher IL-10 levels; and TGFB1 +29 CC genotype higher TGF- β plasma levels in PTB patients at T2. |
| 1576 | 23634300 | The present study suggests that IFNG +874T/A, IFNG +2109A/G, IL12B +1188A/C, IL10 -819C/T, and TGFB1 +21C/T are associated with differential cytokine levels in pulmonary tuberculosis patients and may play a role in the initiation and maintenance of acquired cellular immunity to tuberculosis and in the outcome of the active disease while on antituberculosis treatment. |
| 1577 | 23634300 | The present study suggests that IFNG +874T/A, IFNG +2109A/G, IL12B +1188A/C, IL10 -819C/T, and TGFB1 +21C/T are associated with differential cytokine levels in pulmonary tuberculosis patients and may play a role in the initiation and maintenance of acquired cellular immunity to tuberculosis and in the outcome of the active disease while on antituberculosis treatment. |
| 1578 | 23634300 | The present study suggests that IFNG +874T/A, IFNG +2109A/G, IL12B +1188A/C, IL10 -819C/T, and TGFB1 +21C/T are associated with differential cytokine levels in pulmonary tuberculosis patients and may play a role in the initiation and maintenance of acquired cellular immunity to tuberculosis and in the outcome of the active disease while on antituberculosis treatment. |
| 1579 | 23613752 | Interferon gamma suppresses collagen-induced arthritis by regulation of Th17 through the induction of indoleamine-2,3-deoxygenase. |
| 1580 | 23613752 | C57BL/6 mice are known to be resistant to the development of collagen-induced arthritis (CIA). |
| 1581 | 23613752 | Also, production of IL-17 by the splenocytes of the IFN-γ KO mice was increased when cultured with type II collagen. |
| 1582 | 23613752 | The proportion of CD44(high)CD62L(low) memory-like T cells were elevated in the spleen, draining lymph node and mesenteric lymph node of IFN-γ KO CIA mice. |
| 1583 | 23613752 | Meanwhile, CD44(low)CD62L(high) naïve T cells were increased in IFN-γ and IL-17 double KO CIA mice. |
| 1584 | 23613752 | When Th17 polarized CD4+ T cells of IFN-γ KO mice were co-cultured with their own antigen presenting cells (APCs), a greater increase in IL-17 production was observed than in co-culture of the cells from wild type mice. |
| 1585 | 23595134 | Single-leg peak isometric force and blood 25(OH)D, aspartate and alanine aminotransferases, albumin, interferon (IFN)-γ, and interleukin-4 were measured prior to and following intense exercise. |
| 1586 | 23580950 | Mares were inseminated over five estrous cycles and endometrial biopsies were collected at one time point per cycle before (0) and 2, 6, 12, and 24 h after insemination. qPCR analysis for IL1B, IL6, IL8, IFNG, TNF (TNFA), IL10, and IL1RN was performed, and endometrial inflammatory cells were counted for each sample. |
| 1587 | 23580950 | Cytokine mRNA increased at 2 h, peaked between 2 and 12 h, and then decreased.Differences were detected between groups of mares 6 h after challenge; resistant mares had higher mRNA expression of IL6, IL1RN,and IL10 than susceptible mares. |
| 1588 | 23490048 | Intracranial infection of IRF7 KO mice was associated with delayed onset of LCM, increased survival and significantly reduced expression of the Ifng gene in the brain but not in the periphery. |
| 1589 | 23490048 | Intracranial infection of IRF7 KO mice was associated with delayed onset of LCM, increased survival and significantly reduced expression of the Ifng gene in the brain but not in the periphery. |
| 1590 | 23490048 | Similar numbers of activated anti-LCMV-GP(33-41) CD8+ T cells were present in the brain and spleens of infected WT and IRF7 KO mice. |
| 1591 | 23490048 | Similar numbers of activated anti-LCMV-GP(33-41) CD8+ T cells were present in the brain and spleens of infected WT and IRF7 KO mice. |
| 1592 | 23490048 | In conclusion, IRF7 (1) is required for the early innate control of LCMV infection, likely through the regulation of the appropriate type I IFN response, and (2) is not required for the antiviral CD8+ T cell-dependent clearance of LCMV from infected tissues. |
| 1593 | 23490048 | In conclusion, IRF7 (1) is required for the early innate control of LCMV infection, likely through the regulation of the appropriate type I IFN response, and (2) is not required for the antiviral CD8+ T cell-dependent clearance of LCMV from infected tissues. |
| 1594 | 23487038 | BAL1/ARTD9 represses the anti-proliferative and pro-apoptotic IFNγ-STAT1-IRF1-p53 axis in diffuse large B-cell lymphoma. |
| 1595 | 23487038 | Here we identify BAL1 as a novel oncogenic survival factor in DLBCL and show that constitutive overexpression of BAL1 in DLBCL tightly associates with intrinsic interferon-gamma (IFNγ) signaling and constitutive activity of signal transducer and activator of transcription (STAT)-1. |
| 1596 | 23487038 | Remarkably, BAL1 stimulates the phosphorylation of both STAT1 isoforms, STAT1α and STAT1β, on Y701 and thereby promotes the nuclear accumulation of the antagonistically acting and transcriptionally repressive isoform STAT1β. |
| 1597 | 23487038 | BAL1 directly inhibits, together with STAT1β, the expression of tumor suppressor and interferon response factor (IRF)-1. |
| 1598 | 23487038 | Conversely, BAL1 enhances the expression of the proto-oncogenes IRF2 and B-cell CLL/lymphoma (BCL)-6 in DLBCL. |
| 1599 | 23487038 | Our results show for the first time that BAL1 represses the anti-proliferative and pro-apoptotic IFNγ-STAT1-IRF1-p53 axis and mediates proliferation, survival and chemo-resistance in DLBCL. |
| 1600 | 23487038 | Our results suggest that BAL1 may induce an switch in STAT1 from a tumor suppressor to an oncogene in high-risk DLBCL. |
| 1601 | 23419269 | It can be further induced by various stimuli including starvation, hypoxia, and treatment with cytokines such as IFNG/IFNγ and TGFB/TGFβ. |
| 1602 | 23408540 | In contrast to the normal adult Type II cells, there was notable expression of inflammation-associated genes (Ccl2, Cxcl2, Ifng) as well as genes associated with epithelial growth (Ereg, Lep). |
| 1603 | 23349499 | Cereal-SPF rats displayed increased gut CD3(+) and CD8α(+) lymphocytes, ratio of Ifng to Il4 mRNA, and Lck expression, indicating T-cell activation. |
| 1604 | 23349499 | The cathelicidin antimicrobial peptide (Camp) gene was upregulated in the jejunum of HC diet-protected rats, and CAMP(+) cells colocalized with CD163. |
| 1605 | 23333334 | It down-regulates pro-inflammatory cytokines: TNF, IFNG and ICAM-1, resulting in decreased adherence of Plasmodium falciparum parasitized RBC to capillary wall, entry into the brain and delayed onset of death. |
| 1606 | 23313588 | During delayed export, nuclear NFAT constituted a short-term imprint of transient TCR signals and remained transcriptionally active for the T cell tolerance gene Egr2, but not for the effector gene Ifng, which required continuous TCR triggering for expression. |
| 1607 | 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. |
| 1608 | 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. |
| 1609 | 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). |
| 1610 | 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). |
| 1611 | 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). |
| 1612 | 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). |
| 1613 | 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. |
| 1614 | 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. |
| 1615 | 23255246 | Loss of methylation at the IFNG promoter and CNS-1 is associated with the development of functional IFN-γ memory in human CD4(+) T lymphocytes. |
| 1616 | 23221969 | IFNB1/interferon (IFN)-β belongs to the type I IFNs and exerts potent antiproliferative, proapoptotic, antiangiogenic and immunemodulatory functions. |
| 1617 | 23221969 | We show here that IFNB1 induces autophagy in MCF-7, MDAMB231 and SKBR3 breast cancer cells by measuring the turnover of two autophagic markers, MAP1LC3B/LC3 and SQSTM1/p62. |
| 1618 | 23221969 | The induction of autophagy in MCF-7 cells occurred upstream of the negative regulator of autophagy MTORC1, and autophagosome formation was dependent on the known core autophagy molecule ATG7 and the IFNB1 signaling molecule STAT1. |
| 1619 | 23221969 | Using siRNA-mediated silencing of several core autophagy molecules and STAT1, we provide evidence that IFNB1 mediates its antiproliferative effects independent of autophagy, while the proapoptotic function of IFNB1 was strongly enhanced in the absence of autophagy. |
| 1620 | 23179933 | The cytokines tumor necrosis factor α (TNFα), macrophage migration inhibitory factor (MIF) and interferon γ (INFγ) are proinflammatory cytokines of the innate immune response. |
| 1621 | 23179933 | The cytokines tumor necrosis factor α (TNFα), macrophage migration inhibitory factor (MIF) and interferon γ (INFγ) are proinflammatory cytokines of the innate immune response. |
| 1622 | 23179933 | We investigated the association between functional allelic variants of MIF (rs35688089), IFNG (rs2234688) and TNFA (rs1800629) in patients with MD. |
| 1623 | 23179933 | We investigated the association between functional allelic variants of MIF (rs35688089), IFNG (rs2234688) and TNFA (rs1800629) in patients with MD. |
| 1624 | 23179933 | Moreover, no genetic associations for variants in either the TNFA or IFNG genes and MD were found. |
| 1625 | 23179933 | Moreover, no genetic associations for variants in either the TNFA or IFNG genes and MD were found. |
| 1626 | 23138119 | IL-2 mRNA declined as pregnancy progressed, while IL-15, IFNG and TGFB1 transcripts increased on day 19 and/or 25. |
| 1627 | 23138119 | Analyses of IL-4 and IL-12 mRNAs demonstrated the increase in these transcripts as pregnancy progressed. |
| 1628 | 23138119 | Increase in CCR5 and CCR4 mRNAs indicated that both Th1 and Th2 cells coexisted in the day 25 pregnant endometrium. |
| 1629 | 23133532 | Polymorphisms in the inflammatory genes CIITA, CLEC16A and IFNG influence BMD, bone loss and fracture in elderly women. |
| 1630 | 23133532 | Polymorphisms in the inflammatory genes CIITA, CLEC16A and IFNG influence BMD, bone loss and fracture in elderly women. |
| 1631 | 23133532 | Polymorphisms in the inflammatory genes CIITA, CLEC16A and IFNG influence BMD, bone loss and fracture in elderly women. |
| 1632 | 23133532 | Osteoclast activity and the fine balance between bone formation and resorption is affected by inflammatory factors such as cytokines and T lymphocyte activity, mediated by major histocompatibility complex (MHC) molecules, in turn regulated by the MHC class II transactivator (MHC2TA). |
| 1633 | 23133532 | Osteoclast activity and the fine balance between bone formation and resorption is affected by inflammatory factors such as cytokines and T lymphocyte activity, mediated by major histocompatibility complex (MHC) molecules, in turn regulated by the MHC class II transactivator (MHC2TA). |
| 1634 | 23133532 | Osteoclast activity and the fine balance between bone formation and resorption is affected by inflammatory factors such as cytokines and T lymphocyte activity, mediated by major histocompatibility complex (MHC) molecules, in turn regulated by the MHC class II transactivator (MHC2TA). |
| 1635 | 23133532 | We investigated the effect of functional polymorphisms in the MHC2TA gene (CIITA), and two additional genes; C-type lectin domain 16A (CLEC16A), in linkage disequilibrium with CIITA and Interferon-γ (IFNG), an inducer of CIITA; on bone density, bone resorption markers, bone loss and fracture risk in 75 year-old women followed for up to 10 years (OPRA n = 1003) and in young adult women (PEAK-25 n = 999). |
| 1636 | 23133532 | We investigated the effect of functional polymorphisms in the MHC2TA gene (CIITA), and two additional genes; C-type lectin domain 16A (CLEC16A), in linkage disequilibrium with CIITA and Interferon-γ (IFNG), an inducer of CIITA; on bone density, bone resorption markers, bone loss and fracture risk in 75 year-old women followed for up to 10 years (OPRA n = 1003) and in young adult women (PEAK-25 n = 999). |
| 1637 | 23133532 | We investigated the effect of functional polymorphisms in the MHC2TA gene (CIITA), and two additional genes; C-type lectin domain 16A (CLEC16A), in linkage disequilibrium with CIITA and Interferon-γ (IFNG), an inducer of CIITA; on bone density, bone resorption markers, bone loss and fracture risk in 75 year-old women followed for up to 10 years (OPRA n = 1003) and in young adult women (PEAK-25 n = 999). |
| 1638 | 23133532 | Carriers of CLEC16A and IFNG variant alleles had lower BMD (p<0.05) and ultrasound parameters and a lower risk of incident fracture (CLEC16A, p = 0.011). |
| 1639 | 23133532 | Carriers of CLEC16A and IFNG variant alleles had lower BMD (p<0.05) and ultrasound parameters and a lower risk of incident fracture (CLEC16A, p = 0.011). |
| 1640 | 23133532 | Carriers of CLEC16A and IFNG variant alleles had lower BMD (p<0.05) and ultrasound parameters and a lower risk of incident fracture (CLEC16A, p = 0.011). |
| 1641 | 23133532 | In conclusion, variation in inflammatory genes CIITA, CLEC-16A and INFG appear to contribute to bone phenotypes in elderly women and suggest a role for low-grade inflammation and MHC class II expression for osteoporosis pathogenesis. |
| 1642 | 23133532 | In conclusion, variation in inflammatory genes CIITA, CLEC-16A and INFG appear to contribute to bone phenotypes in elderly women and suggest a role for low-grade inflammation and MHC class II expression for osteoporosis pathogenesis. |
| 1643 | 23133532 | In conclusion, variation in inflammatory genes CIITA, CLEC-16A and INFG appear to contribute to bone phenotypes in elderly women and suggest a role for low-grade inflammation and MHC class II expression for osteoporosis pathogenesis. |
| 1644 | 23106526 | The expression of cytokines mRNA, namely Ifng, Il2,Il4,Il10 and Il12, was quantitated by real-time PCR. |
| 1645 | 23106526 | The expression of cytokines mRNA, namely Ifng, Il2,Il4,Il10 and Il12, was quantitated by real-time PCR. |
| 1646 | 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. |
| 1647 | 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. |
| 1648 | 23086406 | In this study, we identified hGBP1/2 as important resistance factors against C. trachomatis infection in IFNG-stimulated human macrophages. |
| 1649 | 23086406 | In this study, we identified hGBP1/2 as important resistance factors against C. trachomatis infection in IFNG-stimulated human macrophages. |
| 1650 | 23086406 | In this study, we identified hGBP1/2 as important resistance factors against C. trachomatis infection in IFNG-stimulated human macrophages. |
| 1651 | 23086406 | In this study, we identified hGBP1/2 as important resistance factors against C. trachomatis infection in IFNG-stimulated human macrophages. |
| 1652 | 23086406 | Exogenous IFNG reduced chlamydial infectivity by 50 percent in wild-type cells, whereas shRNA hGBP1/2 knockdown macrophages fully supported chlamydial growth in the presence of exogenous IFNG. hGBP1/2 were recruited to bacterial inclusions in human macrophages upon stimulation with IFNG, which triggered rerouting of the typically nonfusogenic bacterial inclusions for lysosomal degradation. |
| 1653 | 23086406 | Exogenous IFNG reduced chlamydial infectivity by 50 percent in wild-type cells, whereas shRNA hGBP1/2 knockdown macrophages fully supported chlamydial growth in the presence of exogenous IFNG. hGBP1/2 were recruited to bacterial inclusions in human macrophages upon stimulation with IFNG, which triggered rerouting of the typically nonfusogenic bacterial inclusions for lysosomal degradation. |
| 1654 | 23086406 | Exogenous IFNG reduced chlamydial infectivity by 50 percent in wild-type cells, whereas shRNA hGBP1/2 knockdown macrophages fully supported chlamydial growth in the presence of exogenous IFNG. hGBP1/2 were recruited to bacterial inclusions in human macrophages upon stimulation with IFNG, which triggered rerouting of the typically nonfusogenic bacterial inclusions for lysosomal degradation. |
| 1655 | 23086406 | Exogenous IFNG reduced chlamydial infectivity by 50 percent in wild-type cells, whereas shRNA hGBP1/2 knockdown macrophages fully supported chlamydial growth in the presence of exogenous IFNG. hGBP1/2 were recruited to bacterial inclusions in human macrophages upon stimulation with IFNG, which triggered rerouting of the typically nonfusogenic bacterial inclusions for lysosomal degradation. |
| 1656 | 23086406 | Thus, hGBP1/2 are critical effectors of antichlamydial IFNG responses in human macrophages. |
| 1657 | 23086406 | Thus, hGBP1/2 are critical effectors of antichlamydial IFNG responses in human macrophages. |
| 1658 | 23086406 | Thus, hGBP1/2 are critical effectors of antichlamydial IFNG responses in human macrophages. |
| 1659 | 23086406 | Thus, hGBP1/2 are critical effectors of antichlamydial IFNG responses in human macrophages. |
| 1660 | 23086406 | Through their capacity to remodel classically nonfusogenic chlamydial inclusions and stimulate fusion with autophagosomes, hGBP1/2 disable a major chlamydial virulence mechanism and contribute to IFNG-mediated pathogen clearance. |
| 1661 | 23086406 | Through their capacity to remodel classically nonfusogenic chlamydial inclusions and stimulate fusion with autophagosomes, hGBP1/2 disable a major chlamydial virulence mechanism and contribute to IFNG-mediated pathogen clearance. |
| 1662 | 23086406 | Through their capacity to remodel classically nonfusogenic chlamydial inclusions and stimulate fusion with autophagosomes, hGBP1/2 disable a major chlamydial virulence mechanism and contribute to IFNG-mediated pathogen clearance. |
| 1663 | 23086406 | Through their capacity to remodel classically nonfusogenic chlamydial inclusions and stimulate fusion with autophagosomes, hGBP1/2 disable a major chlamydial virulence mechanism and contribute to IFNG-mediated pathogen clearance. |
| 1664 | 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. |
| 1665 | 23071669 | MYC/MYCN, TGFB1, and IL2) and to 4 weeks (e.g. |
| 1666 | 23071669 | IFNG, beta-estradiol, p53, NFKB, AKT, PRKCA, IL12, and HLA-C). |
| 1667 | 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. |
| 1668 | 23063468 | Therefore, the DNA methylation status of the Ifng promoter in CD4(+) cells from neonatal foal was determined using a methylation-specific PCR (MSP), and its relevance to IFN-γ mRNA expression was estimated. |
| 1669 | 22940185 | A cytokine profile revealed the Th1- lineage development of dominant IFNg and IL-2 from RECD4T. |
| 1670 | 22912446 | Downregulated genes in tumorous spleens mainly enriched in the cytokine-cytokine receptor interaction pathway, and commonly investigated genes in Marek's disease study, IL6, IL18, IFNA, and IFNG were nondifferentially expressed, which indicates host inflammatory response was impaired. |
| 1671 | 22912446 | The IL10 and TNFRSF8 genes were upregulated in tumorous spleens. |
| 1672 | 22896638 | The Ifng gene is essential for Vdr gene expression and vitamin D₃-mediated reduction of the pathogenic T cell burden in the central nervous system in experimental autoimmune encephalomyelitis, a multiple sclerosis model. |
| 1673 | 22896638 | The Ifng gene is essential for Vdr gene expression and vitamin D₃-mediated reduction of the pathogenic T cell burden in the central nervous system in experimental autoimmune encephalomyelitis, a multiple sclerosis model. |
| 1674 | 22896638 | The Ifng gene is essential for Vdr gene expression and vitamin D₃-mediated reduction of the pathogenic T cell burden in the central nervous system in experimental autoimmune encephalomyelitis, a multiple sclerosis model. |
| 1675 | 22896638 | The two strains did not differ in Cyp27b1 and Cyp24a1 gene expression, implying equivalent vitamin D3 metabolism in the CNS. |
| 1676 | 22896638 | The two strains did not differ in Cyp27b1 and Cyp24a1 gene expression, implying equivalent vitamin D3 metabolism in the CNS. |
| 1677 | 22896638 | The two strains did not differ in Cyp27b1 and Cyp24a1 gene expression, implying equivalent vitamin D3 metabolism in the CNS. |
| 1678 | 22896638 | Thus, the Ifng gene was needed for CNS Vdr gene expression and vitamin D3-dependent mechanisms that inhibit EAE. |
| 1679 | 22896638 | Thus, the Ifng gene was needed for CNS Vdr gene expression and vitamin D3-dependent mechanisms that inhibit EAE. |
| 1680 | 22896638 | Thus, the Ifng gene was needed for CNS Vdr gene expression and vitamin D3-dependent mechanisms that inhibit EAE. |
| 1681 | 22896638 | Individuals with inadequate Ifng expression may have increased MS risk despite high ambient UV irradiation because of low Vdr gene expression and a high encephalitogenic T cell burden in the CNS. |
| 1682 | 22896638 | Individuals with inadequate Ifng expression may have increased MS risk despite high ambient UV irradiation because of low Vdr gene expression and a high encephalitogenic T cell burden in the CNS. |
| 1683 | 22896638 | Individuals with inadequate Ifng expression may have increased MS risk despite high ambient UV irradiation because of low Vdr gene expression and a high encephalitogenic T cell burden in the CNS. |
| 1684 | 22875907 | CD3E (CD3)-IL2RB (CD122)+DBA cells were identified as the dominant Ifng transcript source. |
| 1685 | 22875907 | In contrast, CD3E-IL2RB+DBA+ uNK cells expressed genes compatible with significantly greater potential for IL22 synthesis, angiogenesis, and participation in regulation mediated by the renin-angiotensin system (RAS). |
| 1686 | 22874566 | IFNG and autophagy: a critical role for the ER-stress mediator ATF6 in controlling bacterial infections. |
| 1687 | 22874566 | IFNG and autophagy: a critical role for the ER-stress mediator ATF6 in controlling bacterial infections. |
| 1688 | 22874566 | IFNG and autophagy: a critical role for the ER-stress mediator ATF6 in controlling bacterial infections. |
| 1689 | 22874566 | IFNG and autophagy: a critical role for the ER-stress mediator ATF6 in controlling bacterial infections. |
| 1690 | 22874566 | IFNG and autophagy: a critical role for the ER-stress mediator ATF6 in controlling bacterial infections. |
| 1691 | 22874566 | IFNG and autophagy: a critical role for the ER-stress mediator ATF6 in controlling bacterial infections. |
| 1692 | 22874566 | The death-associated protein kinase 1 (DAPK1), originally identified as an activator of IFNG-induced cell death, controls autophagy. |
| 1693 | 22874566 | The death-associated protein kinase 1 (DAPK1), originally identified as an activator of IFNG-induced cell death, controls autophagy. |
| 1694 | 22874566 | The death-associated protein kinase 1 (DAPK1), originally identified as an activator of IFNG-induced cell death, controls autophagy. |
| 1695 | 22874566 | The death-associated protein kinase 1 (DAPK1), originally identified as an activator of IFNG-induced cell death, controls autophagy. |
| 1696 | 22874566 | The death-associated protein kinase 1 (DAPK1), originally identified as an activator of IFNG-induced cell death, controls autophagy. |
| 1697 | 22874566 | The death-associated protein kinase 1 (DAPK1), originally identified as an activator of IFNG-induced cell death, controls autophagy. |
| 1698 | 22874566 | Previously, we have shown that transcription factor CEBPB (C/EBP-β) regulates IFNG-induced expression of Dapk1 through a CRE/ATF motif in its enhancer. |
| 1699 | 22874566 | Previously, we have shown that transcription factor CEBPB (C/EBP-β) regulates IFNG-induced expression of Dapk1 through a CRE/ATF motif in its enhancer. |
| 1700 | 22874566 | Previously, we have shown that transcription factor CEBPB (C/EBP-β) regulates IFNG-induced expression of Dapk1 through a CRE/ATF motif in its enhancer. |
| 1701 | 22874566 | Previously, we have shown that transcription factor CEBPB (C/EBP-β) regulates IFNG-induced expression of Dapk1 through a CRE/ATF motif in its enhancer. |
| 1702 | 22874566 | Previously, we have shown that transcription factor CEBPB (C/EBP-β) regulates IFNG-induced expression of Dapk1 through a CRE/ATF motif in its enhancer. |
| 1703 | 22874566 | Previously, we have shown that transcription factor CEBPB (C/EBP-β) regulates IFNG-induced expression of Dapk1 through a CRE/ATF motif in its enhancer. |
| 1704 | 22874566 | In this paper we have shown that ATF6, an ER-resident transcription factor regulates IFNG-induced Dapk1 expression through the CRE/ATF site, in association with CEBPB. |
| 1705 | 22874566 | In this paper we have shown that ATF6, an ER-resident transcription factor regulates IFNG-induced Dapk1 expression through the CRE/ATF site, in association with CEBPB. |
| 1706 | 22874566 | In this paper we have shown that ATF6, an ER-resident transcription factor regulates IFNG-induced Dapk1 expression through the CRE/ATF site, in association with CEBPB. |
| 1707 | 22874566 | In this paper we have shown that ATF6, an ER-resident transcription factor regulates IFNG-induced Dapk1 expression through the CRE/ATF site, in association with CEBPB. |
| 1708 | 22874566 | In this paper we have shown that ATF6, an ER-resident transcription factor regulates IFNG-induced Dapk1 expression through the CRE/ATF site, in association with CEBPB. |
| 1709 | 22874566 | In this paper we have shown that ATF6, an ER-resident transcription factor regulates IFNG-induced Dapk1 expression through the CRE/ATF site, in association with CEBPB. |
| 1710 | 22874566 | IFNG-stimulated proteolytic cleavage of ATF6, and MAPK1/3 (ERK2/1)-dependent phosphorylation of CEBPB together control the expression of Dapk1. |
| 1711 | 22874566 | IFNG-stimulated proteolytic cleavage of ATF6, and MAPK1/3 (ERK2/1)-dependent phosphorylation of CEBPB together control the expression of Dapk1. |
| 1712 | 22874566 | IFNG-stimulated proteolytic cleavage of ATF6, and MAPK1/3 (ERK2/1)-dependent phosphorylation of CEBPB together control the expression of Dapk1. |
| 1713 | 22874566 | IFNG-stimulated proteolytic cleavage of ATF6, and MAPK1/3 (ERK2/1)-dependent phosphorylation of CEBPB together control the expression of Dapk1. |
| 1714 | 22874566 | IFNG-stimulated proteolytic cleavage of ATF6, and MAPK1/3 (ERK2/1)-dependent phosphorylation of CEBPB together control the expression of Dapk1. |
| 1715 | 22874566 | IFNG-stimulated proteolytic cleavage of ATF6, and MAPK1/3 (ERK2/1)-dependent phosphorylation of CEBPB together control the expression of Dapk1. |
| 1716 | 22874566 | Consistent with their requirement for DAPK1 expression, IFNG fails to induce autophagy in cells lacking either Atf6 or Cebpb. |
| 1717 | 22874566 | Consistent with their requirement for DAPK1 expression, IFNG fails to induce autophagy in cells lacking either Atf6 or Cebpb. |
| 1718 | 22874566 | Consistent with their requirement for DAPK1 expression, IFNG fails to induce autophagy in cells lacking either Atf6 or Cebpb. |
| 1719 | 22874566 | Consistent with their requirement for DAPK1 expression, IFNG fails to induce autophagy in cells lacking either Atf6 or Cebpb. |
| 1720 | 22874566 | Consistent with their requirement for DAPK1 expression, IFNG fails to induce autophagy in cells lacking either Atf6 or Cebpb. |
| 1721 | 22874566 | Consistent with their requirement for DAPK1 expression, IFNG fails to induce autophagy in cells lacking either Atf6 or Cebpb. |
| 1722 | 22851706 | In this study, we show that transcription of both mouse and human TMEVPG1 genes is Th1 selective and dependent on Stat4 and T-bet, transcription factors that drive the Th1 differentiation program. |
| 1723 | 22851706 | Ifng expression is partially restored in Stat4-/-Tbx21-/- cells through coexpression of T-bet and Tmevpg1, and Tmevpg1 expression contributes to, but alone is not sufficient to, drive Th1-dependent Ifng expression. |
| 1724 | 22847916 | The purpose of the present study was to elucidate if tumor necrosis factor-α (TNF), interferon γ (IFNG), and/or progesterone (P4) play roles in regulating NO generating system in LECs. |
| 1725 | 22847916 | The purpose of the present study was to elucidate if tumor necrosis factor-α (TNF), interferon γ (IFNG), and/or progesterone (P4) play roles in regulating NO generating system in LECs. |
| 1726 | 22847916 | The purpose of the present study was to elucidate if tumor necrosis factor-α (TNF), interferon γ (IFNG), and/or progesterone (P4) play roles in regulating NO generating system in LECs. |
| 1727 | 22847916 | The purpose of the present study was to elucidate if tumor necrosis factor-α (TNF), interferon γ (IFNG), and/or progesterone (P4) play roles in regulating NO generating system in LECs. |
| 1728 | 22847916 | The purpose of the present study was to elucidate if tumor necrosis factor-α (TNF), interferon γ (IFNG), and/or progesterone (P4) play roles in regulating NO generating system in LECs. |
| 1729 | 22847916 | The purpose of the present study was to elucidate if tumor necrosis factor-α (TNF), interferon γ (IFNG), and/or progesterone (P4) play roles in regulating NO generating system in LECs. |
| 1730 | 22847916 | Cultured bovine LECs obtained from the CL at the mid-luteal stage (Days 8-12 of the cycle) were treated for 24 hr with TNF (2.9 nM), IFNG (2.5 nM), or P4 (0.032-32 µM). |
| 1731 | 22847916 | Cultured bovine LECs obtained from the CL at the mid-luteal stage (Days 8-12 of the cycle) were treated for 24 hr with TNF (2.9 nM), IFNG (2.5 nM), or P4 (0.032-32 µM). |
| 1732 | 22847916 | Cultured bovine LECs obtained from the CL at the mid-luteal stage (Days 8-12 of the cycle) were treated for 24 hr with TNF (2.9 nM), IFNG (2.5 nM), or P4 (0.032-32 µM). |
| 1733 | 22847916 | Cultured bovine LECs obtained from the CL at the mid-luteal stage (Days 8-12 of the cycle) were treated for 24 hr with TNF (2.9 nM), IFNG (2.5 nM), or P4 (0.032-32 µM). |
| 1734 | 22847916 | Cultured bovine LECs obtained from the CL at the mid-luteal stage (Days 8-12 of the cycle) were treated for 24 hr with TNF (2.9 nM), IFNG (2.5 nM), or P4 (0.032-32 µM). |
| 1735 | 22847916 | Cultured bovine LECs obtained from the CL at the mid-luteal stage (Days 8-12 of the cycle) were treated for 24 hr with TNF (2.9 nM), IFNG (2.5 nM), or P4 (0.032-32 µM). |
| 1736 | 22847916 | NO production was increased by TNF and IFNG, but decreased by P4 (P < 0.05). |
| 1737 | 22847916 | NO production was increased by TNF and IFNG, but decreased by P4 (P < 0.05). |
| 1738 | 22847916 | NO production was increased by TNF and IFNG, but decreased by P4 (P < 0.05). |
| 1739 | 22847916 | NO production was increased by TNF and IFNG, but decreased by P4 (P < 0.05). |
| 1740 | 22847916 | NO production was increased by TNF and IFNG, but decreased by P4 (P < 0.05). |
| 1741 | 22847916 | NO production was increased by TNF and IFNG, but decreased by P4 (P < 0.05). |
| 1742 | 22847916 | TNF and IFNG stimulated the relative steady-state amounts of inducible nitric oxide synthase (iNOS) mRNA and iNOS protein expression (P < 0.05), whereas P4 inhibited relative steady-state amounts of iNOS mRNA and iNOS protein expression (P < 0.05). |
| 1743 | 22847916 | TNF and IFNG stimulated the relative steady-state amounts of inducible nitric oxide synthase (iNOS) mRNA and iNOS protein expression (P < 0.05), whereas P4 inhibited relative steady-state amounts of iNOS mRNA and iNOS protein expression (P < 0.05). |
| 1744 | 22847916 | TNF and IFNG stimulated the relative steady-state amounts of inducible nitric oxide synthase (iNOS) mRNA and iNOS protein expression (P < 0.05), whereas P4 inhibited relative steady-state amounts of iNOS mRNA and iNOS protein expression (P < 0.05). |
| 1745 | 22847916 | TNF and IFNG stimulated the relative steady-state amounts of inducible nitric oxide synthase (iNOS) mRNA and iNOS protein expression (P < 0.05), whereas P4 inhibited relative steady-state amounts of iNOS mRNA and iNOS protein expression (P < 0.05). |
| 1746 | 22847916 | TNF and IFNG stimulated the relative steady-state amounts of inducible nitric oxide synthase (iNOS) mRNA and iNOS protein expression (P < 0.05), whereas P4 inhibited relative steady-state amounts of iNOS mRNA and iNOS protein expression (P < 0.05). |
| 1747 | 22847916 | TNF and IFNG stimulated the relative steady-state amounts of inducible nitric oxide synthase (iNOS) mRNA and iNOS protein expression (P < 0.05), whereas P4 inhibited relative steady-state amounts of iNOS mRNA and iNOS protein expression (P < 0.05). |
| 1748 | 22847916 | TNF and IFNG stimulated NOS activity (P < 0.05) and 1400W, a specific inhibitor of iNOS, reduced NO production stimulated by TNF and IFNG in LECs (P < 0.05). |
| 1749 | 22847916 | TNF and IFNG stimulated NOS activity (P < 0.05) and 1400W, a specific inhibitor of iNOS, reduced NO production stimulated by TNF and IFNG in LECs (P < 0.05). |
| 1750 | 22847916 | TNF and IFNG stimulated NOS activity (P < 0.05) and 1400W, a specific inhibitor of iNOS, reduced NO production stimulated by TNF and IFNG in LECs (P < 0.05). |
| 1751 | 22847916 | TNF and IFNG stimulated NOS activity (P < 0.05) and 1400W, a specific inhibitor of iNOS, reduced NO production stimulated by TNF and IFNG in LECs (P < 0.05). |
| 1752 | 22847916 | TNF and IFNG stimulated NOS activity (P < 0.05) and 1400W, a specific inhibitor of iNOS, reduced NO production stimulated by TNF and IFNG in LECs (P < 0.05). |
| 1753 | 22847916 | TNF and IFNG stimulated NOS activity (P < 0.05) and 1400W, a specific inhibitor of iNOS, reduced NO production stimulated by TNF and IFNG in LECs (P < 0.05). |
| 1754 | 22847916 | The overall findings suggest that TNF and IFNG accelerate luteolysis by increasing NO production via stimulation of iNOS expression and NOS activity in bovine LECs. |
| 1755 | 22847916 | The overall findings suggest that TNF and IFNG accelerate luteolysis by increasing NO production via stimulation of iNOS expression and NOS activity in bovine LECs. |
| 1756 | 22847916 | The overall findings suggest that TNF and IFNG accelerate luteolysis by increasing NO production via stimulation of iNOS expression and NOS activity in bovine LECs. |
| 1757 | 22847916 | The overall findings suggest that TNF and IFNG accelerate luteolysis by increasing NO production via stimulation of iNOS expression and NOS activity in bovine LECs. |
| 1758 | 22847916 | The overall findings suggest that TNF and IFNG accelerate luteolysis by increasing NO production via stimulation of iNOS expression and NOS activity in bovine LECs. |
| 1759 | 22847916 | The overall findings suggest that TNF and IFNG accelerate luteolysis by increasing NO production via stimulation of iNOS expression and NOS activity in bovine LECs. |
| 1760 | 22847916 | P4, on the other hand, may act in maintaining CL function by suppressing iNOS expression in bovine LECs. |
| 1761 | 22847916 | P4, on the other hand, may act in maintaining CL function by suppressing iNOS expression in bovine LECs. |
| 1762 | 22847916 | P4, on the other hand, may act in maintaining CL function by suppressing iNOS expression in bovine LECs. |
| 1763 | 22847916 | P4, on the other hand, may act in maintaining CL function by suppressing iNOS expression in bovine LECs. |
| 1764 | 22847916 | P4, on the other hand, may act in maintaining CL function by suppressing iNOS expression in bovine LECs. |
| 1765 | 22847916 | P4, on the other hand, may act in maintaining CL function by suppressing iNOS expression in bovine LECs. |
| 1766 | 22735807 | We have previously shown that vaccination with the natural tumor peptide Melan-A-induced T cells with superior effector functions as compared with vaccination with the analog peptide optimized for enhanced HLA-A*0201 binding. |
| 1767 | 22735807 | Here we found that natural peptide vaccination induced tumor-reactive CD8 T cells with frequent coexpression of both memory/homing-associated genes (CD27, IL7R, EOMES, CXCR3, and CCR5) and effector-related genes (IFNG, KLRD1, PRF1, and GZMB), comparable with protective Epstein-Barr virus-specific and cytomegalovirus-specific T cells. |
| 1768 | 22685317 | Naturally occurring effector CD8(+) T cells, with a KLRG1(hi) CD62L(lo) phenotype typical of short-lived effector CD8(+) T cells (SLECs), can be found in increased numbers in autoimmune-prone mice, most notably in mice homozygous for the san allele of Roquin. |
| 1769 | 22685317 | When Roquin is mutated (Roquin(san)), effector CD8(+) T cells accumulate in a cell-autonomous manner, most prominently as SLEC-like effectors. |
| 1770 | 22685317 | Excessive IFN-γ promotes the accumulation of SLEC-like cells, increases their T-bet expression, and enhances their granzyme B production in vivo. |
| 1771 | 22685317 | This study identifies a novel mechanism that prevents accumulation of self-reactive cytotoxic effectors, highlighting the importance of regulating Ifng mRNA stability to maintain CD8(+) T cell homeostasis and prevent CD8-mediated autoimmunity. |
| 1772 | 22685315 | Twist1 regulates Ifng expression in Th1 cells by interfering with Runx3 function. |
| 1773 | 22685315 | Twist1 regulates Ifng expression in Th1 cells by interfering with Runx3 function. |
| 1774 | 22685315 | Twist1 regulates Ifng expression in Th1 cells by interfering with Runx3 function. |
| 1775 | 22685315 | A transcription factor network that includes STAT4, T-bet, and Runx3 promotes the differentiation of Th1 cells and inflammatory immune responses. |
| 1776 | 22685315 | A transcription factor network that includes STAT4, T-bet, and Runx3 promotes the differentiation of Th1 cells and inflammatory immune responses. |
| 1777 | 22685315 | A transcription factor network that includes STAT4, T-bet, and Runx3 promotes the differentiation of Th1 cells and inflammatory immune responses. |
| 1778 | 22685315 | In this study we show that the negative regulatory factor Twist1 decreases expression of T-bet, Runx3, and IL-12Rβ2 as it inhibits IFN-γ production. |
| 1779 | 22685315 | In this study we show that the negative regulatory factor Twist1 decreases expression of T-bet, Runx3, and IL-12Rβ2 as it inhibits IFN-γ production. |
| 1780 | 22685315 | In this study we show that the negative regulatory factor Twist1 decreases expression of T-bet, Runx3, and IL-12Rβ2 as it inhibits IFN-γ production. |
| 1781 | 22685315 | Ectopic expression of Runx3, but not T-bet or IL-12Rβ2, compensates for the effects of Twist1 on IFN-γ production, and Twist1 regulation of Ifng depends on complex formation with Runx3. |
| 1782 | 22685315 | Ectopic expression of Runx3, but not T-bet or IL-12Rβ2, compensates for the effects of Twist1 on IFN-γ production, and Twist1 regulation of Ifng depends on complex formation with Runx3. |
| 1783 | 22685315 | Ectopic expression of Runx3, but not T-bet or IL-12Rβ2, compensates for the effects of Twist1 on IFN-γ production, and Twist1 regulation of Ifng depends on complex formation with Runx3. |
| 1784 | 22685315 | Twist1 decreases Runx3 and T-bet binding at the Ifng locus, and it decreases chromatin looping within the Ifng locus. |
| 1785 | 22685315 | Twist1 decreases Runx3 and T-bet binding at the Ifng locus, and it decreases chromatin looping within the Ifng locus. |
| 1786 | 22685315 | Twist1 decreases Runx3 and T-bet binding at the Ifng locus, and it decreases chromatin looping within the Ifng locus. |
| 1787 | 22685315 | These data define an IL-12/STAT4-induced negative regulatory loop that impacts multiple components of the Th1 transcriptional network and provide further insight into regulation of Th1 differentiation. |
| 1788 | 22685315 | These data define an IL-12/STAT4-induced negative regulatory loop that impacts multiple components of the Th1 transcriptional network and provide further insight into regulation of Th1 differentiation. |
| 1789 | 22685315 | These data define an IL-12/STAT4-induced negative regulatory loop that impacts multiple components of the Th1 transcriptional network and provide further insight into regulation of Th1 differentiation. |
| 1790 | 22674296 | After controlling for multiple comparisons, single nucleotide polymorphisms (SNPs) from four genes, IL3, IL6R, IL8, IL15, were associated with increased colon cancer risk, and CXCR1 and CXCR2 were significantly associated with increased rectal cancer risk. |
| 1791 | 22674296 | Only SNPs from genes within the IL-8 pathway (IL8, CXCR1 and CXCR2) showed a significant association with both colon and rectal cancer risk. |
| 1792 | 22674296 | Several SNPs interacted significantly with IL8 and IFNG SNPs and with aspirin/non-steroidal anti-inflammatory drug (NSAID), cigarette smoking, estrogen use and BMI. |
| 1793 | 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. |
| 1794 | 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. |
| 1795 | 22659089 | The CCBs nimodipine (NDP) and verapamil (VPM) both significantly suppressed toxic secretions from human astrocytes and astrocytoma U-373 MG cells that were induced by interferon (IFN)-γ. |
| 1796 | 22659089 | In human astrocytes, both NDP and VPM reduced IFN-γ-induced phosphorylation of signal transducer and activator of transcription (STAT) 3. |
| 1797 | 22578563 | To test this hypothesis, mice deficient in genes regulating IFN-γ expression (Casp1, Nlrp3, Il12a, Il12b, Stat4) or function (Ifngr1, Irf1) were examined for mHgIA susceptibility. |
| 1798 | 22578563 | Absence of either Ifngr1 or Irf1 resulted in a striking reduction of disease, while deficiency of genes promoting IFN-γ expression had modest to no effect. |
| 1799 | 22578563 | Furthermore, both Irf1- and Ifng-deficiency only modestly reduced the expansion of CD44(hi) and CD44(hi)CD55(lo) CD4(+) T cells, indicating that they are not absolutely required for T cell activation. |
| 1800 | 22492973 | Therefore, the purpose of this study was to evaluate the role of cytokines--tumor necrosis factor alpha (TNF), interferon gamma (IFNG) and Fas ligand (FASL)--on in vitro modulation of angiogenic activity and mRNA level of vascular endothelial growth factor A (VEGF), its receptor VEGFR2, thrombospondin 1 (TSP1), and its receptor CD36 in equine corpus luteum (CL) throughout the luteal phase. |
| 1801 | 22492973 | Therefore, the purpose of this study was to evaluate the role of cytokines--tumor necrosis factor alpha (TNF), interferon gamma (IFNG) and Fas ligand (FASL)--on in vitro modulation of angiogenic activity and mRNA level of vascular endothelial growth factor A (VEGF), its receptor VEGFR2, thrombospondin 1 (TSP1), and its receptor CD36 in equine corpus luteum (CL) throughout the luteal phase. |
| 1802 | 22492973 | Therefore, the purpose of this study was to evaluate the role of cytokines--tumor necrosis factor alpha (TNF), interferon gamma (IFNG) and Fas ligand (FASL)--on in vitro modulation of angiogenic activity and mRNA level of vascular endothelial growth factor A (VEGF), its receptor VEGFR2, thrombospondin 1 (TSP1), and its receptor CD36 in equine corpus luteum (CL) throughout the luteal phase. |
| 1803 | 22492973 | The role of VEGF on regulation of luteal secretory capacity was assessed by progesterone (P(4)) and prostaglandin E(2) (PGE(2)) production and by mRNA levels for steroidogenic enzymes 3-beta-hydroxysteroid dehydrogenase (3betaHSD) and PGE synthase (PGES). |
| 1804 | 22492973 | The role of VEGF on regulation of luteal secretory capacity was assessed by progesterone (P(4)) and prostaglandin E(2) (PGE(2)) production and by mRNA levels for steroidogenic enzymes 3-beta-hydroxysteroid dehydrogenase (3betaHSD) and PGE synthase (PGES). |
| 1805 | 22492973 | The role of VEGF on regulation of luteal secretory capacity was assessed by progesterone (P(4)) and prostaglandin E(2) (PGE(2)) production and by mRNA levels for steroidogenic enzymes 3-beta-hydroxysteroid dehydrogenase (3betaHSD) and PGE synthase (PGES). |
| 1806 | 22492973 | In early CL cells, TNF increased angiogenic activity (bovine aortic endothelial cell viability) and VEGF and VEGFR2 mRNA levels and decreased CD36 (real-time PCR relative quantification). |
| 1807 | 22492973 | In early CL cells, TNF increased angiogenic activity (bovine aortic endothelial cell viability) and VEGF and VEGFR2 mRNA levels and decreased CD36 (real-time PCR relative quantification). |
| 1808 | 22492973 | In early CL cells, TNF increased angiogenic activity (bovine aortic endothelial cell viability) and VEGF and VEGFR2 mRNA levels and decreased CD36 (real-time PCR relative quantification). |
| 1809 | 22492973 | In mid-CL cells, TNF increased VEGF mRNA and protein expression (Western blot analysis) and reduced CD36 mRNA levels, while FASL and TNF+IFNG+FASL decreased VEGF protein expression. |
| 1810 | 22492973 | In mid-CL cells, TNF increased VEGF mRNA and protein expression (Western blot analysis) and reduced CD36 mRNA levels, while FASL and TNF+IFNG+FASL decreased VEGF protein expression. |
| 1811 | 22492973 | In mid-CL cells, TNF increased VEGF mRNA and protein expression (Western blot analysis) and reduced CD36 mRNA levels, while FASL and TNF+IFNG+FASL decreased VEGF protein expression. |
| 1812 | 22492973 | In late CL cells, TNF and TNF+IFNG+FASL reduced VEGFR2 mRNA, but TNF+IFNG+FASL increased TSP1 and CD36 mRNA. |
| 1813 | 22492973 | In late CL cells, TNF and TNF+IFNG+FASL reduced VEGFR2 mRNA, but TNF+IFNG+FASL increased TSP1 and CD36 mRNA. |
| 1814 | 22492973 | In late CL cells, TNF and TNF+IFNG+FASL reduced VEGFR2 mRNA, but TNF+IFNG+FASL increased TSP1 and CD36 mRNA. |
| 1815 | 22492973 | VEGF treatment increased mRNA levels of 3betaHSD and PGES and secretion of P(4) and PGE(2). |
| 1816 | 22492973 | VEGF treatment increased mRNA levels of 3betaHSD and PGES and secretion of P(4) and PGE(2). |
| 1817 | 22492973 | VEGF treatment increased mRNA levels of 3betaHSD and PGES and secretion of P(4) and PGE(2). |
| 1818 | 22492973 | In conclusion, these findings suggest a novel auto/paracrine action of cytokines, specifically TNF, on the up-regulation of VEGF for angiogenesis stimulation in equine early CL, while at luteolysis, cytokines down-regulated angiogenesis. |
| 1819 | 22492973 | In conclusion, these findings suggest a novel auto/paracrine action of cytokines, specifically TNF, on the up-regulation of VEGF for angiogenesis stimulation in equine early CL, while at luteolysis, cytokines down-regulated angiogenesis. |
| 1820 | 22492973 | In conclusion, these findings suggest a novel auto/paracrine action of cytokines, specifically TNF, on the up-regulation of VEGF for angiogenesis stimulation in equine early CL, while at luteolysis, cytokines down-regulated angiogenesis. |
| 1821 | 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. |
| 1822 | 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. |
| 1823 | 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. |
| 1824 | 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. |
| 1825 | 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. |
| 1826 | 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. |
| 1827 | 22392581 | Genetic variants of the MRC1 gene and the IFNG gene are associated with leprosy in Han Chinese from Southwest China. |
| 1828 | 22392581 | Genetic variants of the MRC1 gene and the IFNG gene are associated with leprosy in Han Chinese from Southwest China. |
| 1829 | 22392581 | Genetic variants of the MRC1 gene and the IFNG gene are associated with leprosy in Han Chinese from Southwest China. |
| 1830 | 22392581 | Genetic variants of the MRC1 gene and the IFNG gene are associated with leprosy in Han Chinese from Southwest China. |
| 1831 | 22392581 | Genetic variants of the MRC1 gene and the IFNG gene are associated with leprosy in Han Chinese from Southwest China. |
| 1832 | 22392581 | In the present study, we genotyped 12 genetic variants of the MRC1 gene and the IFNG gene in 527 Han Chinese with leprosy and 583 healthy individuals from Yunnan, China, to discern potential association of these two genes with leprosy. |
| 1833 | 22392581 | In the present study, we genotyped 12 genetic variants of the MRC1 gene and the IFNG gene in 527 Han Chinese with leprosy and 583 healthy individuals from Yunnan, China, to discern potential association of these two genes with leprosy. |
| 1834 | 22392581 | In the present study, we genotyped 12 genetic variants of the MRC1 gene and the IFNG gene in 527 Han Chinese with leprosy and 583 healthy individuals from Yunnan, China, to discern potential association of these two genes with leprosy. |
| 1835 | 22392581 | In the present study, we genotyped 12 genetic variants of the MRC1 gene and the IFNG gene in 527 Han Chinese with leprosy and 583 healthy individuals from Yunnan, China, to discern potential association of these two genes with leprosy. |
| 1836 | 22392581 | In the present study, we genotyped 12 genetic variants of the MRC1 gene and the IFNG gene in 527 Han Chinese with leprosy and 583 healthy individuals from Yunnan, China, to discern potential association of these two genes with leprosy. |
| 1837 | 22392581 | In particular, we aimed to validate the recently reported association of MRC1 variant rs1926736 (p.G396S) and IFNG variant rs2430561 (+874 T>A) with leprosy, which were initially observed in Vietnamese and Brazilian populations, respectively. |
| 1838 | 22392581 | In particular, we aimed to validate the recently reported association of MRC1 variant rs1926736 (p.G396S) and IFNG variant rs2430561 (+874 T>A) with leprosy, which were initially observed in Vietnamese and Brazilian populations, respectively. |
| 1839 | 22392581 | In particular, we aimed to validate the recently reported association of MRC1 variant rs1926736 (p.G396S) and IFNG variant rs2430561 (+874 T>A) with leprosy, which were initially observed in Vietnamese and Brazilian populations, respectively. |
| 1840 | 22392581 | In particular, we aimed to validate the recently reported association of MRC1 variant rs1926736 (p.G396S) and IFNG variant rs2430561 (+874 T>A) with leprosy, which were initially observed in Vietnamese and Brazilian populations, respectively. |
| 1841 | 22392581 | In particular, we aimed to validate the recently reported association of MRC1 variant rs1926736 (p.G396S) and IFNG variant rs2430561 (+874 T>A) with leprosy, which were initially observed in Vietnamese and Brazilian populations, respectively. |
| 1842 | 22392581 | However, we found that variants rs692527 (P = 0.022) and rs34856358 (P = 0.022) of the MRC1 gene were associated with paucibacillary leprosy, and rs3138557 of the IFNG gene was significantly associated with multibacillary leprosy. |
| 1843 | 22392581 | However, we found that variants rs692527 (P = 0.022) and rs34856358 (P = 0.022) of the MRC1 gene were associated with paucibacillary leprosy, and rs3138557 of the IFNG gene was significantly associated with multibacillary leprosy. |
| 1844 | 22392581 | However, we found that variants rs692527 (P = 0.022) and rs34856358 (P = 0.022) of the MRC1 gene were associated with paucibacillary leprosy, and rs3138557 of the IFNG gene was significantly associated with multibacillary leprosy. |
| 1845 | 22392581 | However, we found that variants rs692527 (P = 0.022) and rs34856358 (P = 0.022) of the MRC1 gene were associated with paucibacillary leprosy, and rs3138557 of the IFNG gene was significantly associated with multibacillary leprosy. |
| 1846 | 22392581 | However, we found that variants rs692527 (P = 0.022) and rs34856358 (P = 0.022) of the MRC1 gene were associated with paucibacillary leprosy, and rs3138557 of the IFNG gene was significantly associated with multibacillary leprosy. |
| 1847 | 22392581 | The exact role of the MRC1 gene and the IFNG gene in leprosy awaits future study. |
| 1848 | 22392581 | The exact role of the MRC1 gene and the IFNG gene in leprosy awaits future study. |
| 1849 | 22392581 | The exact role of the MRC1 gene and the IFNG gene in leprosy awaits future study. |
| 1850 | 22392581 | The exact role of the MRC1 gene and the IFNG gene in leprosy awaits future study. |
| 1851 | 22392581 | The exact role of the MRC1 gene and the IFNG gene in leprosy awaits future study. |
| 1852 | 22378921 | β (CCL2) and α (CXCL10) chemokine modulations by cytokines and peroxisome proliferator-activated receptor-α agonists in Graves' ophthalmopathy. |
| 1853 | 22378921 | No data are present in the literature about the effect of cytokines on the prototype β chemokine (C-C motif) ligand 2 (CCL2) or of peroxisome proliferator-activated receptor α (PPARα (PPARA)) activation on CCL2 and CXCL10 chemokines secretion in fibroblasts or preadipocytes in Graves' ophthalmopathy (GO). |
| 1854 | 22378921 | We have tested the effect of interferon γ (IFNγ (IFNG)) and tumor necrosis factor α (TNFα) on CCL2, and for comparison on the prototype α chemokine (C-X-C motif) ligand 10 (CXCL10), and the possible modulatory role of PPARα activation on secretion of these chemokines in normal and GO fibroblasts or preadipocytes in primary cell cultures. |
| 1855 | 22378921 | PPARα activators were able to inhibit the secretion of CXCL10 and CCL2, while PPARγ activators were confirmed to be able to inhibit CXCL10 but had no effect on CCL2. |
| 1856 | 22378921 | In conclusion, CCL2 and CXCL10 are modulated by IFNγ and TNFα in GO. |
| 1857 | 22378921 | PPARα activators inhibit the secretion of the main prototype α (CXCL10) and β (CCL2) chemokines in GO fibroblasts or preadipocytes, suggesting that PPARα may be involved in the modulation of the immune response in GO. |
| 1858 | 22345648 | The production of M. tuberculosis and purified protein derivative-induced IFN-γ, TNF-α, IL-1β, and IL-6 was reduced in a DEP dose-dependent manner. |
| 1859 | 22345648 | Furthermore, DEP stimulation prior to M. tuberculosis infection altered the expression of TLR3, -4, -7, and -10 mRNAs and of a subset of M. tuberculosis-induced host genes including inhibition of expression of many NF-κB (e.g., CSF3, IFNG, IFNA, IFNB, IL1A, IL6, and NFKBIA) and IFN regulatory factor (e.g., IFNG, IFNA1, IFNB1, and CXCL10) pathway target genes. |
| 1860 | 22345648 | We propose that DEP downregulate M. tuberculosis-induced host gene expression via MyD88-dependent (IL6, IL1A, and PTGS2) as well as MyD88-independent (IFNA, IFNB) pathways. |
| 1861 | 22327783 | IFN-gamma and IL-12B polymorphisms in women with cervical intraepithellial neoplasia caused by human papillomavirus. |
| 1862 | 22327783 | IFN-gamma and IL-12B polymorphisms in women with cervical intraepithellial neoplasia caused by human papillomavirus. |
| 1863 | 22327783 | In this study, we evaluated the presence of functional polymorphisms at +874 (T/A) IFNG and +1188 (A/C) IL-12B genes in cervical smears samples from 76 healthy women and 162 women, HPV positive, with CIN lesion--CIN I (45), CIN II (55), CIN III (53) and cervical cancer (9)--in Brazilian population. |
| 1864 | 22327783 | In this study, we evaluated the presence of functional polymorphisms at +874 (T/A) IFNG and +1188 (A/C) IL-12B genes in cervical smears samples from 76 healthy women and 162 women, HPV positive, with CIN lesion--CIN I (45), CIN II (55), CIN III (53) and cervical cancer (9)--in Brazilian population. |
| 1865 | 22308202 | Neopterin, a Marker of Interferon-Gamma-Inducible Inflammation, Correlates with Pyridoxal-5'-Phosphate, Waist Circumference, HDL-Cholesterol, Insulin Resistance and Mortality Risk in Adult Boston Community Dwellers of Puerto Rican Origin. |
| 1866 | 22308202 | Neopterin, a Marker of Interferon-Gamma-Inducible Inflammation, Correlates with Pyridoxal-5'-Phosphate, Waist Circumference, HDL-Cholesterol, Insulin Resistance and Mortality Risk in Adult Boston Community Dwellers of Puerto Rican Origin. |
| 1867 | 22308202 | Neopterin, a Marker of Interferon-Gamma-Inducible Inflammation, Correlates with Pyridoxal-5'-Phosphate, Waist Circumference, HDL-Cholesterol, Insulin Resistance and Mortality Risk in Adult Boston Community Dwellers of Puerto Rican Origin. |
| 1868 | 22308202 | Neopterin concentrations correlated with abdominal obesity (waist circumference, r = 0.085, p < 0.038), HDL cholesterol (r = -0.15, p < 0.0001), insulin resistance (HOMA-IR, r = 0.08, P < 0.03), and plasma pyridoxal-5'-phosphate (PLP (r = -0.13, P = 0.002). |
| 1869 | 22308202 | Neopterin concentrations correlated with abdominal obesity (waist circumference, r = 0.085, p < 0.038), HDL cholesterol (r = -0.15, p < 0.0001), insulin resistance (HOMA-IR, r = 0.08, P < 0.03), and plasma pyridoxal-5'-phosphate (PLP (r = -0.13, P = 0.002). |
| 1870 | 22308202 | Neopterin concentrations correlated with abdominal obesity (waist circumference, r = 0.085, p < 0.038), HDL cholesterol (r = -0.15, p < 0.0001), insulin resistance (HOMA-IR, r = 0.08, P < 0.03), and plasma pyridoxal-5'-phosphate (PLP (r = -0.13, P = 0.002). |
| 1871 | 22308202 | PLP is a cofactor of IFNG-induced key enzymes of tryptophan-kynurenine metabolism. |
| 1872 | 22308202 | PLP is a cofactor of IFNG-induced key enzymes of tryptophan-kynurenine metabolism. |
| 1873 | 22308202 | PLP is a cofactor of IFNG-induced key enzymes of tryptophan-kynurenine metabolism. |
| 1874 | 22308202 | Since PLP deficiency is associated with the increased production of diabetogenic kynurenine derivative, xanthurenic acid, our results suggest that up-regulated IFNG production might contribute to the development of insulin resistance. |
| 1875 | 22308202 | Since PLP deficiency is associated with the increased production of diabetogenic kynurenine derivative, xanthurenic acid, our results suggest that up-regulated IFNG production might contribute to the development of insulin resistance. |
| 1876 | 22308202 | Since PLP deficiency is associated with the increased production of diabetogenic kynurenine derivative, xanthurenic acid, our results suggest that up-regulated IFNG production might contribute to the development of insulin resistance. |
| 1877 | 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). |
| 1878 | 22295566 | Complex association analysis of copaxone (glatiramer acetate) immunotherapy efficacy with allelic polymorphism in the number of immune response genes, which encode interferone beta (IFNB1), transforming growth factor beta1 (TGFB1), interferone gamma (IFNG), tumor necrosis factor (TNF), interferon alpha/beta receptor 1 (IFNAR1), CC chemokine receptor 5 (CCR5), interleukin 7 receptor alpha subunit (IL7RA), cytotoxic T-lymphocyte antigen 4 (CTLA4) and HLA class II histocompatibility antigen beta chain (DRB1) was performed with APSampler algorithm for 285 multiple sclerosis patients of Russian ethnicity. |
| 1879 | 22295566 | Complex association analysis of copaxone (glatiramer acetate) immunotherapy efficacy with allelic polymorphism in the number of immune response genes, which encode interferone beta (IFNB1), transforming growth factor beta1 (TGFB1), interferone gamma (IFNG), tumor necrosis factor (TNF), interferon alpha/beta receptor 1 (IFNAR1), CC chemokine receptor 5 (CCR5), interleukin 7 receptor alpha subunit (IL7RA), cytotoxic T-lymphocyte antigen 4 (CTLA4) and HLA class II histocompatibility antigen beta chain (DRB1) was performed with APSampler algorithm for 285 multiple sclerosis patients of Russian ethnicity. |
| 1880 | 22295566 | The results show evidence for the contribution of polymorphic variants in CCRS, DRB1, IFNG, TGFB1, IFNAR1, IL7RA and, probably, TNF and CTLA4 genes to copaxone treatment response. |
| 1881 | 22295566 | The results show evidence for the contribution of polymorphic variants in CCRS, DRB1, IFNG, TGFB1, IFNAR1, IL7RA and, probably, TNF and CTLA4 genes to copaxone treatment response. |
| 1882 | 22295566 | Single alleles of CCR5 and DRB1 genes are reliably associated with treatment efficacy. |
| 1883 | 22295566 | Single alleles of CCR5 and DRB1 genes are reliably associated with treatment efficacy. |
| 1884 | 22263663 | Association of interleukin 10 and interferon gamma gene polymorphisms with enterovirus 71 encephalitis in patients with hand, foot and mouth disease. |
| 1885 | 22263663 | Association of interleukin 10 and interferon gamma gene polymorphisms with enterovirus 71 encephalitis in patients with hand, foot and mouth disease. |
| 1886 | 22263663 | This study investigated the polymorphisms of interferon gamma (IFN-γ)+874 T/A and interleukin 10 (IL-10)-1082 G/A in 65 Chinese patients with EV71 encephalitis and 113 Chinese HFMD patients without complications. |
| 1887 | 22263663 | This study investigated the polymorphisms of interferon gamma (IFN-γ)+874 T/A and interleukin 10 (IL-10)-1082 G/A in 65 Chinese patients with EV71 encephalitis and 113 Chinese HFMD patients without complications. |
| 1888 | 22186103 | In this study, the presence of cytokines tumor necrosis factor alpha (TNF) and interferon gamma (IFNG), and their receptors (TNFRI, TNFRII and IFNRI), was investigated in equine CL throughout the luteal phase. |
| 1889 | 22186103 | In this study, the presence of cytokines tumor necrosis factor alpha (TNF) and interferon gamma (IFNG), and their receptors (TNFRI, TNFRII and IFNRI), was investigated in equine CL throughout the luteal phase. |
| 1890 | 22186103 | In this study, the presence of cytokines tumor necrosis factor alpha (TNF) and interferon gamma (IFNG), and their receptors (TNFRI, TNFRII and IFNRI), was investigated in equine CL throughout the luteal phase. |
| 1891 | 22186103 | In this study, the presence of cytokines tumor necrosis factor alpha (TNF) and interferon gamma (IFNG), and their receptors (TNFRI, TNFRII and IFNRI), was investigated in equine CL throughout the luteal phase. |
| 1892 | 22186103 | In this study, the presence of cytokines tumor necrosis factor alpha (TNF) and interferon gamma (IFNG), and their receptors (TNFRI, TNFRII and IFNRI), was investigated in equine CL throughout the luteal phase. |
| 1893 | 22186103 | In this study, the presence of cytokines tumor necrosis factor alpha (TNF) and interferon gamma (IFNG), and their receptors (TNFRI, TNFRII and IFNRI), was investigated in equine CL throughout the luteal phase. |
| 1894 | 22186103 | The effects of TNF and IFNG on secretory function and viability of luteal cells were defined in vitro. |
| 1895 | 22186103 | The effects of TNF and IFNG on secretory function and viability of luteal cells were defined in vitro. |
| 1896 | 22186103 | The effects of TNF and IFNG on secretory function and viability of luteal cells were defined in vitro. |
| 1897 | 22186103 | The effects of TNF and IFNG on secretory function and viability of luteal cells were defined in vitro. |
| 1898 | 22186103 | The effects of TNF and IFNG on secretory function and viability of luteal cells were defined in vitro. |
| 1899 | 22186103 | The effects of TNF and IFNG on secretory function and viability of luteal cells were defined in vitro. |
| 1900 | 22186103 | In the mid luteal phase, TNF increased PGF(2α) secretion and TNF+IFNG decreased PGE(2) secretion. |
| 1901 | 22186103 | In the mid luteal phase, TNF increased PGF(2α) secretion and TNF+IFNG decreased PGE(2) secretion. |
| 1902 | 22186103 | In the mid luteal phase, TNF increased PGF(2α) secretion and TNF+IFNG decreased PGE(2) secretion. |
| 1903 | 22186103 | In the mid luteal phase, TNF increased PGF(2α) secretion and TNF+IFNG decreased PGE(2) secretion. |
| 1904 | 22186103 | In the mid luteal phase, TNF increased PGF(2α) secretion and TNF+IFNG decreased PGE(2) secretion. |
| 1905 | 22186103 | In the mid luteal phase, TNF increased PGF(2α) secretion and TNF+IFNG decreased PGE(2) secretion. |
| 1906 | 22186103 | In the regressing luteal phase, TNF, IFNG and TNF+IFNG decreased P(4) and PGE(2) secretion, but TNF and TNF+IFNG increased PGF(2α) secretion by luteal cells. |
| 1907 | 22186103 | In the regressing luteal phase, TNF, IFNG and TNF+IFNG decreased P(4) and PGE(2) secretion, but TNF and TNF+IFNG increased PGF(2α) secretion by luteal cells. |
| 1908 | 22186103 | In the regressing luteal phase, TNF, IFNG and TNF+IFNG decreased P(4) and PGE(2) secretion, but TNF and TNF+IFNG increased PGF(2α) secretion by luteal cells. |
| 1909 | 22186103 | In the regressing luteal phase, TNF, IFNG and TNF+IFNG decreased P(4) and PGE(2) secretion, but TNF and TNF+IFNG increased PGF(2α) secretion by luteal cells. |
| 1910 | 22186103 | In the regressing luteal phase, TNF, IFNG and TNF+IFNG decreased P(4) and PGE(2) secretion, but TNF and TNF+IFNG increased PGF(2α) secretion by luteal cells. |
| 1911 | 22186103 | In the regressing luteal phase, TNF, IFNG and TNF+IFNG decreased P(4) and PGE(2) secretion, but TNF and TNF+IFNG increased PGF(2α) secretion by luteal cells. |
| 1912 | 22186103 | Cell viability was reduced by TNF+IFNG in regressing CL. |
| 1913 | 22186103 | Cell viability was reduced by TNF+IFNG in regressing CL. |
| 1914 | 22186103 | Cell viability was reduced by TNF+IFNG in regressing CL. |
| 1915 | 22186103 | Cell viability was reduced by TNF+IFNG in regressing CL. |
| 1916 | 22186103 | Cell viability was reduced by TNF+IFNG in regressing CL. |
| 1917 | 22186103 | Cell viability was reduced by TNF+IFNG in regressing CL. |
| 1918 | 22186103 | These data show the presence of cytokines TNF and IFNG, and their receptors, in the equine CL and indicate their potential involvement in regulation of luteal function. |
| 1919 | 22186103 | These data show the presence of cytokines TNF and IFNG, and their receptors, in the equine CL and indicate their potential involvement in regulation of luteal function. |
| 1920 | 22186103 | These data show the presence of cytokines TNF and IFNG, and their receptors, in the equine CL and indicate their potential involvement in regulation of luteal function. |
| 1921 | 22186103 | These data show the presence of cytokines TNF and IFNG, and their receptors, in the equine CL and indicate their potential involvement in regulation of luteal function. |
| 1922 | 22186103 | These data show the presence of cytokines TNF and IFNG, and their receptors, in the equine CL and indicate their potential involvement in regulation of luteal function. |
| 1923 | 22186103 | These data show the presence of cytokines TNF and IFNG, and their receptors, in the equine CL and indicate their potential involvement in regulation of luteal function. |
| 1924 | 22116824 | The 1MOG244 T cell expresses dual TCRA chains, one of which, when combined with the single TCRB present, promotes the development of CD8(+) T cells with specificity for hair follicles. |
| 1925 | 22116824 | Pathologic T cells primarily express IFNG and IL-17 early in disease, with dramatic increases in cytokine production and recruitment of IL-4 and IL-10 production with disease progression. |
| 1926 | 22101570 | Present study evaluated the effect of recombinant human interferon gamma (rIFN-gamma: Gamma Immunex, Exir Pharmaceutical Company, Iran) on severity of AD (SCORAD), dermatology life quality index (DLQI) as well as serum levels of IL-4, IgE and IL-6 in AD patients. |
| 1927 | 22101570 | IL-4, IL-6 and IgE were measured in blood samples before and after 1 month treatment with rIFN-gamma. |
| 1928 | 22101570 | Treatment with rIFN-gamma decreased serum levels of IL-4 and IL-6 (P < 0.05), but IgE remained unchanged. |
| 1929 | 22098465 | In animals, inflammatory lesions track with IFNγ and IL-10 expression and infection of Ifng(-/-) mice leads to increased pathogen load but inhibition of inflammation. |
| 1930 | 22098465 | With severe disease, tissues can demonstrate hemophagocytosis, and measures of macrophage activation/hemophagocytic syndromes (MAS/HPS) support the concept of human granulocytic anaplasmosis as an immunopathologic disease. |
| 1931 | 22098465 | MAS/HPS are related to defective cytotoxic lymphocytes that ordinarily diminish inflammation. |
| 1932 | 22098465 | Pilot studies in mice show cytotoxic lymphocyte activation with A. phagocytophilum infection, yet suppression of cytotoxic responses from both NKT and CD8 cells, consistent with the development of MAS/HPS. |
| 1933 | 22052597 | A total of 10 single nucleotide polymorphisms distributed in 6 genes (TNFRSF1A, IL12A, IL12B, IFNG, IL4, and IL10) were genotyped in 214 high-responders [hepatitis B surface antibody (anti-HBs) ≥1,000 mIU/ml] and 107 low-responders (anti-HBs: 10-99 mIU/ml). |
| 1934 | 22052597 | In addition, a significant gene-gene interaction was found: the frequency of the combined genotypes IL12A rs2243115 TT and IL12B rs17860508 CTCTAA/CTCTAA was significantly higher in the low-response group than in the high-response group (P = 0.008, odds ratio = 2.19, 95% confidence interval = 1.23-3.93). |
| 1935 | 22052597 | These findings suggest that polymorphisms in the IL12A and IL12B genes might play an important role jointly in determining the response to hepatitis B vaccination. |
| 1936 | 22048764 | We isolated in vivo-differentiated human Th1 and Th17 cells, as well as intermediate Th1/17 cells, and identified distinct epigenetic signatures at cytokine (IFNG and IL17A) and transcription factor (TBX21, RORC, and RORA) loci. |
| 1937 | 22048764 | We also examined the phenotypic and epigenetic stability of human Th17 cells exposed to Th1-polarizing conditions and found that although they could upregulate TBX21 and IFN-γ, this occurred without loss of IL-17 or RORC expression, and resulted in cells with a Th1/17 phenotype. |
| 1938 | 22019771 | We used a gene panel of regulatory/inflammatory molecules (FOXP3, GATA3, IL10, TGFB1, TGFBR1/ TBX21, TNF and IFNG) to investigate the gene expression profile in peripheral blood mononuclear cells of renal-transplanted individuals experiencing OT compared to transplanted individuals not displaying OT and healthy individuals (HI). |
| 1939 | 22019771 | OT subjects showed a predominant regulatory (REG) profile with higher gene expression of GATA3, FOXP3, TGFB1 and TGFB receptor 1 compared to the other groups. |
| 1940 | 21976969 | Microarray and qRT-PCR data analyses showed significant upregulation of some cytotoxicity-related genes, including those from the granzyme family, tumor necrosis factor, Fas Ligand, and chemokines, in the spleen cells of IFNg KO mice. |
| 1941 | 21976969 | Microarray and qRT-PCR data analyses showed significant upregulation of some cytotoxicity-related genes, including those from the granzyme family, tumor necrosis factor, Fas Ligand, and chemokines, in the spleen cells of IFNg KO mice. |
| 1942 | 21976969 | Microarray and qRT-PCR data analyses showed significant upregulation of some cytotoxicity-related genes, including those from the granzyme family, tumor necrosis factor, Fas Ligand, and chemokines, in the spleen cells of IFNg KO mice. |
| 1943 | 21976969 | Furthermore, CD8+ cells instead of NK cells of IFNg KO mice exhibited increased transcription of cytotoxic genes compared with WT mice. |
| 1944 | 21976969 | Furthermore, CD8+ cells instead of NK cells of IFNg KO mice exhibited increased transcription of cytotoxic genes compared with WT mice. |
| 1945 | 21976969 | Furthermore, CD8+ cells instead of NK cells of IFNg KO mice exhibited increased transcription of cytotoxic genes compared with WT mice. |
| 1946 | 21976969 | Additionally, Schistosoma japonicum-specific egg antigen immunization also could activate CD8+ T cells to upregulate the expression of cytotoxic genes in IFNg KO mice. |
| 1947 | 21976969 | Additionally, Schistosoma japonicum-specific egg antigen immunization also could activate CD8+ T cells to upregulate the expression of cytotoxic genes in IFNg KO mice. |
| 1948 | 21976969 | Additionally, Schistosoma japonicum-specific egg antigen immunization also could activate CD8+ T cells to upregulate the expression of cytotoxic genes in IFNg KO mice. |
| 1949 | 21900681 | We concluded that the major NK cell population in rhesus early pregnancy decidua are CD56(bright) CD16(+)NKp30(-) decidual NK cells, with minor CD56(dim) and CD56(neg) dNK cells. |
| 1950 | 21900681 | Intracellular cytokine staining demonstrated that CD56(dim) and not CD56(bright) dNK cells are the primary interferon-gamma (IFNG) producers. |
| 1951 | 21880854 | Dexamethasone reduced IFNG transcription by day 12 and IL-8 and IL-18 by days 7 to 9 and increased IL-4 on day 7. |
| 1952 | 21880854 | Dexamethasone reduced IFNG transcription by day 12 and IL-8 and IL-18 by days 7 to 9 and increased IL-4 on day 7. |
| 1953 | 21880854 | The ratio of IL-10 to IFNG was increased by dexamethasone on day 9. |
| 1954 | 21880854 | The ratio of IL-10 to IFNG was increased by dexamethasone on day 9. |
| 1955 | 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. |
| 1956 | 21876173 | Such proliferation-dependent variation in cytokine production appears tied to the epigenetic signatures within the ifnG and tnfA proximal promoters. |
| 1957 | 21859832 | In this study we examine genetic variation in IFNG, IFNGR1, IFNGR2 and interferon regulatory factors (IRFs) to determine associations with colon and rectal cancer and survival after diagnosis. |
| 1958 | 21859832 | In this study we examine genetic variation in IFNG, IFNGR1, IFNGR2 and interferon regulatory factors (IRFs) to determine associations with colon and rectal cancer and survival after diagnosis. |
| 1959 | 21859832 | Five tagSNPs in IFNG, IRF2 and IRF3 were associated with colon cancer and eight tagSNPs in IFNGR1, IFNGR2, IRF2, IRF4, IRF6 and IRF8 were associated with rectal cancer. |
| 1960 | 21859832 | Five tagSNPs in IFNG, IRF2 and IRF3 were associated with colon cancer and eight tagSNPs in IFNGR1, IFNGR2, IRF2, IRF4, IRF6 and IRF8 were associated with rectal cancer. |
| 1961 | 21859832 | IRF3 rs2304204 was associated with the strongest direct association and IRF2 3775554 with the strongest inverse association for colon cancer [odds ratios (ORs) 1.43, 95% confidence interval (CI) 1.12-1.82 for recessive model and 0.52, 95% CI 0.28-0.97 for unrestricted model]. |
| 1962 | 21859832 | IRF3 rs2304204 was associated with the strongest direct association and IRF2 3775554 with the strongest inverse association for colon cancer [odds ratios (ORs) 1.43, 95% confidence interval (CI) 1.12-1.82 for recessive model and 0.52, 95% CI 0.28-0.97 for unrestricted model]. |
| 1963 | 21859832 | For rectal cancer, IFNGR1 rs3799488 was directly associated with risk (OR 2.30, 95% CI 1.04-5.09 for recessive model), whereas IRF6 rs861020 was inversely associated with risk (OR 0.57, 95% CI 0.34-0.95). |
| 1964 | 21859832 | For rectal cancer, IFNGR1 rs3799488 was directly associated with risk (OR 2.30, 95% CI 1.04-5.09 for recessive model), whereas IRF6 rs861020 was inversely associated with risk (OR 0.57, 95% CI 0.34-0.95). |
| 1965 | 21734265 | During reprogramming of porcine mesenchymal cells with a four-factor (POU5F1/SOX2/KLF4/MYC) mixture of vectors, a fraction of the colonies had an atypical phenotype and arose earlier than the recognizable porcine induced pluripotent stem (iPS) cell colonies. |
| 1966 | 21734265 | Relative to gene expression of the iPS cells, there was up-regulation of genes for transcription factors associated with trophoblast (TR) lineage emergence, e.g., GATA2, PPARG, MSX2, DLX3, HAND1, GCM1, CDX2, ID2, ELF5, TCFAP2C, and TEAD4 and for genes required for synthesis of products more typical of differentiated TR, such as steroids (HSD17B1, CYP11A1, and STAR), pregnancy-associated glycoproteins (PAG6), and select cytokines (IFND, IFNG, and IL1B). |
| 1967 | 21712187 | Gene ontology and networks analyses revealed that these regions included the genes encoding oculocutaneous albinism II (OCA2), hect domain and RLD 2 (HERC2), ectodysplasin A receptor (EDAR) and solute carrier family 45, member 2 (SLC45A2). |
| 1968 | 21712187 | We also identified the genes encoding interferon-γ (IFNG) and death-associated protein kinase 1 (DAPK1), which are associated with cell death, inflammatory and immunological diseases. |
| 1969 | 21712101 | We assessed variation in eight genes (CD46, IFNG, IL4, IL8, IL10, RARa, SLAM and TLR2) encoding key proteins involved in host cellular interactions with Morbilliviruses and the relationship of variants to disease status. |
| 1970 | 21712101 | We found no variation in harbour seals from across Europe in the protein coding domains of the viral receptors SLAM and CD46, but SNPs were present in SLAM intron 2. |
| 1971 | 21698796 | However, the expressions of ACE, ACLY, PRKCB1, SLC2A4, SNAP23, VAPA, IGF2BP2, and IFNG were significantly enhanced when FPG increased (P<0.05). |
| 1972 | 21685942 | Comparative analysis of inflammation-related genes showed that Ifng, Il1b and Nos2 had expression concordant with methylation induction whereas Il2, Il6, Il10, Tnf did not. |
| 1973 | 21632975 | On the other hand, GATA3 inhibits T(h)1 cell differentiation by preventing up-regulation of IL-12 receptor β2 and STAT4 (signal transducer and activator of transcription 4) and neutralization of Runx3 (runt-related transcription factor 3) function through protein-protein interaction. |
| 1974 | 21632975 | GATA3 may also directly act on the Ifng gene. |
| 1975 | 21628330 | Improved host defense against septic peritonitis in mice lacking MyD88 and TRIF is linked to a normal interferon response. |
| 1976 | 21628330 | Improved host defense against septic peritonitis in mice lacking MyD88 and TRIF is linked to a normal interferon response. |
| 1977 | 21628330 | Improved host defense against septic peritonitis in mice lacking MyD88 and TRIF is linked to a normal interferon response. |
| 1978 | 21628330 | Improved host defense against septic peritonitis in mice lacking MyD88 and TRIF is linked to a normal interferon response. |
| 1979 | 21628330 | The signaling adapters MyD88 and TRIF are engaged by TLRs and/or receptors of the IL-1 family and are considered important for innate immune responses that combat bacterial infections. |
| 1980 | 21628330 | The signaling adapters MyD88 and TRIF are engaged by TLRs and/or receptors of the IL-1 family and are considered important for innate immune responses that combat bacterial infections. |
| 1981 | 21628330 | The signaling adapters MyD88 and TRIF are engaged by TLRs and/or receptors of the IL-1 family and are considered important for innate immune responses that combat bacterial infections. |
| 1982 | 21628330 | The signaling adapters MyD88 and TRIF are engaged by TLRs and/or receptors of the IL-1 family and are considered important for innate immune responses that combat bacterial infections. |
| 1983 | 21628330 | Here, the consequences of a combined MyD88 and TRIF deficiency for the innate immune response against severe septic peritonitis was examined. |
| 1984 | 21628330 | Here, the consequences of a combined MyD88 and TRIF deficiency for the innate immune response against severe septic peritonitis was examined. |
| 1985 | 21628330 | Here, the consequences of a combined MyD88 and TRIF deficiency for the innate immune response against severe septic peritonitis was examined. |
| 1986 | 21628330 | Here, the consequences of a combined MyD88 and TRIF deficiency for the innate immune response against severe septic peritonitis was examined. |
| 1987 | 21628330 | We demonstrate that Myd88(-/-);Trif(Lps2/Lps2) mice had markedly reduced bacterial numbers in the peritoneal cavity and peripheral blood, indicating that bacterial clearance in this model is improved in the absence of MyD88/TRIF signals. |
| 1988 | 21628330 | We demonstrate that Myd88(-/-);Trif(Lps2/Lps2) mice had markedly reduced bacterial numbers in the peritoneal cavity and peripheral blood, indicating that bacterial clearance in this model is improved in the absence of MyD88/TRIF signals. |
| 1989 | 21628330 | We demonstrate that Myd88(-/-);Trif(Lps2/Lps2) mice had markedly reduced bacterial numbers in the peritoneal cavity and peripheral blood, indicating that bacterial clearance in this model is improved in the absence of MyD88/TRIF signals. |
| 1990 | 21628330 | We demonstrate that Myd88(-/-);Trif(Lps2/Lps2) mice had markedly reduced bacterial numbers in the peritoneal cavity and peripheral blood, indicating that bacterial clearance in this model is improved in the absence of MyD88/TRIF signals. |
| 1991 | 21628330 | The lack of MyD88/TRIF signaling prevented the excessive production of inflammatory cytokines and of IL-10. |
| 1992 | 21628330 | The lack of MyD88/TRIF signaling prevented the excessive production of inflammatory cytokines and of IL-10. |
| 1993 | 21628330 | The lack of MyD88/TRIF signaling prevented the excessive production of inflammatory cytokines and of IL-10. |
| 1994 | 21628330 | The lack of MyD88/TRIF signaling prevented the excessive production of inflammatory cytokines and of IL-10. |
| 1995 | 21628330 | In contrast, Ifng mRNA was expressed at WT levels, and induction of Ifnb mRNA was reduced only by one-half. |
| 1996 | 21628330 | In contrast, Ifng mRNA was expressed at WT levels, and induction of Ifnb mRNA was reduced only by one-half. |
| 1997 | 21628330 | In contrast, Ifng mRNA was expressed at WT levels, and induction of Ifnb mRNA was reduced only by one-half. |
| 1998 | 21628330 | In contrast, Ifng mRNA was expressed at WT levels, and induction of Ifnb mRNA was reduced only by one-half. |
| 1999 | 21628330 | Consistent with these findings, numerous IFN-regulated genes, including p47 and p65 GTPases, as well as CXCL10, were expressed in a MyD88/TRIF-independent manner. |
| 2000 | 21628330 | Consistent with these findings, numerous IFN-regulated genes, including p47 and p65 GTPases, as well as CXCL10, were expressed in a MyD88/TRIF-independent manner. |
| 2001 | 21628330 | Consistent with these findings, numerous IFN-regulated genes, including p47 and p65 GTPases, as well as CXCL10, were expressed in a MyD88/TRIF-independent manner. |
| 2002 | 21628330 | Consistent with these findings, numerous IFN-regulated genes, including p47 and p65 GTPases, as well as CXCL10, were expressed in a MyD88/TRIF-independent manner. |
| 2003 | 21628330 | The production of p47 GTPases and CXCL10 in septic peritonitis was found to be dependent on the presence of IFNAR1, but not IFN-γ, indicating a normal induction of the type I IFN response in Myd88(-/-);Trif(Lps2/Lps2) mice, despite attenuated IFN-β production. |
| 2004 | 21628330 | The production of p47 GTPases and CXCL10 in septic peritonitis was found to be dependent on the presence of IFNAR1, but not IFN-γ, indicating a normal induction of the type I IFN response in Myd88(-/-);Trif(Lps2/Lps2) mice, despite attenuated IFN-β production. |
| 2005 | 21628330 | The production of p47 GTPases and CXCL10 in septic peritonitis was found to be dependent on the presence of IFNAR1, but not IFN-γ, indicating a normal induction of the type I IFN response in Myd88(-/-);Trif(Lps2/Lps2) mice, despite attenuated IFN-β production. |
| 2006 | 21628330 | The production of p47 GTPases and CXCL10 in septic peritonitis was found to be dependent on the presence of IFNAR1, but not IFN-γ, indicating a normal induction of the type I IFN response in Myd88(-/-);Trif(Lps2/Lps2) mice, despite attenuated IFN-β production. |
| 2007 | 21628330 | Together, these results provide evidence that in severe septic peritonitis, the absence of MyD88 and TRIF balances the innate immune response in a favorable manner by attenuating deleterious responses such as excessive cytokine release, while leaving intact protective IFN responses. |
| 2008 | 21628330 | Together, these results provide evidence that in severe septic peritonitis, the absence of MyD88 and TRIF balances the innate immune response in a favorable manner by attenuating deleterious responses such as excessive cytokine release, while leaving intact protective IFN responses. |
| 2009 | 21628330 | Together, these results provide evidence that in severe septic peritonitis, the absence of MyD88 and TRIF balances the innate immune response in a favorable manner by attenuating deleterious responses such as excessive cytokine release, while leaving intact protective IFN responses. |
| 2010 | 21628330 | Together, these results provide evidence that in severe septic peritonitis, the absence of MyD88 and TRIF balances the innate immune response in a favorable manner by attenuating deleterious responses such as excessive cytokine release, while leaving intact protective IFN responses. |
| 2011 | 21597988 | Bovine IFNGR2, IL12RB1, IL12RB2, and IL23R polymorphisms and MAP infection status. |
| 2012 | 21597988 | Twenty previously reported polymorphisms in genes encoding bovine interferon gamma (IFNG), IFNGR1, IFNGR2, IL22, IL22RA1, IL12RB1, IL12RB2, and IL23R were genotyped in a resource population of 446 dairy Holsteins with known MAP infection status, and logistic regression was used to assess the statistical association with a binomial MAP infection status phenotype. |
| 2013 | 21597988 | Four SNPs in IFNGR2, IL12RB1, IL12RB2, and IL23R were found to be associated with the MAP infection status of the resource population. |
| 2014 | 21585261 | During the early events of host-pathogen interaction identified genes are involved in pattern recognition receptors, and mycobacterial uptake (TLRs, NOD2 and MRC1), which modulate autophagy. |
| 2015 | 21585261 | Together, the activation of these pathways regulates cellular metabolism upon infection, activating cytokine production through NF-κB and vitamin D-vitamin D receptor pathways, while PARK2 and LRRK2 participate in the regulation of host-cell apoptosis. |
| 2016 | 21585261 | Concomitantly, genes triggered to form and maintain granulomas (TNF, LTA and IFNG) and genes involved in activating and differentiating T-helper cells (HLA, IL10, as well as the TNF/LTA axis and the IFNG/IL12 axis) bridge immunological regulation towards adaptive immunity. |
| 2017 | 21566463 | We show, using this co-culture system, that the same experimental conditions that result in an autophagic microenvironment, also drive in the production of numerous inflammatory mediators (including IL-6, IL-8, IL-10, MIP1a, IFNg, RANTES (CCL5) and GMCSF). |
| 2018 | 21518797 | The lineage-defining factors T-bet and Bcl-6 collaborate to regulate Th1 gene expression patterns. |
| 2019 | 21518797 | The T-box transcription factor T-bet is important for the differentiation of naive CD4(+) T helper cells (Th cells) into the Th1 phenotype. |
| 2020 | 21518797 | In this study, we first identify Socs1, Socs3, and Tcf7 (TCF-1) as gene targets that are negatively regulated by T-bet. |
| 2021 | 21518797 | Consistent with this, we identified two T-bet DNA-binding elements in the Socs1 promoter that are functionally used to down-regulate transcription in primary Th1 cells. |
| 2022 | 21518797 | Furthermore, T-bet functionally recruits Bcl-6 to the Ifng locus in late stages of Th1 differentiation to repress its activity, possibly to prevent the overproduction of IFN-γ, which could result in autoimmunity. |
| 2023 | 21516112 | Here we report that interleukin 23 (IL-23) and the transcription factor RORγt drove expression of the cytokine GM-CSF in helper T cells, whereas IL-12, interferon-γ (IFN-γ) and IL-27 acted as negative regulators. |
| 2024 | 21516112 | Autoreactive helper T cells specifically lacking GM-CSF failed to initiate neuroinflammation despite expression of IL-17A or IFN-γ, whereas GM-CSF secretion by Ifng(-/-)Il17a(-/-) helper T cells was sufficient to induce experimental autoimmune encephalomyelitis (EAE). |
| 2025 | 21480212 | Rapamycin-sensitive signals control TCR/CD28-driven Ifng, Il4 and Foxp3 transcription and promoter region methylation. |
| 2026 | 21480212 | Rapamycin-sensitive signals control TCR/CD28-driven Ifng, Il4 and Foxp3 transcription and promoter region methylation. |
| 2027 | 21480212 | Here, we report that both mTOR complex 1 and mTOR complex 2 are readily activated following TCR/CD28 engagement and are critical for early expression of Ifng, Il4 and Foxp3, and for effector T cell differentiation in the absence of polarizing cytokines. |
| 2028 | 21480212 | Here, we report that both mTOR complex 1 and mTOR complex 2 are readily activated following TCR/CD28 engagement and are critical for early expression of Ifng, Il4 and Foxp3, and for effector T cell differentiation in the absence of polarizing cytokines. |
| 2029 | 21480212 | While inhibition of mTOR complex 1 and cell division were evident at low doses of RAPA, inhibition of mTOR complex 2, Ifng, Il4 and Foxp3 expression, and T-cell polarization required higher doses and more prolonged treatments. |
| 2030 | 21480212 | While inhibition of mTOR complex 1 and cell division were evident at low doses of RAPA, inhibition of mTOR complex 2, Ifng, Il4 and Foxp3 expression, and T-cell polarization required higher doses and more prolonged treatments. |
| 2031 | 21480212 | We found that while T-bet and GATA3 were readily induced following TCR/CD28 engagement, administration of RAPA delayed their expression, and interfered with the loss of DNA methylation within Ifng and Il4 promoter regions. |
| 2032 | 21480212 | We found that while T-bet and GATA3 were readily induced following TCR/CD28 engagement, administration of RAPA delayed their expression, and interfered with the loss of DNA methylation within Ifng and Il4 promoter regions. |
| 2033 | 21463712 | In the current study we investigated genotype variants pertaining to five cytokine genes namely IFNG, TNFA, IL4, IL10 and IL12 in the north Indian population with active pulmonary tuberculosis (APTB) and correlated the serum cytokine levels with the corresponding genotypes. |
| 2034 | 21463712 | Compared to HC mean serum IFN-γ, IL-12, IL-4, and IL-10 levels were higher in APTB (p = 0.3661, p = 0.0186, p = 0.003, p = 0.7, respectively). |
| 2035 | 21463712 | In contrast the genotypes of the selected rsIDs in the TNFA, IL12 and IL10 genes showed significant association with the varying serum levels of corresponding cytokines. |
| 2036 | 21463712 | The variant of the TNFA gene at rs3093662, the IL12 gene at rs3213094 and rs3212220 and the IL10 gene at rs3024498 did show a strong indication to be of relevance to the immunity to tuberculosis. |
| 2037 | 21448974 | Here, we defined the levels of naturally occurring variation in the three specific genes controlling the IFN-γ pathway (IFNG, IFNGR1, IFNGR2) and assessed whether and how natural selection has acted on them. |
| 2038 | 21448974 | Conversely, IFNGR1 and IFNGR2 evolve under more relaxed selective constraints, although they are not completely free to accumulate amino acid variation having a major impact on protein function. |
| 2039 | 21404309 | Genes identified in these functional categories, such as Ccl21c, Cxcl9, Cxcl10, Ifng and Il12rb1, were found to have functional relevance. |
| 2040 | 21402756 | The pulmonary bacterial counts (number of CFU) and transcript levels of select cytokines (e.g., Ifng, Il12b, and Il4) at 1, 3, and 6 weeks postinfection were measured as biological and mechanistic phenotypes, respectively. |
| 2041 | 21393251 | Expression of proinflammatory cytokines, including Tnfa, Il17a, and Ifng, was up-regulated, whereas expression of antimicrobial peptides was down-regulated in the colon of Traf2(-/-) mice. |
| 2042 | 21393251 | Moreover, a number of IL-17-producing helper T cells were increased in the colonic lamina propria of Traf2(-/-) mice. |
| 2043 | 21393251 | Finally, deletion of Tnfr1, but not Il17a, dramatically ameliorated colitis in Traf2(-/-) mice by preventing apoptosis of colonic epithelial cells, down-regulation of proinflammatory cytokines, and restoration of wild-type commensal bacteria. |
| 2044 | 26760552 | Contrasting roles of donor and recipient TGFB1 and IFNG gene polymorphic variants in chronic kidney transplant rejection. |
| 2045 | 21328101 | Identification of SNPs in interferon gamma, interleukin-22, and their receptors and associations with health and production-related traits in Canadian Holstein bulls. |
| 2046 | 21328101 | Identification of SNPs in interferon gamma, interleukin-22, and their receptors and associations with health and production-related traits in Canadian Holstein bulls. |
| 2047 | 21328101 | Therefore, in the following study, the genes coding interferon gamma (IFNG), IFNG receptor 1 and 2 domains, interleukin-22 (IL22), and IL22 receptor alpha 1, were investigated for single nucleotide polymorphisms (SNPs) in Holstein bulls. |
| 2048 | 21328101 | Therefore, in the following study, the genes coding interferon gamma (IFNG), IFNG receptor 1 and 2 domains, interleukin-22 (IL22), and IL22 receptor alpha 1, were investigated for single nucleotide polymorphisms (SNPs) in Holstein bulls. |
| 2049 | 21328101 | These SNPs, along with SNPs previously identified in IL10, IL10 receptor, and transforming growth factor beta 1 (TGFB1) genes, were evaluated for statistical associations to estimated breeding values for milk somatic cell score (SCS), a trait highly correlated to mastitis incidence, and various production-related traits, including milk yield, protein yield, fat yield, and lactation persistency. |
| 2050 | 21328101 | These SNPs, along with SNPs previously identified in IL10, IL10 receptor, and transforming growth factor beta 1 (TGFB1) genes, were evaluated for statistical associations to estimated breeding values for milk somatic cell score (SCS), a trait highly correlated to mastitis incidence, and various production-related traits, including milk yield, protein yield, fat yield, and lactation persistency. |
| 2051 | 21328101 | While no significant associations were found between these SNPs and SCS, SNPs in IL10 receptor beta subunit showed a significant effect on protein yield and lactation persistency. |
| 2052 | 21328101 | While no significant associations were found between these SNPs and SCS, SNPs in IL10 receptor beta subunit showed a significant effect on protein yield and lactation persistency. |
| 2053 | 21328101 | While there is evidence that IL10 plays an important role during lactation, it is also likely that the effects of SNPs in IL10 receptor beta subunit on protein yield and lactation persistency are due to linkage disequilibrium with a neighboring QTL. |
| 2054 | 21328101 | While there is evidence that IL10 plays an important role during lactation, it is also likely that the effects of SNPs in IL10 receptor beta subunit on protein yield and lactation persistency are due to linkage disequilibrium with a neighboring QTL. |
| 2055 | 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. |
| 2056 | 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. |
| 2057 | 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. |
| 2058 | 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. |
| 2059 | 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. |
| 2060 | 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. |
| 2061 | 21278341 | We sought to understand transcriptional control of the effector genes IFN-γ (Ifng), granzyme B (Gzmb), and perforin 1 (Prf1) in murine memory CD8(+) T cells by characterizing their transcriptional profiles and chromatin states during lymphocytic choriomeningitis virus infection. |
| 2062 | 21278341 | We sought to understand transcriptional control of the effector genes IFN-γ (Ifng), granzyme B (Gzmb), and perforin 1 (Prf1) in murine memory CD8(+) T cells by characterizing their transcriptional profiles and chromatin states during lymphocytic choriomeningitis virus infection. |
| 2063 | 21278341 | We sought to understand transcriptional control of the effector genes IFN-γ (Ifng), granzyme B (Gzmb), and perforin 1 (Prf1) in murine memory CD8(+) T cells by characterizing their transcriptional profiles and chromatin states during lymphocytic choriomeningitis virus infection. |
| 2064 | 21278341 | Primary infection leads to reduced nucleosomal density near the transcription start sites and reduced H3K27 methylation throughout the Ifng and Gzmb loci, and these chromatin changes persist in the memory phase. |
| 2065 | 21278341 | Primary infection leads to reduced nucleosomal density near the transcription start sites and reduced H3K27 methylation throughout the Ifng and Gzmb loci, and these chromatin changes persist in the memory phase. |
| 2066 | 21278341 | Primary infection leads to reduced nucleosomal density near the transcription start sites and reduced H3K27 methylation throughout the Ifng and Gzmb loci, and these chromatin changes persist in the memory phase. |
| 2067 | 21278341 | Despite similarities in chromatin at the memory stage, PolII recruitment and continuous transcription occur at the Ifng locus but not the Gzmb locus. |
| 2068 | 21278341 | Despite similarities in chromatin at the memory stage, PolII recruitment and continuous transcription occur at the Ifng locus but not the Gzmb locus. |
| 2069 | 21278341 | Despite similarities in chromatin at the memory stage, PolII recruitment and continuous transcription occur at the Ifng locus but not the Gzmb locus. |
| 2070 | 21215285 | Chlamydia trachomatis-induced fallopian tube damage leading to tubal factor infertility (TFI) is linked with TNF, IL-10, and probably IFNG gene polymorphisms. |
| 2071 | 21215285 | Chlamydia trachomatis-induced fallopian tube damage leading to tubal factor infertility (TFI) is linked with TNF, IL-10, and probably IFNG gene polymorphisms. |
| 2072 | 21215285 | Chlamydia trachomatis-induced fallopian tube damage leading to tubal factor infertility (TFI) is linked with TNF, IL-10, and probably IFNG gene polymorphisms. |
| 2073 | 21215285 | Chlamydia trachomatis-induced fallopian tube damage leading to tubal factor infertility (TFI) is linked with TNF, IL-10, and probably IFNG gene polymorphisms. |
| 2074 | 21215285 | Cytokine polymorphisms (IL-10 -1082A/G, -819T/C, and -592A/C, IFNG +874T/A, and TNF -308G/A) were genotyped by polymerase chain reaction in 139 women. |
| 2075 | 21215285 | Cytokine polymorphisms (IL-10 -1082A/G, -819T/C, and -592A/C, IFNG +874T/A, and TNF -308G/A) were genotyped by polymerase chain reaction in 139 women. |
| 2076 | 21215285 | Cytokine polymorphisms (IL-10 -1082A/G, -819T/C, and -592A/C, IFNG +874T/A, and TNF -308G/A) were genotyped by polymerase chain reaction in 139 women. |
| 2077 | 21215285 | Cytokine polymorphisms (IL-10 -1082A/G, -819T/C, and -592A/C, IFNG +874T/A, and TNF -308G/A) were genotyped by polymerase chain reaction in 139 women. |
| 2078 | 21215285 | IL-10 -1082/-819/-592 and IFNG +874 SNPs were associated with the intensity of LP responses to C trachomatis antigens. |
| 2079 | 21215285 | IL-10 -1082/-819/-592 and IFNG +874 SNPs were associated with the intensity of LP responses to C trachomatis antigens. |
| 2080 | 21215285 | IL-10 -1082/-819/-592 and IFNG +874 SNPs were associated with the intensity of LP responses to C trachomatis antigens. |
| 2081 | 21215285 | IL-10 -1082/-819/-592 and IFNG +874 SNPs were associated with the intensity of LP responses to C trachomatis antigens. |
| 2082 | 21215285 | These cytokines also interact with each other and a cumulative effect of IL-10 -1082 and IFNG +874 genotypes was seen in LP responses to C trachomatis antigens. |
| 2083 | 21215285 | These cytokines also interact with each other and a cumulative effect of IL-10 -1082 and IFNG +874 genotypes was seen in LP responses to C trachomatis antigens. |
| 2084 | 21215285 | These cytokines also interact with each other and a cumulative effect of IL-10 -1082 and IFNG +874 genotypes was seen in LP responses to C trachomatis antigens. |
| 2085 | 21215285 | These cytokines also interact with each other and a cumulative effect of IL-10 -1082 and IFNG +874 genotypes was seen in LP responses to C trachomatis antigens. |
| 2086 | 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. |
| 2087 | 21176971 | MHYO infection significantly (P<0.05) stimulated innate cytokines, IL1B and IL8. |
| 2088 | 21176971 | MHYO infection significantly (P<0.05) stimulated innate cytokines, IL1B and IL8. |
| 2089 | 21176971 | MHYO infection significantly (P<0.05) stimulated innate cytokines, IL1B and IL8. |
| 2090 | 21176971 | PCV2 infection significantly stimulated expression of IFNG, IL8, NOS2A and chemokines CCL2, CCL5, and CXCL10. |
| 2091 | 21176971 | PCV2 infection significantly stimulated expression of IFNG, IL8, NOS2A and chemokines CCL2, CCL5, and CXCL10. |
| 2092 | 21176971 | PCV2 infection significantly stimulated expression of IFNG, IL8, NOS2A and chemokines CCL2, CCL5, and CXCL10. |
| 2093 | 21176971 | IFNB, IL1B and IL12 were slightly increased with PCV2 infection and IFNA and IL4 were significantly downregulated. |
| 2094 | 21176971 | IFNB, IL1B and IL12 were slightly increased with PCV2 infection and IFNA and IL4 were significantly downregulated. |
| 2095 | 21176971 | IFNB, IL1B and IL12 were slightly increased with PCV2 infection and IFNA and IL4 were significantly downregulated. |
| 2096 | 21176971 | Compared to NEG pigs, coinfection resulted in a significant increase in expression of IFNG, IL1B, IL8, CCL5, CXCL10, and weak stimulation of IFNB, IL6 and IL10; IL13 and IFNA were significantly downregulated. |
| 2097 | 21176971 | Compared to NEG pigs, coinfection resulted in a significant increase in expression of IFNG, IL1B, IL8, CCL5, CXCL10, and weak stimulation of IFNB, IL6 and IL10; IL13 and IFNA were significantly downregulated. |
| 2098 | 21176971 | Compared to NEG pigs, coinfection resulted in a significant increase in expression of IFNG, IL1B, IL8, CCL5, CXCL10, and weak stimulation of IFNB, IL6 and IL10; IL13 and IFNA were significantly downregulated. |
| 2099 | 21176971 | Overall MHYO potentiated PCV2 infection by increasing IFNG and IL10 mRNA expression levels. |
| 2100 | 21176971 | Overall MHYO potentiated PCV2 infection by increasing IFNG and IL10 mRNA expression levels. |
| 2101 | 21176971 | Overall MHYO potentiated PCV2 infection by increasing IFNG and IL10 mRNA expression levels. |
| 2102 | 21161299 | Interferon-gamma (+874) T/A genotypes and risk of IFN-alpha-induced depression. |
| 2103 | 21161299 | Interferon-gamma (+874) T/A genotypes and risk of IFN-alpha-induced depression. |
| 2104 | 21161299 | Interferon-gamma (+874) T/A genotypes and risk of IFN-alpha-induced depression. |
| 2105 | 21161299 | Interferon-gamma (+874) T/A genotypes and risk of IFN-alpha-induced depression. |
| 2106 | 21161299 | Interferon-gamma (+874) T/A genotypes and risk of IFN-alpha-induced depression. |
| 2107 | 21161299 | Depression is a frequent side effect of interferon (IFN)-alpha therapy of hepatitis C (HCV) and is of great relevance with regard to adherence, compliance, and premature therapy discontinuation. |
| 2108 | 21161299 | Depression is a frequent side effect of interferon (IFN)-alpha therapy of hepatitis C (HCV) and is of great relevance with regard to adherence, compliance, and premature therapy discontinuation. |
| 2109 | 21161299 | Depression is a frequent side effect of interferon (IFN)-alpha therapy of hepatitis C (HCV) and is of great relevance with regard to adherence, compliance, and premature therapy discontinuation. |
| 2110 | 21161299 | Depression is a frequent side effect of interferon (IFN)-alpha therapy of hepatitis C (HCV) and is of great relevance with regard to adherence, compliance, and premature therapy discontinuation. |
| 2111 | 21161299 | Depression is a frequent side effect of interferon (IFN)-alpha therapy of hepatitis C (HCV) and is of great relevance with regard to adherence, compliance, and premature therapy discontinuation. |
| 2112 | 21161299 | We retrospectively studied distribution of IFN-gamma (IFNG) (+874) T/A genotypes in 170 Caucasian HCV patients treated by IFN-alpha. |
| 2113 | 21161299 | We retrospectively studied distribution of IFN-gamma (IFNG) (+874) T/A genotypes in 170 Caucasian HCV patients treated by IFN-alpha. |
| 2114 | 21161299 | We retrospectively studied distribution of IFN-gamma (IFNG) (+874) T/A genotypes in 170 Caucasian HCV patients treated by IFN-alpha. |
| 2115 | 21161299 | We retrospectively studied distribution of IFN-gamma (IFNG) (+874) T/A genotypes in 170 Caucasian HCV patients treated by IFN-alpha. |
| 2116 | 21161299 | We retrospectively studied distribution of IFN-gamma (IFNG) (+874) T/A genotypes in 170 Caucasian HCV patients treated by IFN-alpha. |
| 2117 | 21161299 | Assessment of IFNG (+874) genotypes might help to identify patients-at-risk for IFN-alpha-induced depression. |
| 2118 | 21161299 | Assessment of IFNG (+874) genotypes might help to identify patients-at-risk for IFN-alpha-induced depression. |
| 2119 | 21161299 | Assessment of IFNG (+874) genotypes might help to identify patients-at-risk for IFN-alpha-induced depression. |
| 2120 | 21161299 | Assessment of IFNG (+874) genotypes might help to identify patients-at-risk for IFN-alpha-induced depression. |
| 2121 | 21161299 | Assessment of IFNG (+874) genotypes might help to identify patients-at-risk for IFN-alpha-induced depression. |
| 2122 | 21161299 | IFNG and IFN-alpha transcriptionally induce indoleamine-2,3-dioxygenase (IDO), the rate-limiting enzyme of the kynurenine (KYN) pathway of tryptophan (TRY) metabolism. |
| 2123 | 21161299 | IFNG and IFN-alpha transcriptionally induce indoleamine-2,3-dioxygenase (IDO), the rate-limiting enzyme of the kynurenine (KYN) pathway of tryptophan (TRY) metabolism. |
| 2124 | 21161299 | IFNG and IFN-alpha transcriptionally induce indoleamine-2,3-dioxygenase (IDO), the rate-limiting enzyme of the kynurenine (KYN) pathway of tryptophan (TRY) metabolism. |
| 2125 | 21161299 | IFNG and IFN-alpha transcriptionally induce indoleamine-2,3-dioxygenase (IDO), the rate-limiting enzyme of the kynurenine (KYN) pathway of tryptophan (TRY) metabolism. |
| 2126 | 21161299 | IFNG and IFN-alpha transcriptionally induce indoleamine-2,3-dioxygenase (IDO), the rate-limiting enzyme of the kynurenine (KYN) pathway of tryptophan (TRY) metabolism. |
| 2127 | 21090238 | [Analysis of linkage and association of alleles of proinflammatory cytokines genes IL-6, IFNg and TNF with multiple sclerosis using transmission disequilibrium test (TDT)]. |
| 2128 | 21090238 | [Analysis of linkage and association of alleles of proinflammatory cytokines genes IL-6, IFNg and TNF with multiple sclerosis using transmission disequilibrium test (TDT)]. |
| 2129 | 21090238 | [Analysis of linkage and association of alleles of proinflammatory cytokines genes IL-6, IFNg and TNF with multiple sclerosis using transmission disequilibrium test (TDT)]. |
| 2130 | 21090238 | [Analysis of linkage and association of alleles of proinflammatory cytokines genes IL-6, IFNg and TNF with multiple sclerosis using transmission disequilibrium test (TDT)]. |
| 2131 | 21090238 | Proinflammatory cytokines Interleukin-6 (IL-6), Interferon-gamma (IFNg) and Tumor necrosis factor (TNF) are known as participants of inflammation and play an important role in pathogenesis of multiple sclerosis (MS). |
| 2132 | 21090238 | Proinflammatory cytokines Interleukin-6 (IL-6), Interferon-gamma (IFNg) and Tumor necrosis factor (TNF) are known as participants of inflammation and play an important role in pathogenesis of multiple sclerosis (MS). |
| 2133 | 21090238 | Proinflammatory cytokines Interleukin-6 (IL-6), Interferon-gamma (IFNg) and Tumor necrosis factor (TNF) are known as participants of inflammation and play an important role in pathogenesis of multiple sclerosis (MS). |
| 2134 | 21090238 | Proinflammatory cytokines Interleukin-6 (IL-6), Interferon-gamma (IFNg) and Tumor necrosis factor (TNF) are known as participants of inflammation and play an important role in pathogenesis of multiple sclerosis (MS). |
| 2135 | 21090238 | Based on literature data about influence of SNPs G(-308)A of TNF gene, A(+874)T of IFNG gene and G(-174)C of IL-6 gene on production of these cytokines, we investigated association of these polymorphic sites with MS. |
| 2136 | 21090238 | Based on literature data about influence of SNPs G(-308)A of TNF gene, A(+874)T of IFNG gene and G(-174)C of IL-6 gene on production of these cytokines, we investigated association of these polymorphic sites with MS. |
| 2137 | 21090238 | Based on literature data about influence of SNPs G(-308)A of TNF gene, A(+874)T of IFNG gene and G(-174)C of IL-6 gene on production of these cytokines, we investigated association of these polymorphic sites with MS. |
| 2138 | 21090238 | Based on literature data about influence of SNPs G(-308)A of TNF gene, A(+874)T of IFNG gene and G(-174)C of IL-6 gene on production of these cytokines, we investigated association of these polymorphic sites with MS. |
| 2139 | 21090238 | Linkage/association of IFNG and IL-6 alleles with MS was not revealed. |
| 2140 | 21090238 | Linkage/association of IFNG and IL-6 alleles with MS was not revealed. |
| 2141 | 21090238 | Linkage/association of IFNG and IL-6 alleles with MS was not revealed. |
| 2142 | 21090238 | Linkage/association of IFNG and IL-6 alleles with MS was not revealed. |
| 2143 | 21067287 | Multiple sclerosis risk markers in HLA-DRA, HLA-C, and IFNG genes are associated with sex-specific childhood leukemia risk. |
| 2144 | 21067287 | Two other SNPs in superkiller viralicidic activity 2-like and tenascin XB that are markers for systemic lupus erythematosus susceptibility showed female-specific associations but due to linkage disequilibrium with HLA-DRB1*15. |
| 2145 | 20963786 | Changes in histone acetylation and methylation that are important for persistent but not transient expression of CCR4 in human CD4+ T cells. |
| 2146 | 20963786 | Although regulation of CXCR3 and CCR4 is related to Th1 and Th2 differentiation, respectively, many CXCR3(+) and CCR4(+) cells do not express IFN-γ and/or IL-4, suggesting that the chemokine receptor genes might be inducible by mechanisms that are lineage-independent. |
| 2147 | 20963786 | We investigated the regulation of CXCR3 versus IFNG, and CCR4 versus IL4 in human CD4(+) T cells by analyzing modifications of histone H3. |
| 2148 | 20963786 | In naïve cord-blood cells, under nonpolarizing conditions not inducing IL4, CCR4 was induced to high levels without many of the activation-associated changes in promoter histone H3 found for both IL4 and CCR4 in Th2 cells. |
| 2149 | 20963786 | Patterns of histone H3 modifications in CXCR3(+) CCR4(-) and CXCR3(-) CCR4(+) CD4(+) T-cell subsets from adult blood matched those in cells cultured under polarizing conditions in vitro. |
| 2150 | 20953611 | We genotyped ten polymorphisms in three cytokine genes (IFNG, TNF, and TGFB1) and FAS gene. |
| 2151 | 20953611 | We genotyped ten polymorphisms in three cytokine genes (IFNG, TNF, and TGFB1) and FAS gene. |
| 2152 | 20953611 | In addition, it was found that polymorphisms in IFNG and TGFB1 are associated with response to IST. |
| 2153 | 20953611 | In addition, it was found that polymorphisms in IFNG and TGFB1 are associated with response to IST. |
| 2154 | 20947410 | Interleukin-26: an IL-10-related cytokine produced by Th17 cells. |
| 2155 | 20947410 | IL-26 is classified as a member of the IL-10 cytokine family because it has limited sequence homology to IL-10 and the IL-10-related cytokines. |
| 2156 | 20947410 | The human IL-26 gene, IL26, is located on chromosome 12q15 between the genes for two other important class-2 cytokines, IFNG (IFN-γ) and IL22 (IL-22). |
| 2157 | 20947410 | IL-26 is often co-expressed with IL-22 by activated T cells, especially Th17 cells. |
| 2158 | 20947410 | It signals through a heterodimeric receptor complex composed of the IL-20R1 and IL-10R2 chains. |
| 2159 | 20947410 | Signaling through IL-26 receptor complexes results in the activation of STAT1 and STAT3 with subsequent induction of IL-26-responsive genes. |
| 2160 | 20944005 | PRDM1 response elements are defined at the IFNG and TNF loci. |
| 2161 | 20921622 | Enhanced cell cycle and metabolic activity was restricted to the acute phase of the response, but at all stages, HCMV-specific CD8+ T cells expressed the Th1-associated transcription factors T-bet (TBX21) and eomesodermin (EOMES), in parallel with continuous expression of IFNG mRNA and IFN-γ-regulated genes. |
| 2162 | 20921622 | The cytolytic proteins granzyme B and perforin as well as the fractalkine-binding chemokine receptor CX3CR1 were found in virus-reactive cells throughout the response. |
| 2163 | 20876105 | IκBζ is essential for natural killer cell activation in response to IL-12 and IL-18. |
| 2164 | 20876105 | IκBζ is essential for natural killer cell activation in response to IL-12 and IL-18. |
| 2165 | 20876105 | IκBζ is essential for natural killer cell activation in response to IL-12 and IL-18. |
| 2166 | 20876105 | Analysis of Nfkbiz(-/-) mice revealed that IκBζ was essential for the production of IFN-γ production and cytotoxic activity in NK cells in response to IL-12 and/or IL-18 stimulation. |
| 2167 | 20876105 | Analysis of Nfkbiz(-/-) mice revealed that IκBζ was essential for the production of IFN-γ production and cytotoxic activity in NK cells in response to IL-12 and/or IL-18 stimulation. |
| 2168 | 20876105 | Analysis of Nfkbiz(-/-) mice revealed that IκBζ was essential for the production of IFN-γ production and cytotoxic activity in NK cells in response to IL-12 and/or IL-18 stimulation. |
| 2169 | 20876105 | IL-12/IL-18-mediated gene induction was profoundly impaired in Nfkbiz(-/-) NK cells. |
| 2170 | 20876105 | IL-12/IL-18-mediated gene induction was profoundly impaired in Nfkbiz(-/-) NK cells. |
| 2171 | 20876105 | IL-12/IL-18-mediated gene induction was profoundly impaired in Nfkbiz(-/-) NK cells. |
| 2172 | 20876105 | Whereas the phosphorylation of STAT4 was normally induced by IL-12 stimulation, STAT4 was not recruited to the Ifng gene regions in Nfkbiz(-/-) NK cells. |
| 2173 | 20876105 | Whereas the phosphorylation of STAT4 was normally induced by IL-12 stimulation, STAT4 was not recruited to the Ifng gene regions in Nfkbiz(-/-) NK cells. |
| 2174 | 20876105 | Whereas the phosphorylation of STAT4 was normally induced by IL-12 stimulation, STAT4 was not recruited to the Ifng gene regions in Nfkbiz(-/-) NK cells. |
| 2175 | 20876105 | Acetylation of histone 3 K9 on Ifng regions was also abrogated in Nfkbiz(-/-) NK cells. |
| 2176 | 20876105 | Acetylation of histone 3 K9 on Ifng regions was also abrogated in Nfkbiz(-/-) NK cells. |
| 2177 | 20876105 | Acetylation of histone 3 K9 on Ifng regions was also abrogated in Nfkbiz(-/-) NK cells. |
| 2178 | 20876105 | IκBζ was recruited on the proximal promoter region of the Ifng gene, and overexpression of IκBζ together with IL-12 activated the Ifng promoter. |
| 2179 | 20876105 | IκBζ was recruited on the proximal promoter region of the Ifng gene, and overexpression of IκBζ together with IL-12 activated the Ifng promoter. |
| 2180 | 20876105 | IκBζ was recruited on the proximal promoter region of the Ifng gene, and overexpression of IκBζ together with IL-12 activated the Ifng promoter. |
| 2181 | 20811799 | IFNG-inducible KYN/pteridines inflammation cascade is characterized by up-regulation of nitric oxide synthase (NOS) activity (induced by KYN) and decreased formation of NOS cofactor, BH4, that results in uncoupling of NOS that shifting arginine from NO to superoxide anion production. |
| 2182 | 20811799 | IFNG-inducible KYN/pteridines inflammation cascade is characterized by up-regulation of nitric oxide synthase (NOS) activity (induced by KYN) and decreased formation of NOS cofactor, BH4, that results in uncoupling of NOS that shifting arginine from NO to superoxide anion production. |
| 2183 | 20811799 | IFNG-induced up-regulation of indoleamine 2,3-dioxygenase (IDO), rate-limiting enzyme of TRY-KYN pathway, decreases TRY conversion into serotonin (substrate of antidepressant effect) and increases production of KYN associated with diabetes [xanthurenic acid (XA)], anxiety (KYN), psychoses and cognitive impairment (kynurenic acid). |
| 2184 | 20811799 | IFNG-induced up-regulation of indoleamine 2,3-dioxygenase (IDO), rate-limiting enzyme of TRY-KYN pathway, decreases TRY conversion into serotonin (substrate of antidepressant effect) and increases production of KYN associated with diabetes [xanthurenic acid (XA)], anxiety (KYN), psychoses and cognitive impairment (kynurenic acid). |
| 2185 | 20811799 | In addition to literature data on KYN/TRY ratio (IDO activity index), we observe neopterin levels (index of activity of rate-limiting enzyme of guanine-BH4 pathway) to be higher in carriers of high (T) than of low (A) producers alleles; and to correlate with AAMPD markers (e.g., insulin resistance, body mass index, mortality risk), and with IFN-alpha-induced depression in hepatitis C patients. |
| 2186 | 20811799 | In addition to literature data on KYN/TRY ratio (IDO activity index), we observe neopterin levels (index of activity of rate-limiting enzyme of guanine-BH4 pathway) to be higher in carriers of high (T) than of low (A) producers alleles; and to correlate with AAMPD markers (e.g., insulin resistance, body mass index, mortality risk), and with IFN-alpha-induced depression in hepatitis C patients. |
| 2187 | 20722470 | Cystic fibrosis conductance regulator, tumor necrosis factor, interferon alpha-10, interferon alpha-17, and interferon gamma genotyping as potential risk markers in pulmonary sarcoidosis pathogenesis in Greek patients. |
| 2188 | 20722470 | Cystic fibrosis conductance regulator, tumor necrosis factor, interferon alpha-10, interferon alpha-17, and interferon gamma genotyping as potential risk markers in pulmonary sarcoidosis pathogenesis in Greek patients. |
| 2189 | 20722470 | Cystic fibrosis conductance regulator, tumor necrosis factor, interferon alpha-10, interferon alpha-17, and interferon gamma genotyping as potential risk markers in pulmonary sarcoidosis pathogenesis in Greek patients. |
| 2190 | 20722470 | We have screened for mutations in the cystic fibrosis conductance regulator (CFTR) gene and genotyped single-nucleotide polymorphisms in the tumor necrosis factor (TNF), interferon alpha-10 (IFNA10), IFNA17, and interferon gamma (IFNG) genes in 89 Greek patients with sarcoidosis and 212 control subjects to detect possible association between them and the risk for developing sarcoidosis. |
| 2191 | 20722470 | We have screened for mutations in the cystic fibrosis conductance regulator (CFTR) gene and genotyped single-nucleotide polymorphisms in the tumor necrosis factor (TNF), interferon alpha-10 (IFNA10), IFNA17, and interferon gamma (IFNG) genes in 89 Greek patients with sarcoidosis and 212 control subjects to detect possible association between them and the risk for developing sarcoidosis. |
| 2192 | 20722470 | We have screened for mutations in the cystic fibrosis conductance regulator (CFTR) gene and genotyped single-nucleotide polymorphisms in the tumor necrosis factor (TNF), interferon alpha-10 (IFNA10), IFNA17, and interferon gamma (IFNG) genes in 89 Greek patients with sarcoidosis and 212 control subjects to detect possible association between them and the risk for developing sarcoidosis. |
| 2193 | 20722470 | Our study did not reproduce the associations previously noted with the TNF, IFNA10, IFNA17, and IFNG genes, which highlights the genetic complexity of the disorder and is in agreement with previous studies showing that CFTR might be an important factor in the clinical course of the disease. |
| 2194 | 20722470 | Our study did not reproduce the associations previously noted with the TNF, IFNA10, IFNA17, and IFNG genes, which highlights the genetic complexity of the disorder and is in agreement with previous studies showing that CFTR might be an important factor in the clinical course of the disease. |
| 2195 | 20722470 | Our study did not reproduce the associations previously noted with the TNF, IFNA10, IFNA17, and IFNG genes, which highlights the genetic complexity of the disorder and is in agreement with previous studies showing that CFTR might be an important factor in the clinical course of the disease. |
| 2196 | 20720169 | Is FAS/Fas ligand system involved in equine corpus luteum functional regression? |
| 2197 | 20720169 | Is FAS/Fas ligand system involved in equine corpus luteum functional regression? |
| 2198 | 20720169 | Is FAS/Fas ligand system involved in equine corpus luteum functional regression? |
| 2199 | 20720169 | Proapoptotic factor Fas ligand (FASL) and its cell surface receptor FAS are tumor necrosis factor superfamily members that trigger apoptosis in different cell types. |
| 2200 | 20720169 | Proapoptotic factor Fas ligand (FASL) and its cell surface receptor FAS are tumor necrosis factor superfamily members that trigger apoptosis in different cell types. |
| 2201 | 20720169 | Proapoptotic factor Fas ligand (FASL) and its cell surface receptor FAS are tumor necrosis factor superfamily members that trigger apoptosis in different cell types. |
| 2202 | 20720169 | The aim of the present work was to determine (i) the presence of the cytokine FASL and its receptor FAS in the mare's corpus luteum (CL) throughout the luteal phase, as well as (ii) the influence of FASL alone, or together with the cytokines tumor necrosis factor alpha (TNF) and interferon gamma (IFNG), on equine luteal cell production of luteotrophic and luteolytic factors, cell viability, and apoptosis. |
| 2203 | 20720169 | The aim of the present work was to determine (i) the presence of the cytokine FASL and its receptor FAS in the mare's corpus luteum (CL) throughout the luteal phase, as well as (ii) the influence of FASL alone, or together with the cytokines tumor necrosis factor alpha (TNF) and interferon gamma (IFNG), on equine luteal cell production of luteotrophic and luteolytic factors, cell viability, and apoptosis. |
| 2204 | 20720169 | The aim of the present work was to determine (i) the presence of the cytokine FASL and its receptor FAS in the mare's corpus luteum (CL) throughout the luteal phase, as well as (ii) the influence of FASL alone, or together with the cytokines tumor necrosis factor alpha (TNF) and interferon gamma (IFNG), on equine luteal cell production of luteotrophic and luteolytic factors, cell viability, and apoptosis. |
| 2205 | 20720169 | FASL and FAS protein expression and mRNA transcription were evaluated in different luteal stages of the equine CL by Western blotting and real-time PCR assays, respectively. |
| 2206 | 20720169 | FASL and FAS protein expression and mRNA transcription were evaluated in different luteal stages of the equine CL by Western blotting and real-time PCR assays, respectively. |
| 2207 | 20720169 | FASL and FAS protein expression and mRNA transcription were evaluated in different luteal stages of the equine CL by Western blotting and real-time PCR assays, respectively. |
| 2208 | 20720169 | Also, FAS and FASL proteins were present in large steroidogenic and endothelial CL cells throughout the luteal phase, as demonstrated by immunohistochemistry. |
| 2209 | 20720169 | Also, FAS and FASL proteins were present in large steroidogenic and endothelial CL cells throughout the luteal phase, as demonstrated by immunohistochemistry. |
| 2210 | 20720169 | Also, FAS and FASL proteins were present in large steroidogenic and endothelial CL cells throughout the luteal phase, as demonstrated by immunohistochemistry. |
| 2211 | 20720169 | Equine luteal cells isolated from midluteal phase CL were stimulated without (control) or with exogenous cytokines: FASL (10 ng/ml); TNF+IFNG (10 ng/ml each; positive control) or FASL+TNF+IFNG (10 ng/ml each). |
| 2212 | 20720169 | Equine luteal cells isolated from midluteal phase CL were stimulated without (control) or with exogenous cytokines: FASL (10 ng/ml); TNF+IFNG (10 ng/ml each; positive control) or FASL+TNF+IFNG (10 ng/ml each). |
| 2213 | 20720169 | Equine luteal cells isolated from midluteal phase CL were stimulated without (control) or with exogenous cytokines: FASL (10 ng/ml); TNF+IFNG (10 ng/ml each; positive control) or FASL+TNF+IFNG (10 ng/ml each). |
| 2214 | 20720169 | Furthermore, FASL effect on equine luteal cell viability depended on the presence of cytokines TNF and IFNG. |
| 2215 | 20720169 | Furthermore, FASL effect on equine luteal cell viability depended on the presence of cytokines TNF and IFNG. |
| 2216 | 20720169 | Furthermore, FASL effect on equine luteal cell viability depended on the presence of cytokines TNF and IFNG. |
| 2217 | 20720169 | In conclusion, this study shows the presence of FASL and FAS in the equine CL and suggests their importance in functional luteolysis. |
| 2218 | 20720169 | In conclusion, this study shows the presence of FASL and FAS in the equine CL and suggests their importance in functional luteolysis. |
| 2219 | 20720169 | In conclusion, this study shows the presence of FASL and FAS in the equine CL and suggests their importance in functional luteolysis. |
| 2220 | 20709293 | Fidelity of pathogen-specific CD4+ T cells to the Th1 lineage is controlled by exogenous cytokines, interferon-gamma expression, and pathogen lifestyle. |
| 2221 | 20655098 | IFNG, IFNGR1 and IFNGR2 expression was analysed using qRT-PCR profiling in the inflammatory granulation tissue and atheroma. |
| 2222 | 20655098 | IFNG, IFNGR1 and IFNGR2 expression was analysed using qRT-PCR profiling in the inflammatory granulation tissue and atheroma. |
| 2223 | 20655098 | Granulation tissue samples obtained from non-atherosclerotic group showed a significant increase in IFNG and a decrease of IFNGR1, IFNGR2 expression whereas granulation tissue and atheromata of patients with systemic disease demonstrated lower IFNG and higher IFNGR1 and IFNGR2 expression. |
| 2224 | 20655098 | Granulation tissue samples obtained from non-atherosclerotic group showed a significant increase in IFNG and a decrease of IFNGR1, IFNGR2 expression whereas granulation tissue and atheromata of patients with systemic disease demonstrated lower IFNG and higher IFNGR1 and IFNGR2 expression. |
| 2225 | 20574006 | This distal regulatory element is a Runx3 binding site in Th1 cells and is needed for RNA polymerase II recruitment to IFNG, but it is not absolutely required for histone acetylation of the IFNG locus. |
| 2226 | 20562522 | Cell death of LSCs and LECs is essential for structural luteolysis. |
| 2227 | 20562522 | Cell death of LSCs and LECs is essential for structural luteolysis. |
| 2228 | 20562522 | Cell death of LSCs and LECs is essential for structural luteolysis. |
| 2229 | 20562522 | Cell death of LSCs and LECs is essential for structural luteolysis. |
| 2230 | 20562522 | Cell death of LSCs and LECs is essential for structural luteolysis. |
| 2231 | 20562522 | Cell death of LSCs and LECs is essential for structural luteolysis. |
| 2232 | 20562522 | Cell death of LSCs and LECs is essential for structural luteolysis. |
| 2233 | 20562522 | Cell death of LSCs and LECs is essential for structural luteolysis. |
| 2234 | 20562522 | We previously reported that a treatment combining tumor necrosis factor α (TNF) and interferon γ (IFNG) induced cell death in LSCs and that LECs express TNF receptor type I (TNFRI). |
| 2235 | 20562522 | We previously reported that a treatment combining tumor necrosis factor α (TNF) and interferon γ (IFNG) induced cell death in LSCs and that LECs express TNF receptor type I (TNFRI). |
| 2236 | 20562522 | We previously reported that a treatment combining tumor necrosis factor α (TNF) and interferon γ (IFNG) induced cell death in LSCs and that LECs express TNF receptor type I (TNFRI). |
| 2237 | 20562522 | We previously reported that a treatment combining tumor necrosis factor α (TNF) and interferon γ (IFNG) induced cell death in LSCs and that LECs express TNF receptor type I (TNFRI). |
| 2238 | 20562522 | We previously reported that a treatment combining tumor necrosis factor α (TNF) and interferon γ (IFNG) induced cell death in LSCs and that LECs express TNF receptor type I (TNFRI). |
| 2239 | 20562522 | We previously reported that a treatment combining tumor necrosis factor α (TNF) and interferon γ (IFNG) induced cell death in LSCs and that LECs express TNF receptor type I (TNFRI). |
| 2240 | 20562522 | We previously reported that a treatment combining tumor necrosis factor α (TNF) and interferon γ (IFNG) induced cell death in LSCs and that LECs express TNF receptor type I (TNFRI). |
| 2241 | 20562522 | We previously reported that a treatment combining tumor necrosis factor α (TNF) and interferon γ (IFNG) induced cell death in LSCs and that LECs express TNF receptor type I (TNFRI). |
| 2242 | 20562522 | To induce cell death in LECs, LECs were treated with TNF or IFNG (0, 0.05, 0.5, 1.0, 2.5 nM) and a combination of TNF (0.5 nM) and IFNG (0.5 nM) for 24 h. |
| 2243 | 20562522 | To induce cell death in LECs, LECs were treated with TNF or IFNG (0, 0.05, 0.5, 1.0, 2.5 nM) and a combination of TNF (0.5 nM) and IFNG (0.5 nM) for 24 h. |
| 2244 | 20562522 | To induce cell death in LECs, LECs were treated with TNF or IFNG (0, 0.05, 0.5, 1.0, 2.5 nM) and a combination of TNF (0.5 nM) and IFNG (0.5 nM) for 24 h. |
| 2245 | 20562522 | To induce cell death in LECs, LECs were treated with TNF or IFNG (0, 0.05, 0.5, 1.0, 2.5 nM) and a combination of TNF (0.5 nM) and IFNG (0.5 nM) for 24 h. |
| 2246 | 20562522 | To induce cell death in LECs, LECs were treated with TNF or IFNG (0, 0.05, 0.5, 1.0, 2.5 nM) and a combination of TNF (0.5 nM) and IFNG (0.5 nM) for 24 h. |
| 2247 | 20562522 | To induce cell death in LECs, LECs were treated with TNF or IFNG (0, 0.05, 0.5, 1.0, 2.5 nM) and a combination of TNF (0.5 nM) and IFNG (0.5 nM) for 24 h. |
| 2248 | 20562522 | To induce cell death in LECs, LECs were treated with TNF or IFNG (0, 0.05, 0.5, 1.0, 2.5 nM) and a combination of TNF (0.5 nM) and IFNG (0.5 nM) for 24 h. |
| 2249 | 20562522 | To induce cell death in LECs, LECs were treated with TNF or IFNG (0, 0.05, 0.5, 1.0, 2.5 nM) and a combination of TNF (0.5 nM) and IFNG (0.5 nM) for 24 h. |
| 2250 | 20562522 | The viability of LECs was reduced by a single treatment with TNF or IFNG dose-dependently (P<0.05). |
| 2251 | 20562522 | The viability of LECs was reduced by a single treatment with TNF or IFNG dose-dependently (P<0.05). |
| 2252 | 20562522 | The viability of LECs was reduced by a single treatment with TNF or IFNG dose-dependently (P<0.05). |
| 2253 | 20562522 | The viability of LECs was reduced by a single treatment with TNF or IFNG dose-dependently (P<0.05). |
| 2254 | 20562522 | The viability of LECs was reduced by a single treatment with TNF or IFNG dose-dependently (P<0.05). |
| 2255 | 20562522 | The viability of LECs was reduced by a single treatment with TNF or IFNG dose-dependently (P<0.05). |
| 2256 | 20562522 | The viability of LECs was reduced by a single treatment with TNF or IFNG dose-dependently (P<0.05). |
| 2257 | 20562522 | The viability of LECs was reduced by a single treatment with TNF or IFNG dose-dependently (P<0.05). |
| 2258 | 20562522 | Cell viability was further decreased by treatment with a combination of TNF and IFNG (P<0.05). |
| 2259 | 20562522 | Cell viability was further decreased by treatment with a combination of TNF and IFNG (P<0.05). |
| 2260 | 20562522 | Cell viability was further decreased by treatment with a combination of TNF and IFNG (P<0.05). |
| 2261 | 20562522 | Cell viability was further decreased by treatment with a combination of TNF and IFNG (P<0.05). |
| 2262 | 20562522 | Cell viability was further decreased by treatment with a combination of TNF and IFNG (P<0.05). |
| 2263 | 20562522 | Cell viability was further decreased by treatment with a combination of TNF and IFNG (P<0.05). |
| 2264 | 20562522 | Cell viability was further decreased by treatment with a combination of TNF and IFNG (P<0.05). |
| 2265 | 20562522 | Cell viability was further decreased by treatment with a combination of TNF and IFNG (P<0.05). |
| 2266 | 20562522 | Cells with DNA fragmentation (TUNEL-positive cells) were observed after the treatment with TNF and IFNG. |
| 2267 | 20562522 | Cells with DNA fragmentation (TUNEL-positive cells) were observed after the treatment with TNF and IFNG. |
| 2268 | 20562522 | Cells with DNA fragmentation (TUNEL-positive cells) were observed after the treatment with TNF and IFNG. |
| 2269 | 20562522 | Cells with DNA fragmentation (TUNEL-positive cells) were observed after the treatment with TNF and IFNG. |
| 2270 | 20562522 | Cells with DNA fragmentation (TUNEL-positive cells) were observed after the treatment with TNF and IFNG. |
| 2271 | 20562522 | Cells with DNA fragmentation (TUNEL-positive cells) were observed after the treatment with TNF and IFNG. |
| 2272 | 20562522 | Cells with DNA fragmentation (TUNEL-positive cells) were observed after the treatment with TNF and IFNG. |
| 2273 | 20562522 | Cells with DNA fragmentation (TUNEL-positive cells) were observed after the treatment with TNF and IFNG. |
| 2274 | 20562522 | Semi-quantitative RT-PCR analysis revealed that treatment with IFNG alone or in combination with TNF increased the expression of TNFRI mRNA compared with the control (P<0.05). |
| 2275 | 20562522 | Semi-quantitative RT-PCR analysis revealed that treatment with IFNG alone or in combination with TNF increased the expression of TNFRI mRNA compared with the control (P<0.05). |
| 2276 | 20562522 | Semi-quantitative RT-PCR analysis revealed that treatment with IFNG alone or in combination with TNF increased the expression of TNFRI mRNA compared with the control (P<0.05). |
| 2277 | 20562522 | Semi-quantitative RT-PCR analysis revealed that treatment with IFNG alone or in combination with TNF increased the expression of TNFRI mRNA compared with the control (P<0.05). |
| 2278 | 20562522 | Semi-quantitative RT-PCR analysis revealed that treatment with IFNG alone or in combination with TNF increased the expression of TNFRI mRNA compared with the control (P<0.05). |
| 2279 | 20562522 | Semi-quantitative RT-PCR analysis revealed that treatment with IFNG alone or in combination with TNF increased the expression of TNFRI mRNA compared with the control (P<0.05). |
| 2280 | 20562522 | Semi-quantitative RT-PCR analysis revealed that treatment with IFNG alone or in combination with TNF increased the expression of TNFRI mRNA compared with the control (P<0.05). |
| 2281 | 20562522 | Semi-quantitative RT-PCR analysis revealed that treatment with IFNG alone or in combination with TNF increased the expression of TNFRI mRNA compared with the control (P<0.05). |
| 2282 | 20562522 | In summary, TNF and IFNG increased cell death in cultured bovine LECs. |
| 2283 | 20562522 | In summary, TNF and IFNG increased cell death in cultured bovine LECs. |
| 2284 | 20562522 | In summary, TNF and IFNG increased cell death in cultured bovine LECs. |
| 2285 | 20562522 | In summary, TNF and IFNG increased cell death in cultured bovine LECs. |
| 2286 | 20562522 | In summary, TNF and IFNG increased cell death in cultured bovine LECs. |
| 2287 | 20562522 | In summary, TNF and IFNG increased cell death in cultured bovine LECs. |
| 2288 | 20562522 | In summary, TNF and IFNG increased cell death in cultured bovine LECs. |
| 2289 | 20562522 | In summary, TNF and IFNG increased cell death in cultured bovine LECs. |
| 2290 | 20562522 | The upregulation of TNFRI mRNA expression by IFNG suggests that TNF and IFNG synergistically affect the death of LECs resulting in acute luteolysis. |
| 2291 | 20562522 | The upregulation of TNFRI mRNA expression by IFNG suggests that TNF and IFNG synergistically affect the death of LECs resulting in acute luteolysis. |
| 2292 | 20562522 | The upregulation of TNFRI mRNA expression by IFNG suggests that TNF and IFNG synergistically affect the death of LECs resulting in acute luteolysis. |
| 2293 | 20562522 | The upregulation of TNFRI mRNA expression by IFNG suggests that TNF and IFNG synergistically affect the death of LECs resulting in acute luteolysis. |
| 2294 | 20562522 | The upregulation of TNFRI mRNA expression by IFNG suggests that TNF and IFNG synergistically affect the death of LECs resulting in acute luteolysis. |
| 2295 | 20562522 | The upregulation of TNFRI mRNA expression by IFNG suggests that TNF and IFNG synergistically affect the death of LECs resulting in acute luteolysis. |
| 2296 | 20562522 | The upregulation of TNFRI mRNA expression by IFNG suggests that TNF and IFNG synergistically affect the death of LECs resulting in acute luteolysis. |
| 2297 | 20562522 | The upregulation of TNFRI mRNA expression by IFNG suggests that TNF and IFNG synergistically affect the death of LECs resulting in acute luteolysis. |
| 2298 | 20484740 | Murine trophoblast cells induce NK cell interferon-gamma production through KLRK1. |
| 2299 | 20484740 | Murine trophoblast cells induce NK cell interferon-gamma production through KLRK1. |
| 2300 | 20484740 | We suggest that the interaction of KLRK1 and RAET1 may be involved in IFNG production by uNK cells, and thus, this receptor-ligand pair may contribute to successful murine implantation site development. |
| 2301 | 20484740 | We suggest that the interaction of KLRK1 and RAET1 may be involved in IFNG production by uNK cells, and thus, this receptor-ligand pair may contribute to successful murine implantation site development. |
| 2302 | 20427761 | The cytokines interferon tau (IFNT), interferon gamma (IFNG), and interleukin 4 (IL4) significantly increased luciferase expression in NC1 promoter reporter constructs and endogenous NC1 mRNA levels in a bovine endometrial cell line. |
| 2303 | 20427761 | The cytokines interferon tau (IFNT), interferon gamma (IFNG), and interleukin 4 (IL4) significantly increased luciferase expression in NC1 promoter reporter constructs and endogenous NC1 mRNA levels in a bovine endometrial cell line. |
| 2304 | 20427761 | The cytokines interferon tau (IFNT), interferon gamma (IFNG), and interleukin 4 (IL4) significantly increased luciferase expression in NC1 promoter reporter constructs and endogenous NC1 mRNA levels in a bovine endometrial cell line. |
| 2305 | 20427761 | In addition, IFNG, IL3, IL4, and progesterone significantly increased Day 7 bovine blastocyst NC1 mRNA expression when supplemented during in vitro embryo culture. |
| 2306 | 20427761 | In addition, IFNG, IL3, IL4, and progesterone significantly increased Day 7 bovine blastocyst NC1 mRNA expression when supplemented during in vitro embryo culture. |
| 2307 | 20427761 | In addition, IFNG, IL3, IL4, and progesterone significantly increased Day 7 bovine blastocyst NC1 mRNA expression when supplemented during in vitro embryo culture. |
| 2308 | 20427761 | The promoter is responsive to IFNT, IFNG, and IL4, suggesting possible roles for these cytokines in bovine preimplantation embryo survival and/or maternal-fetal tolerance. |
| 2309 | 20427761 | The promoter is responsive to IFNT, IFNG, and IL4, suggesting possible roles for these cytokines in bovine preimplantation embryo survival and/or maternal-fetal tolerance. |
| 2310 | 20427761 | The promoter is responsive to IFNT, IFNG, and IL4, suggesting possible roles for these cytokines in bovine preimplantation embryo survival and/or maternal-fetal tolerance. |
| 2311 | 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). |
| 2312 | 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). |
| 2313 | 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). |
| 2314 | 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. |
| 2315 | 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. |
| 2316 | 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. |
| 2317 | 20421878 | Over-expression of PHF11 did not increase IL2 gene transcription, suggesting some specificity in promoter recognition. |
| 2318 | 20421878 | Over-expression of PHF11 did not increase IL2 gene transcription, suggesting some specificity in promoter recognition. |
| 2319 | 20421878 | Over-expression of PHF11 did not increase IL2 gene transcription, suggesting some specificity in promoter recognition. |
| 2320 | 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. |
| 2321 | 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. |
| 2322 | 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. |
| 2323 | 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. |
| 2324 | 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. |
| 2325 | 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. |
| 2326 | 20404426 | Association of interleukin-10, interferon-gamma, transforming growth factor-beta, and tumor necrosis factor-alpha gene polymorphisms with long-term kidney allograft survival. |
| 2327 | 20399120 | The transcription factor GATA3 actively represses RUNX3 protein-regulated production of interferon-gamma. |
| 2328 | 20399120 | The transcription factor GATA3 actively represses RUNX3 protein-regulated production of interferon-gamma. |
| 2329 | 20399120 | The transcription factor GATA3 actively represses RUNX3 protein-regulated production of interferon-gamma. |
| 2330 | 20399120 | The transcription factor GATA3 actively represses RUNX3 protein-regulated production of interferon-gamma. |
| 2331 | 20399120 | The transcription factor GATA3 actively represses RUNX3 protein-regulated production of interferon-gamma. |
| 2332 | 20399120 | The transcription factor GATA3 actively represses RUNX3 protein-regulated production of interferon-gamma. |
| 2333 | 20399120 | The transcription factor GATA3 actively represses RUNX3 protein-regulated production of interferon-gamma. |
| 2334 | 20399120 | The transcription factor GATA3 is crucial for the differentiation of naive CD4(+) T cells into T helper 2 (Th2) cells. |
| 2335 | 20399120 | The transcription factor GATA3 is crucial for the differentiation of naive CD4(+) T cells into T helper 2 (Th2) cells. |
| 2336 | 20399120 | The transcription factor GATA3 is crucial for the differentiation of naive CD4(+) T cells into T helper 2 (Th2) cells. |
| 2337 | 20399120 | The transcription factor GATA3 is crucial for the differentiation of naive CD4(+) T cells into T helper 2 (Th2) cells. |
| 2338 | 20399120 | The transcription factor GATA3 is crucial for the differentiation of naive CD4(+) T cells into T helper 2 (Th2) cells. |
| 2339 | 20399120 | The transcription factor GATA3 is crucial for the differentiation of naive CD4(+) T cells into T helper 2 (Th2) cells. |
| 2340 | 20399120 | The transcription factor GATA3 is crucial for the differentiation of naive CD4(+) T cells into T helper 2 (Th2) cells. |
| 2341 | 20399120 | Here, we show that deletion of Gata3 allowed the appearance of interferon-gamma (IFN-gamma)-producing cells in the absence of interleukin-12 (IL-12) and IFN-gamma. |
| 2342 | 20399120 | Here, we show that deletion of Gata3 allowed the appearance of interferon-gamma (IFN-gamma)-producing cells in the absence of interleukin-12 (IL-12) and IFN-gamma. |
| 2343 | 20399120 | Here, we show that deletion of Gata3 allowed the appearance of interferon-gamma (IFN-gamma)-producing cells in the absence of interleukin-12 (IL-12) and IFN-gamma. |
| 2344 | 20399120 | Here, we show that deletion of Gata3 allowed the appearance of interferon-gamma (IFN-gamma)-producing cells in the absence of interleukin-12 (IL-12) and IFN-gamma. |
| 2345 | 20399120 | Here, we show that deletion of Gata3 allowed the appearance of interferon-gamma (IFN-gamma)-producing cells in the absence of interleukin-12 (IL-12) and IFN-gamma. |
| 2346 | 20399120 | Here, we show that deletion of Gata3 allowed the appearance of interferon-gamma (IFN-gamma)-producing cells in the absence of interleukin-12 (IL-12) and IFN-gamma. |
| 2347 | 20399120 | Here, we show that deletion of Gata3 allowed the appearance of interferon-gamma (IFN-gamma)-producing cells in the absence of interleukin-12 (IL-12) and IFN-gamma. |
| 2348 | 20399120 | Such IFN-gamma production was transcription factor T-bet independent. |
| 2349 | 20399120 | Such IFN-gamma production was transcription factor T-bet independent. |
| 2350 | 20399120 | Such IFN-gamma production was transcription factor T-bet independent. |
| 2351 | 20399120 | Such IFN-gamma production was transcription factor T-bet independent. |
| 2352 | 20399120 | Such IFN-gamma production was transcription factor T-bet independent. |
| 2353 | 20399120 | Such IFN-gamma production was transcription factor T-bet independent. |
| 2354 | 20399120 | Such IFN-gamma production was transcription factor T-bet independent. |
| 2355 | 20399120 | Another T-box-containing transcription factor Eomes, but not T-bet, was induced both in GATA3-deficient CD4(+) T cells differentiated under Th2 cell conditions and in Th2 cells with enforced Runx3 expression, contributing to IFN-gamma production. |
| 2356 | 20399120 | Another T-box-containing transcription factor Eomes, but not T-bet, was induced both in GATA3-deficient CD4(+) T cells differentiated under Th2 cell conditions and in Th2 cells with enforced Runx3 expression, contributing to IFN-gamma production. |
| 2357 | 20399120 | Another T-box-containing transcription factor Eomes, but not T-bet, was induced both in GATA3-deficient CD4(+) T cells differentiated under Th2 cell conditions and in Th2 cells with enforced Runx3 expression, contributing to IFN-gamma production. |
| 2358 | 20399120 | Another T-box-containing transcription factor Eomes, but not T-bet, was induced both in GATA3-deficient CD4(+) T cells differentiated under Th2 cell conditions and in Th2 cells with enforced Runx3 expression, contributing to IFN-gamma production. |
| 2359 | 20399120 | Another T-box-containing transcription factor Eomes, but not T-bet, was induced both in GATA3-deficient CD4(+) T cells differentiated under Th2 cell conditions and in Th2 cells with enforced Runx3 expression, contributing to IFN-gamma production. |
| 2360 | 20399120 | Another T-box-containing transcription factor Eomes, but not T-bet, was induced both in GATA3-deficient CD4(+) T cells differentiated under Th2 cell conditions and in Th2 cells with enforced Runx3 expression, contributing to IFN-gamma production. |
| 2361 | 20399120 | Another T-box-containing transcription factor Eomes, but not T-bet, was induced both in GATA3-deficient CD4(+) T cells differentiated under Th2 cell conditions and in Th2 cells with enforced Runx3 expression, contributing to IFN-gamma production. |
| 2362 | 20399120 | GATA3 overexpression blocked Runx3-mediated Eomes induction and IFN-gamma production, and GATA3 protein physically interacted with Runx3 protein. |
| 2363 | 20399120 | GATA3 overexpression blocked Runx3-mediated Eomes induction and IFN-gamma production, and GATA3 protein physically interacted with Runx3 protein. |
| 2364 | 20399120 | GATA3 overexpression blocked Runx3-mediated Eomes induction and IFN-gamma production, and GATA3 protein physically interacted with Runx3 protein. |
| 2365 | 20399120 | GATA3 overexpression blocked Runx3-mediated Eomes induction and IFN-gamma production, and GATA3 protein physically interacted with Runx3 protein. |
| 2366 | 20399120 | GATA3 overexpression blocked Runx3-mediated Eomes induction and IFN-gamma production, and GATA3 protein physically interacted with Runx3 protein. |
| 2367 | 20399120 | GATA3 overexpression blocked Runx3-mediated Eomes induction and IFN-gamma production, and GATA3 protein physically interacted with Runx3 protein. |
| 2368 | 20399120 | GATA3 overexpression blocked Runx3-mediated Eomes induction and IFN-gamma production, and GATA3 protein physically interacted with Runx3 protein. |
| 2369 | 20399120 | Furthermore, we found that Runx3 directly bound to multiple regulatory elements of the Ifng gene and that blocking Runx3 function in either Th1 or GATA3-deficient "Th2" cells results in diminished IFN-gamma production by these cells. |
| 2370 | 20399120 | Furthermore, we found that Runx3 directly bound to multiple regulatory elements of the Ifng gene and that blocking Runx3 function in either Th1 or GATA3-deficient "Th2" cells results in diminished IFN-gamma production by these cells. |
| 2371 | 20399120 | Furthermore, we found that Runx3 directly bound to multiple regulatory elements of the Ifng gene and that blocking Runx3 function in either Th1 or GATA3-deficient "Th2" cells results in diminished IFN-gamma production by these cells. |
| 2372 | 20399120 | Furthermore, we found that Runx3 directly bound to multiple regulatory elements of the Ifng gene and that blocking Runx3 function in either Th1 or GATA3-deficient "Th2" cells results in diminished IFN-gamma production by these cells. |
| 2373 | 20399120 | Furthermore, we found that Runx3 directly bound to multiple regulatory elements of the Ifng gene and that blocking Runx3 function in either Th1 or GATA3-deficient "Th2" cells results in diminished IFN-gamma production by these cells. |
| 2374 | 20399120 | Furthermore, we found that Runx3 directly bound to multiple regulatory elements of the Ifng gene and that blocking Runx3 function in either Th1 or GATA3-deficient "Th2" cells results in diminished IFN-gamma production by these cells. |
| 2375 | 20399120 | Furthermore, we found that Runx3 directly bound to multiple regulatory elements of the Ifng gene and that blocking Runx3 function in either Th1 or GATA3-deficient "Th2" cells results in diminished IFN-gamma production by these cells. |
| 2376 | 20399120 | Thus, the Runx3-mediated pathway, actively suppressed by GATA3, induces IFN-gamma production in a STAT4- and T-bet-independent manner. |
| 2377 | 20399120 | Thus, the Runx3-mediated pathway, actively suppressed by GATA3, induces IFN-gamma production in a STAT4- and T-bet-independent manner. |
| 2378 | 20399120 | Thus, the Runx3-mediated pathway, actively suppressed by GATA3, induces IFN-gamma production in a STAT4- and T-bet-independent manner. |
| 2379 | 20399120 | Thus, the Runx3-mediated pathway, actively suppressed by GATA3, induces IFN-gamma production in a STAT4- and T-bet-independent manner. |
| 2380 | 20399120 | Thus, the Runx3-mediated pathway, actively suppressed by GATA3, induces IFN-gamma production in a STAT4- and T-bet-independent manner. |
| 2381 | 20399120 | Thus, the Runx3-mediated pathway, actively suppressed by GATA3, induces IFN-gamma production in a STAT4- and T-bet-independent manner. |
| 2382 | 20399120 | Thus, the Runx3-mediated pathway, actively suppressed by GATA3, induces IFN-gamma production in a STAT4- and T-bet-independent manner. |
| 2383 | 20376717 | In the past we have analysed candidate genes and their role in the course of malaria and could detect some polymorphisms influencing infectious diseases in the genes encoding NOS2, MBL2, IFNa, FCN2, and receptors for IFNg and IFNa. |
| 2384 | 20346061 | In kidney allografts, T cell mediated rejection (TCMR) is characterized by infiltration of the interstitium by T cells and macrophages, intense IFNG and TGFB effects, and epithelial deterioration. |
| 2385 | 20346061 | This event creates the inflammatory compartment that recruits effector and effector memory CD4 and CD8 T cells, both cognate and noncognate, and macrophage precursors. |
| 2386 | 20304822 | Activating transcription factor 3 is a positive regulator of human IFNG gene expression. |
| 2387 | 20304822 | Activating transcription factor 3 is a positive regulator of human IFNG gene expression. |
| 2388 | 20304822 | Activating transcription factor 3 is a positive regulator of human IFNG gene expression. |
| 2389 | 20304822 | IL-12 and IL-18 are essential for Th1 differentiation, whereas the role of IFN-alpha in Th1 development is less understood. |
| 2390 | 20304822 | IL-12 and IL-18 are essential for Th1 differentiation, whereas the role of IFN-alpha in Th1 development is less understood. |
| 2391 | 20304822 | IL-12 and IL-18 are essential for Th1 differentiation, whereas the role of IFN-alpha in Th1 development is less understood. |
| 2392 | 20304822 | In this microarray-based study, we searched for genes that are regulated by IFN-alpha, IL-12, or the combination of IL-12 plus IL-18 during the early differentiation of human umbilical cord blood CD4(+) Th cells. |
| 2393 | 20304822 | In this microarray-based study, we searched for genes that are regulated by IFN-alpha, IL-12, or the combination of IL-12 plus IL-18 during the early differentiation of human umbilical cord blood CD4(+) Th cells. |
| 2394 | 20304822 | In this microarray-based study, we searched for genes that are regulated by IFN-alpha, IL-12, or the combination of IL-12 plus IL-18 during the early differentiation of human umbilical cord blood CD4(+) Th cells. |
| 2395 | 20304822 | Twenty-six genes were similarly regulated in response to treatment with IL-12, IFN-alpha, or the combination of IL-12 plus IL-18. |
| 2396 | 20304822 | Twenty-six genes were similarly regulated in response to treatment with IL-12, IFN-alpha, or the combination of IL-12 plus IL-18. |
| 2397 | 20304822 | Twenty-six genes were similarly regulated in response to treatment with IL-12, IFN-alpha, or the combination of IL-12 plus IL-18. |
| 2398 | 20304822 | Ectopic expression of ATF3 in CD4(+) T cells enhanced the production of IFN-gamma, the hallmark cytokine of Th1 cells, whereas small interfering RNA knockdown of ATF3 reduced IFN-gamma production. |
| 2399 | 20304822 | Ectopic expression of ATF3 in CD4(+) T cells enhanced the production of IFN-gamma, the hallmark cytokine of Th1 cells, whereas small interfering RNA knockdown of ATF3 reduced IFN-gamma production. |
| 2400 | 20304822 | Ectopic expression of ATF3 in CD4(+) T cells enhanced the production of IFN-gamma, the hallmark cytokine of Th1 cells, whereas small interfering RNA knockdown of ATF3 reduced IFN-gamma production. |
| 2401 | 20304822 | Furthermore, ATF3 formed an endogenous complex with JUN in CD4(+) T cells induced to Th1. |
| 2402 | 20304822 | Furthermore, ATF3 formed an endogenous complex with JUN in CD4(+) T cells induced to Th1. |
| 2403 | 20304822 | Furthermore, ATF3 formed an endogenous complex with JUN in CD4(+) T cells induced to Th1. |
| 2404 | 20304822 | Chromatin immunoprecipitation and luciferase reporter assays showed that both ATF3 and JUN are recruited to and transactivate the IFNG promoter during early Th1 differentiation. |
| 2405 | 20304822 | Chromatin immunoprecipitation and luciferase reporter assays showed that both ATF3 and JUN are recruited to and transactivate the IFNG promoter during early Th1 differentiation. |
| 2406 | 20304822 | Chromatin immunoprecipitation and luciferase reporter assays showed that both ATF3 and JUN are recruited to and transactivate the IFNG promoter during early Th1 differentiation. |
| 2407 | 20164427 | Induction of genes implicated in diabetes, such as Il18, Tnfa, and Inos but not Il4, Il17 or Ifng, was repressed in splenocytes derived from protected mice. |
| 2408 | 20121742 | Macrophages display two activation states that are considered mutually exclusive: classical macrophage activation (CMA), inducible by IFNG, and alternative macrophage activation (AMA), inducible by IL4 and IL13. |
| 2409 | 20121742 | Macrophages display two activation states that are considered mutually exclusive: classical macrophage activation (CMA), inducible by IFNG, and alternative macrophage activation (AMA), inducible by IL4 and IL13. |
| 2410 | 20121742 | Macrophages display two activation states that are considered mutually exclusive: classical macrophage activation (CMA), inducible by IFNG, and alternative macrophage activation (AMA), inducible by IL4 and IL13. |
| 2411 | 20121742 | In rejecting allografts, unlike interferon gamma (IFNG) effects and T-cell infiltration that developed rapidly and plateaued by day 7, AMA transcripts (Arg1, Mrc1, Mmp12 and Ear1) rose progressively as tubulitis and parenchymal deterioration developed at days 21 and 42, despite persistent IFNG effects. |
| 2412 | 20121742 | In rejecting allografts, unlike interferon gamma (IFNG) effects and T-cell infiltration that developed rapidly and plateaued by day 7, AMA transcripts (Arg1, Mrc1, Mmp12 and Ear1) rose progressively as tubulitis and parenchymal deterioration developed at days 21 and 42, despite persistent IFNG effects. |
| 2413 | 20121742 | In rejecting allografts, unlike interferon gamma (IFNG) effects and T-cell infiltration that developed rapidly and plateaued by day 7, AMA transcripts (Arg1, Mrc1, Mmp12 and Ear1) rose progressively as tubulitis and parenchymal deterioration developed at days 21 and 42, despite persistent IFNG effects. |
| 2414 | 20121742 | AMA in allografts was associated with transcripts for AMA inducers IL4, IL13 and inhibin A, but also occurred when hosts lacked IL4/IL13 receptors, suggesting a role for inhibin A. |
| 2415 | 20121742 | AMA in allografts was associated with transcripts for AMA inducers IL4, IL13 and inhibin A, but also occurred when hosts lacked IL4/IL13 receptors, suggesting a role for inhibin A. |
| 2416 | 20121742 | AMA in allografts was associated with transcripts for AMA inducers IL4, IL13 and inhibin A, but also occurred when hosts lacked IL4/IL13 receptors, suggesting a role for inhibin A. |
| 2417 | 20121742 | Thus kidneys undergoing T-cell-mediated rejection progressively acquire macrophages with alternative activation phenotype despite strong local IFNG effects, independent of IL4 and IL13. |
| 2418 | 20121742 | Thus kidneys undergoing T-cell-mediated rejection progressively acquire macrophages with alternative activation phenotype despite strong local IFNG effects, independent of IL4 and IL13. |
| 2419 | 20121742 | Thus kidneys undergoing T-cell-mediated rejection progressively acquire macrophages with alternative activation phenotype despite strong local IFNG effects, independent of IL4 and IL13. |
| 2420 | 20095398 | Experiments on Wistar rats showed that subacute poisoning by organophosphorus compounds dimethyldichlorovinyl phosphate (DDVF), malation, and dimethylparation (total dose, 1.0 LD50) suppresses both cell and humoral immune responses and significantly decreases the level of blood cytokines (IFNg, IL-4) and the IFNg/IL-4 ratio in comparison to the control, which is evidence for a greater lesion of Th1 cells in comparison to Th2 cells. |
| 2421 | 20084279 | Genes/regions statistically significantly associated with CIN3/cancer included the viral infection and cell entry genes 2',5' oligoadenylate synthetase gene 3 (OAS3), sulfatase 1 (SULF1), and interferon gamma (IFNG); the DNA repair genes deoxyuridine triphosphate (DUT), dosage suppressor of mck 1 homolog (DMC1), and general transcription factor IIH, polypeptide 3 (GTF2H4); and the EVER1 and EVER2 genes (p<0.01). |
| 2422 | 20084279 | Genes/regions statistically significantly associated with CIN3/cancer included the viral infection and cell entry genes 2',5' oligoadenylate synthetase gene 3 (OAS3), sulfatase 1 (SULF1), and interferon gamma (IFNG); the DNA repair genes deoxyuridine triphosphate (DUT), dosage suppressor of mck 1 homolog (DMC1), and general transcription factor IIH, polypeptide 3 (GTF2H4); and the EVER1 and EVER2 genes (p<0.01). |
| 2423 | 20084279 | Genes/regions statistically significantly associated with CIN3/cancer included the viral infection and cell entry genes 2',5' oligoadenylate synthetase gene 3 (OAS3), sulfatase 1 (SULF1), and interferon gamma (IFNG); the DNA repair genes deoxyuridine triphosphate (DUT), dosage suppressor of mck 1 homolog (DMC1), and general transcription factor IIH, polypeptide 3 (GTF2H4); and the EVER1 and EVER2 genes (p<0.01). |
| 2424 | 20084279 | From each region, the single most significant SNPs associated with CIN3/cancer were OAS3 rs12302655, SULF1 rs4737999, IFNG rs11177074, DUT rs3784621, DMC1 rs5757133, GTF2H4 rs2894054, EVER1/EVER2 rs9893818 (p-trends</=0.001). |
| 2425 | 20084279 | From each region, the single most significant SNPs associated with CIN3/cancer were OAS3 rs12302655, SULF1 rs4737999, IFNG rs11177074, DUT rs3784621, DMC1 rs5757133, GTF2H4 rs2894054, EVER1/EVER2 rs9893818 (p-trends</=0.001). |
| 2426 | 20084279 | From each region, the single most significant SNPs associated with CIN3/cancer were OAS3 rs12302655, SULF1 rs4737999, IFNG rs11177074, DUT rs3784621, DMC1 rs5757133, GTF2H4 rs2894054, EVER1/EVER2 rs9893818 (p-trends</=0.001). |
| 2427 | 20084279 | SNPs for OAS3, SULF1, DUT, and GTF2H4 were associated with HPV persistence whereas IFNG and EVER1/EVER2 SNPs were associated with progression to CIN3/cancer. |
| 2428 | 20084279 | SNPs for OAS3, SULF1, DUT, and GTF2H4 were associated with HPV persistence whereas IFNG and EVER1/EVER2 SNPs were associated with progression to CIN3/cancer. |
| 2429 | 20084279 | SNPs for OAS3, SULF1, DUT, and GTF2H4 were associated with HPV persistence whereas IFNG and EVER1/EVER2 SNPs were associated with progression to CIN3/cancer. |
| 2430 | 27534050 | [ALLELE POLYMORPHISM OF THE IFNG AND TGFB GENES AS A FACTOR OF MODULATION OF CYTOKINE SECRETION AND SUSCEPTIBILITY TO PULMONARY TUBERCULOSIS]. |
| 2431 | 27534050 | [ALLELE POLYMORPHISM OF THE IFNG AND TGFB GENES AS A FACTOR OF MODULATION OF CYTOKINE SECRETION AND SUSCEPTIBILITY TO PULMONARY TUBERCULOSIS]. |
| 2432 | 27534050 | [ALLELE POLYMORPHISM OF THE IFNG AND TGFB GENES AS A FACTOR OF MODULATION OF CYTOKINE SECRETION AND SUSCEPTIBILITY TO PULMONARY TUBERCULOSIS]. |
| 2433 | 27534050 | Susceptibility to tuberculosis infection is associated with A allele and with AA and AT genotypes of IFNG gene polymorphism +874A/T and the CTpolymorphic variant G509Tof the TGFB gene. |
| 2434 | 27534050 | Susceptibility to tuberculosis infection is associated with A allele and with AA and AT genotypes of IFNG gene polymorphism +874A/T and the CTpolymorphic variant G509Tof the TGFB gene. |
| 2435 | 27534050 | Susceptibility to tuberculosis infection is associated with A allele and with AA and AT genotypes of IFNG gene polymorphism +874A/T and the CTpolymorphic variant G509Tof the TGFB gene. |
| 2436 | 27534050 | The maximum risk for pulmonary tuberculosis is associated with a combination of the AA genotypes of the polymorphic site +874A/Tof the IFNG gene and TT polymorphism G509T of the TGFB gene (AA/TT). |
| 2437 | 27534050 | The maximum risk for pulmonary tuberculosis is associated with a combination of the AA genotypes of the polymorphic site +874A/Tof the IFNG gene and TT polymorphism G509T of the TGFB gene (AA/TT). |
| 2438 | 27534050 | The maximum risk for pulmonary tuberculosis is associated with a combination of the AA genotypes of the polymorphic site +874A/Tof the IFNG gene and TT polymorphism G509T of the TGFB gene (AA/TT). |
| 2439 | 20038794 | IL-17 produced by neutrophils regulates IFN-gamma-mediated neutrophil migration in mouse kidney ischemia-reperfusion injury. |
| 2440 | 20038794 | IL-17 produced by neutrophils regulates IFN-gamma-mediated neutrophil migration in mouse kidney ischemia-reperfusion injury. |
| 2441 | 20038794 | IL-17 produced by neutrophils regulates IFN-gamma-mediated neutrophil migration in mouse kidney ischemia-reperfusion injury. |
| 2442 | 20038794 | IL-17 produced by neutrophils regulates IFN-gamma-mediated neutrophil migration in mouse kidney ischemia-reperfusion injury. |
| 2443 | 20038794 | IL-17 produced by neutrophils regulates IFN-gamma-mediated neutrophil migration in mouse kidney ischemia-reperfusion injury. |
| 2444 | 20038794 | IL-17 produced by neutrophils regulates IFN-gamma-mediated neutrophil migration in mouse kidney ischemia-reperfusion injury. |
| 2445 | 20038794 | The IL-23/IL-17 and IL-12/IFN-gamma cytokine pathways have a role in chronic autoimmunity, which is considered mainly a dysfunction of adaptive immunity. |
| 2446 | 20038794 | The IL-23/IL-17 and IL-12/IFN-gamma cytokine pathways have a role in chronic autoimmunity, which is considered mainly a dysfunction of adaptive immunity. |
| 2447 | 20038794 | The IL-23/IL-17 and IL-12/IFN-gamma cytokine pathways have a role in chronic autoimmunity, which is considered mainly a dysfunction of adaptive immunity. |
| 2448 | 20038794 | The IL-23/IL-17 and IL-12/IFN-gamma cytokine pathways have a role in chronic autoimmunity, which is considered mainly a dysfunction of adaptive immunity. |
| 2449 | 20038794 | The IL-23/IL-17 and IL-12/IFN-gamma cytokine pathways have a role in chronic autoimmunity, which is considered mainly a dysfunction of adaptive immunity. |
| 2450 | 20038794 | The IL-23/IL-17 and IL-12/IFN-gamma cytokine pathways have a role in chronic autoimmunity, which is considered mainly a dysfunction of adaptive immunity. |
| 2451 | 20038794 | We used a mouse model of acute kidney ischemia-reperfusion injury (IRI) to test the hypothesis that early production of IL-23 and IL-12 following IRI activates downstream IL-17 and IFN-gamma signaling pathways and promotes kidney inflammation. |
| 2452 | 20038794 | We used a mouse model of acute kidney ischemia-reperfusion injury (IRI) to test the hypothesis that early production of IL-23 and IL-12 following IRI activates downstream IL-17 and IFN-gamma signaling pathways and promotes kidney inflammation. |
| 2453 | 20038794 | We used a mouse model of acute kidney ischemia-reperfusion injury (IRI) to test the hypothesis that early production of IL-23 and IL-12 following IRI activates downstream IL-17 and IFN-gamma signaling pathways and promotes kidney inflammation. |
| 2454 | 20038794 | We used a mouse model of acute kidney ischemia-reperfusion injury (IRI) to test the hypothesis that early production of IL-23 and IL-12 following IRI activates downstream IL-17 and IFN-gamma signaling pathways and promotes kidney inflammation. |
| 2455 | 20038794 | We used a mouse model of acute kidney ischemia-reperfusion injury (IRI) to test the hypothesis that early production of IL-23 and IL-12 following IRI activates downstream IL-17 and IFN-gamma signaling pathways and promotes kidney inflammation. |
| 2456 | 20038794 | We used a mouse model of acute kidney ischemia-reperfusion injury (IRI) to test the hypothesis that early production of IL-23 and IL-12 following IRI activates downstream IL-17 and IFN-gamma signaling pathways and promotes kidney inflammation. |
| 2457 | 20038794 | Deficiency in IL-23, IL-17A, or IL-17 receptor (IL-17R) and mAb neutralization of CXCR2, the p19 subunit of IL-23, or IL-17A attenuated neutrophil infiltration in acute kidney IRI in mice. |
| 2458 | 20038794 | Deficiency in IL-23, IL-17A, or IL-17 receptor (IL-17R) and mAb neutralization of CXCR2, the p19 subunit of IL-23, or IL-17A attenuated neutrophil infiltration in acute kidney IRI in mice. |
| 2459 | 20038794 | Deficiency in IL-23, IL-17A, or IL-17 receptor (IL-17R) and mAb neutralization of CXCR2, the p19 subunit of IL-23, or IL-17A attenuated neutrophil infiltration in acute kidney IRI in mice. |
| 2460 | 20038794 | Deficiency in IL-23, IL-17A, or IL-17 receptor (IL-17R) and mAb neutralization of CXCR2, the p19 subunit of IL-23, or IL-17A attenuated neutrophil infiltration in acute kidney IRI in mice. |
| 2461 | 20038794 | Deficiency in IL-23, IL-17A, or IL-17 receptor (IL-17R) and mAb neutralization of CXCR2, the p19 subunit of IL-23, or IL-17A attenuated neutrophil infiltration in acute kidney IRI in mice. |
| 2462 | 20038794 | Deficiency in IL-23, IL-17A, or IL-17 receptor (IL-17R) and mAb neutralization of CXCR2, the p19 subunit of IL-23, or IL-17A attenuated neutrophil infiltration in acute kidney IRI in mice. |
| 2463 | 20038794 | Activation of the IL-12/IFN-gamma pathway and NKT cells by administering alpha-galactosylceramide-primed bone marrow-derived DCs increased IFN-gamma production following moderate IRI in WT mice but did not exacerbate injury or enhance IFN-gamma production in either Il17a-/- or Il17r-/- mice, which suggested that IL-17 signaling was proximal to IFN-gamma signaling. |
| 2464 | 20038794 | Activation of the IL-12/IFN-gamma pathway and NKT cells by administering alpha-galactosylceramide-primed bone marrow-derived DCs increased IFN-gamma production following moderate IRI in WT mice but did not exacerbate injury or enhance IFN-gamma production in either Il17a-/- or Il17r-/- mice, which suggested that IL-17 signaling was proximal to IFN-gamma signaling. |
| 2465 | 20038794 | Activation of the IL-12/IFN-gamma pathway and NKT cells by administering alpha-galactosylceramide-primed bone marrow-derived DCs increased IFN-gamma production following moderate IRI in WT mice but did not exacerbate injury or enhance IFN-gamma production in either Il17a-/- or Il17r-/- mice, which suggested that IL-17 signaling was proximal to IFN-gamma signaling. |
| 2466 | 20038794 | Activation of the IL-12/IFN-gamma pathway and NKT cells by administering alpha-galactosylceramide-primed bone marrow-derived DCs increased IFN-gamma production following moderate IRI in WT mice but did not exacerbate injury or enhance IFN-gamma production in either Il17a-/- or Il17r-/- mice, which suggested that IL-17 signaling was proximal to IFN-gamma signaling. |
| 2467 | 20038794 | Activation of the IL-12/IFN-gamma pathway and NKT cells by administering alpha-galactosylceramide-primed bone marrow-derived DCs increased IFN-gamma production following moderate IRI in WT mice but did not exacerbate injury or enhance IFN-gamma production in either Il17a-/- or Il17r-/- mice, which suggested that IL-17 signaling was proximal to IFN-gamma signaling. |
| 2468 | 20038794 | Activation of the IL-12/IFN-gamma pathway and NKT cells by administering alpha-galactosylceramide-primed bone marrow-derived DCs increased IFN-gamma production following moderate IRI in WT mice but did not exacerbate injury or enhance IFN-gamma production in either Il17a-/- or Il17r-/- mice, which suggested that IL-17 signaling was proximal to IFN-gamma signaling. |
| 2469 | 20038794 | This was confirmed by the finding that IFN-gamma administration reversed the protection seen in Il17a-/- mice subjected to IRI, whereas IL-17A failed to reverse protection in Ifng-/- mice. |
| 2470 | 20038794 | This was confirmed by the finding that IFN-gamma administration reversed the protection seen in Il17a-/- mice subjected to IRI, whereas IL-17A failed to reverse protection in Ifng-/- mice. |
| 2471 | 20038794 | This was confirmed by the finding that IFN-gamma administration reversed the protection seen in Il17a-/- mice subjected to IRI, whereas IL-17A failed to reverse protection in Ifng-/- mice. |
| 2472 | 20038794 | This was confirmed by the finding that IFN-gamma administration reversed the protection seen in Il17a-/- mice subjected to IRI, whereas IL-17A failed to reverse protection in Ifng-/- mice. |
| 2473 | 20038794 | This was confirmed by the finding that IFN-gamma administration reversed the protection seen in Il17a-/- mice subjected to IRI, whereas IL-17A failed to reverse protection in Ifng-/- mice. |
| 2474 | 20038794 | This was confirmed by the finding that IFN-gamma administration reversed the protection seen in Il17a-/- mice subjected to IRI, whereas IL-17A failed to reverse protection in Ifng-/- mice. |
| 2475 | 20038794 | These results demonstrate that the innate immune component of kidney IRI requires dual activation of the IL-12/IFN-gamma and IL-23/IL-17 signaling pathways and that neutrophil production of IL-17A is upstream of IL-12/IFN-gamma. |
| 2476 | 20038794 | These results demonstrate that the innate immune component of kidney IRI requires dual activation of the IL-12/IFN-gamma and IL-23/IL-17 signaling pathways and that neutrophil production of IL-17A is upstream of IL-12/IFN-gamma. |
| 2477 | 20038794 | These results demonstrate that the innate immune component of kidney IRI requires dual activation of the IL-12/IFN-gamma and IL-23/IL-17 signaling pathways and that neutrophil production of IL-17A is upstream of IL-12/IFN-gamma. |
| 2478 | 20038794 | These results demonstrate that the innate immune component of kidney IRI requires dual activation of the IL-12/IFN-gamma and IL-23/IL-17 signaling pathways and that neutrophil production of IL-17A is upstream of IL-12/IFN-gamma. |
| 2479 | 20038794 | These results demonstrate that the innate immune component of kidney IRI requires dual activation of the IL-12/IFN-gamma and IL-23/IL-17 signaling pathways and that neutrophil production of IL-17A is upstream of IL-12/IFN-gamma. |
| 2480 | 20038794 | These results demonstrate that the innate immune component of kidney IRI requires dual activation of the IL-12/IFN-gamma and IL-23/IL-17 signaling pathways and that neutrophil production of IL-17A is upstream of IL-12/IFN-gamma. |
| 2481 | 20035105 | However, cultured mid luteal cells had a higher percentage of cFLIP-positive cells and a lower percentage of TUNEL-positive cells than luteal cells treated with tumor necrosis factor alpha (TNF)/interferon gamma (IFNG; P<0.01). |
| 2482 | 20027288 | Allergen challenge induces Ifng dependent GTPases in the lungs as part of a Th1 transcriptome response in a murine model of allergic asthma. |
| 2483 | 20027288 | Allergen challenge induces Ifng dependent GTPases in the lungs as part of a Th1 transcriptome response in a murine model of allergic asthma. |
| 2484 | 20027288 | Consistent with our hypothesis, RWE challenge concurrently upregulated Th1-associated early target genes of the Il12/Stat4 pathway, such as p47 and p65 GTPases (Iigp, Tgtp and Gbp1), Socs1, Cxcl9, Cxcl10 and Gadd45g with the Th2 genes Il4, Il5, Ccl2 and Ccl7. |
| 2485 | 20027288 | Consistent with our hypothesis, RWE challenge concurrently upregulated Th1-associated early target genes of the Il12/Stat4 pathway, such as p47 and p65 GTPases (Iigp, Tgtp and Gbp1), Socs1, Cxcl9, Cxcl10 and Gadd45g with the Th2 genes Il4, Il5, Ccl2 and Ccl7. |
| 2486 | 20027288 | Augmentation of the local Th1 milieu by administration of Il12 or CpG prior to RWE challenge further upregulated these Th1 genes. |
| 2487 | 20027288 | Augmentation of the local Th1 milieu by administration of Il12 or CpG prior to RWE challenge further upregulated these Th1 genes. |
| 2488 | 20027288 | Abolition of the Th1 response by disrupting the Ifng gene increased allergic airway inflammation and abrogated RWE challenge-induced upregulation of GTPases, Cxcl9, Cxcl10 and Socs1, but not Gadd45g. |
| 2489 | 20027288 | Abolition of the Th1 response by disrupting the Ifng gene increased allergic airway inflammation and abrogated RWE challenge-induced upregulation of GTPases, Cxcl9, Cxcl10 and Socs1, but not Gadd45g. |
| 2490 | 20027288 | Our data demonstrate that allergen challenge induces two sets of Th1-associated genes in the lungs: 1) Ifng-dependent genes such as p47 and p65 GTPases, Socs1, Cxcl9 and Cxcl10 and 2) Ifng-independent Th1-inducing genes like Gadd45g. |
| 2491 | 20027288 | Our data demonstrate that allergen challenge induces two sets of Th1-associated genes in the lungs: 1) Ifng-dependent genes such as p47 and p65 GTPases, Socs1, Cxcl9 and Cxcl10 and 2) Ifng-independent Th1-inducing genes like Gadd45g. |
| 2492 | 20018909 | Blood and decidual CD4(+) T cells from 18 healthy first-trimester pregnant women were analyzed for expression of Treg-cell markers (CD25, FOXP3, CD127, CTLA4, and human leukocyte antigen-DR [HLA-DR]), chemokine receptors (CCR4, CCR6, and CXCR3), and the proliferation antigen MKI67 by six-color flow cytometry. |
| 2493 | 20018909 | Using chemokine receptor expression profiles of CCR4, CCR6, and CXCR3 as markers for T(H)1, T(H)2, and T(H)17 cells, we showed that T(H)17 cells were nearly absent in decidua, whereas T(H)2-cell frequencies were similar in blood and decidua. |
| 2494 | 20018909 | CCR6(+) T(H)1 cells, reported to secrete high levels of interferon gamma (IFNG), were fewer, whereas the moderately IFNG-secreting CCR6(-) T(H)1 cells were more frequent in decidua compared with blood. |
| 2495 | 19904525 | Also, immunohistochemistry (IHC) was used to probe dectin-1 as well as anti-mouse Ccl3, Il1-alpha, and TNF-alpha expression to evaluate dose and time-course (4 and 12 h) postexposure (PE) response patterns in the lungs of intratracheally instilled mice exposed to a single 50 mul dose of curdlan at 10(-7), 10(-8), 10(-9), and 10(-10) M/animal (=4 mug to 4 ng curdlan/kg lung wt). |
| 2496 | 19904525 | Nine gene mRNA transcripts (Ccl3, Ccl11, Ccl17, Ifng, Il1alpha, Il-20, TNF-alpha, Tnfrsf1b, and CD40lg) were significantly expressed at all doses suggesting they may have a central role in immunomodulating curdlan exposures. |
| 2497 | 19904525 | IHC revealed Ccl3, Il1-alpha, and TNF-alpha expression in bronchiolar epithelium, AMs and ATIIs illustrate the important immunomodulatory role that these cells have in the recognition of, and response to glucan. |
| 2498 | 19879772 | TNFalpha and TGF-beta1 influence IL-18-induced IFNgamma production through regulation of IL-18 receptor and T-bet expression. |
| 2499 | 19879772 | TNFalpha and TGF-beta1 influence IL-18-induced IFNgamma production through regulation of IL-18 receptor and T-bet expression. |
| 2500 | 19879772 | TNFalpha and TGF-beta1 influence IL-18-induced IFNgamma production through regulation of IL-18 receptor and T-bet expression. |
| 2501 | 19879772 | TNFalpha and TGF-beta1 influence IL-18-induced IFNgamma production through regulation of IL-18 receptor and T-bet expression. |
| 2502 | 19879772 | TNFalpha and TGF-beta1 influence IL-18-induced IFNgamma production through regulation of IL-18 receptor and T-bet expression. |
| 2503 | 19879772 | TNFalpha and TGF-beta1 influence IL-18-induced IFNgamma production through regulation of IL-18 receptor and T-bet expression. |
| 2504 | 19879772 | TNFalpha and TGF-beta1 influence IL-18-induced IFNgamma production through regulation of IL-18 receptor and T-bet expression. |
| 2505 | 19879772 | IL-18 is a pro-inflammatory cytokine that drives dendritic cell maturation and mediates IFNgamma production. |
| 2506 | 19879772 | IL-18 is a pro-inflammatory cytokine that drives dendritic cell maturation and mediates IFNgamma production. |
| 2507 | 19879772 | IL-18 is a pro-inflammatory cytokine that drives dendritic cell maturation and mediates IFNgamma production. |
| 2508 | 19879772 | IL-18 is a pro-inflammatory cytokine that drives dendritic cell maturation and mediates IFNgamma production. |
| 2509 | 19879772 | IL-18 is a pro-inflammatory cytokine that drives dendritic cell maturation and mediates IFNgamma production. |
| 2510 | 19879772 | IL-18 is a pro-inflammatory cytokine that drives dendritic cell maturation and mediates IFNgamma production. |
| 2511 | 19879772 | IL-18 is a pro-inflammatory cytokine that drives dendritic cell maturation and mediates IFNgamma production. |
| 2512 | 19879772 | In this study, we demonstrate that in the dendritic precursor-like cell line KG-1, IFNgamma production induced by IL-18 is potentiated (>5-fold) by TNFalpha and completely suppressed by TGF-beta1. |
| 2513 | 19879772 | In this study, we demonstrate that in the dendritic precursor-like cell line KG-1, IFNgamma production induced by IL-18 is potentiated (>5-fold) by TNFalpha and completely suppressed by TGF-beta1. |
| 2514 | 19879772 | In this study, we demonstrate that in the dendritic precursor-like cell line KG-1, IFNgamma production induced by IL-18 is potentiated (>5-fold) by TNFalpha and completely suppressed by TGF-beta1. |
| 2515 | 19879772 | In this study, we demonstrate that in the dendritic precursor-like cell line KG-1, IFNgamma production induced by IL-18 is potentiated (>5-fold) by TNFalpha and completely suppressed by TGF-beta1. |
| 2516 | 19879772 | In this study, we demonstrate that in the dendritic precursor-like cell line KG-1, IFNgamma production induced by IL-18 is potentiated (>5-fold) by TNFalpha and completely suppressed by TGF-beta1. |
| 2517 | 19879772 | In this study, we demonstrate that in the dendritic precursor-like cell line KG-1, IFNgamma production induced by IL-18 is potentiated (>5-fold) by TNFalpha and completely suppressed by TGF-beta1. |
| 2518 | 19879772 | In this study, we demonstrate that in the dendritic precursor-like cell line KG-1, IFNgamma production induced by IL-18 is potentiated (>5-fold) by TNFalpha and completely suppressed by TGF-beta1. |
| 2519 | 19879772 | IL-18 stimulation rapidly activates different MAPK signalling pathways but only blocking of p38 activation alleviates IFNgamma production. |
| 2520 | 19879772 | IL-18 stimulation rapidly activates different MAPK signalling pathways but only blocking of p38 activation alleviates IFNgamma production. |
| 2521 | 19879772 | IL-18 stimulation rapidly activates different MAPK signalling pathways but only blocking of p38 activation alleviates IFNgamma production. |
| 2522 | 19879772 | IL-18 stimulation rapidly activates different MAPK signalling pathways but only blocking of p38 activation alleviates IFNgamma production. |
| 2523 | 19879772 | IL-18 stimulation rapidly activates different MAPK signalling pathways but only blocking of p38 activation alleviates IFNgamma production. |
| 2524 | 19879772 | IL-18 stimulation rapidly activates different MAPK signalling pathways but only blocking of p38 activation alleviates IFNgamma production. |
| 2525 | 19879772 | IL-18 stimulation rapidly activates different MAPK signalling pathways but only blocking of p38 activation alleviates IFNgamma production. |
| 2526 | 19879772 | The mechanism through which TNFalpha enhances IL-18 induced IFNgamma production is by promoting IL-18 receptor alpha-chain expression which results in higher levels of p38 activation and induces expression of T-bet, a transcriptional regulator of the IFNG gene. |
| 2527 | 19879772 | The mechanism through which TNFalpha enhances IL-18 induced IFNgamma production is by promoting IL-18 receptor alpha-chain expression which results in higher levels of p38 activation and induces expression of T-bet, a transcriptional regulator of the IFNG gene. |
| 2528 | 19879772 | The mechanism through which TNFalpha enhances IL-18 induced IFNgamma production is by promoting IL-18 receptor alpha-chain expression which results in higher levels of p38 activation and induces expression of T-bet, a transcriptional regulator of the IFNG gene. |
| 2529 | 19879772 | The mechanism through which TNFalpha enhances IL-18 induced IFNgamma production is by promoting IL-18 receptor alpha-chain expression which results in higher levels of p38 activation and induces expression of T-bet, a transcriptional regulator of the IFNG gene. |
| 2530 | 19879772 | The mechanism through which TNFalpha enhances IL-18 induced IFNgamma production is by promoting IL-18 receptor alpha-chain expression which results in higher levels of p38 activation and induces expression of T-bet, a transcriptional regulator of the IFNG gene. |
| 2531 | 19879772 | The mechanism through which TNFalpha enhances IL-18 induced IFNgamma production is by promoting IL-18 receptor alpha-chain expression which results in higher levels of p38 activation and induces expression of T-bet, a transcriptional regulator of the IFNG gene. |
| 2532 | 19879772 | The mechanism through which TNFalpha enhances IL-18 induced IFNgamma production is by promoting IL-18 receptor alpha-chain expression which results in higher levels of p38 activation and induces expression of T-bet, a transcriptional regulator of the IFNG gene. |
| 2533 | 19879772 | In contrast, TGF-beta1 rapidly suppresses IFNgamma production by limiting IL-18 receptor numbers at the cell surface and preventing induction of T-bet expression. |
| 2534 | 19879772 | In contrast, TGF-beta1 rapidly suppresses IFNgamma production by limiting IL-18 receptor numbers at the cell surface and preventing induction of T-bet expression. |
| 2535 | 19879772 | In contrast, TGF-beta1 rapidly suppresses IFNgamma production by limiting IL-18 receptor numbers at the cell surface and preventing induction of T-bet expression. |
| 2536 | 19879772 | In contrast, TGF-beta1 rapidly suppresses IFNgamma production by limiting IL-18 receptor numbers at the cell surface and preventing induction of T-bet expression. |
| 2537 | 19879772 | In contrast, TGF-beta1 rapidly suppresses IFNgamma production by limiting IL-18 receptor numbers at the cell surface and preventing induction of T-bet expression. |
| 2538 | 19879772 | In contrast, TGF-beta1 rapidly suppresses IFNgamma production by limiting IL-18 receptor numbers at the cell surface and preventing induction of T-bet expression. |
| 2539 | 19879772 | In contrast, TGF-beta1 rapidly suppresses IFNgamma production by limiting IL-18 receptor numbers at the cell surface and preventing induction of T-bet expression. |
| 2540 | 19879772 | TGF-beta1 experience by cells leads to sustained long-term inactivation of TNFalpha/IL-18-mediated cell activation but not IL-18 induced p38 activation suggesting transcriptional silencing of the T-BET and/or IFNG promoter independent of MAPK signalling. |
| 2541 | 19879772 | TGF-beta1 experience by cells leads to sustained long-term inactivation of TNFalpha/IL-18-mediated cell activation but not IL-18 induced p38 activation suggesting transcriptional silencing of the T-BET and/or IFNG promoter independent of MAPK signalling. |
| 2542 | 19879772 | TGF-beta1 experience by cells leads to sustained long-term inactivation of TNFalpha/IL-18-mediated cell activation but not IL-18 induced p38 activation suggesting transcriptional silencing of the T-BET and/or IFNG promoter independent of MAPK signalling. |
| 2543 | 19879772 | TGF-beta1 experience by cells leads to sustained long-term inactivation of TNFalpha/IL-18-mediated cell activation but not IL-18 induced p38 activation suggesting transcriptional silencing of the T-BET and/or IFNG promoter independent of MAPK signalling. |
| 2544 | 19879772 | TGF-beta1 experience by cells leads to sustained long-term inactivation of TNFalpha/IL-18-mediated cell activation but not IL-18 induced p38 activation suggesting transcriptional silencing of the T-BET and/or IFNG promoter independent of MAPK signalling. |
| 2545 | 19879772 | TGF-beta1 experience by cells leads to sustained long-term inactivation of TNFalpha/IL-18-mediated cell activation but not IL-18 induced p38 activation suggesting transcriptional silencing of the T-BET and/or IFNG promoter independent of MAPK signalling. |
| 2546 | 19879772 | TGF-beta1 experience by cells leads to sustained long-term inactivation of TNFalpha/IL-18-mediated cell activation but not IL-18 induced p38 activation suggesting transcriptional silencing of the T-BET and/or IFNG promoter independent of MAPK signalling. |
| 2547 | 19876828 | Here, we compared the distribution of the major lymphocyte subsets, the percentage of lymphocytes expressing Interferon Gamma (IFNG) and Interleukin 4 (IL4) and the level of expression of the immunoregulatory transcription factor FOXP3 between pregnant and non-pregnant mares, and between peripheral blood and the endometrium during pregnancy. |
| 2548 | 19876828 | Here, we compared the distribution of the major lymphocyte subsets, the percentage of lymphocytes expressing Interferon Gamma (IFNG) and Interleukin 4 (IL4) and the level of expression of the immunoregulatory transcription factor FOXP3 between pregnant and non-pregnant mares, and between peripheral blood and the endometrium during pregnancy. |
| 2549 | 19876828 | The endometrial cups contained higher numbers of IFNG+ lymphocytes, and lower numbers of lymphocytes expressing IL4. |
| 2550 | 19876828 | The endometrial cups contained higher numbers of IFNG+ lymphocytes, and lower numbers of lymphocytes expressing IL4. |
| 2551 | 19848299 | By Day 12 of pregnancy, estrogens increase the expression of multiple genes in the uterine luminal epithelium including SPP1, STC1, IRF2 and STAT1 that likely have roles for implantation. |
| 2552 | 19848299 | By Day 15 of pregnancy, IFNs upregulate a large array of IFN responsive genes in the underlying stroma and glandular epithelium including ISG15, IRF1, STAT1, SLAs and B2M that likely have roles in uterine remodeling to support placentation. |
| 2553 | 19837722 | Previous studies have shown that methimazole (MMI) reduces MHC class-I expression and inhibits interferon-gamma (IFN-gamma or IFNG as listed in the MGI Database)-induced expression of the MHC class-II genes in TECs. |
| 2554 | 19837722 | Previous studies have shown that methimazole (MMI) reduces MHC class-I expression and inhibits interferon-gamma (IFN-gamma or IFNG as listed in the MGI Database)-induced expression of the MHC class-II genes in TECs. |
| 2555 | 19837722 | In the present study, we show that in Fisher rat thyroid cell line 5 cells, the ability of MMI and its novel derivative phenylmethimazole (C10) to decrease MHC class-I promoter activity is similar to TSH/cAMP suppression of MHC class-I and TSH receptor genes, and involves a 39 bp silencer containing a cAMP response element (CRE)-like site. |
| 2556 | 19837722 | In the present study, we show that in Fisher rat thyroid cell line 5 cells, the ability of MMI and its novel derivative phenylmethimazole (C10) to decrease MHC class-I promoter activity is similar to TSH/cAMP suppression of MHC class-I and TSH receptor genes, and involves a 39 bp silencer containing a cAMP response element (CRE)-like site. |
| 2557 | 19837722 | Furthermore, we show that C10 decreases MHC class-I gene expression to a greater extent than MMI and at 10- to 50-fold lower concentrations. |
| 2558 | 19837722 | Furthermore, we show that C10 decreases MHC class-I gene expression to a greater extent than MMI and at 10- to 50-fold lower concentrations. |
| 2559 | 19837722 | C10 also reduces the IFN-gamma-induced increase in the expression of MHC class-I and MHC class-II genes more effectively than MMI. |
| 2560 | 19837722 | C10 also reduces the IFN-gamma-induced increase in the expression of MHC class-I and MHC class-II genes more effectively than MMI. |
| 2561 | 19837722 | These data support the conclusion that the immunosuppressive mechanism by which MMI and C10 inhibit MHC gene expression mimics 'normal' hormonal suppression by TSH/cAMP. |
| 2562 | 19837722 | These data support the conclusion that the immunosuppressive mechanism by which MMI and C10 inhibit MHC gene expression mimics 'normal' hormonal suppression by TSH/cAMP. |
| 2563 | 19828627 | Ikaros is a regulator of Il10 expression in CD4+ T cells. |
| 2564 | 19828627 | Ikaros is a regulator of Il10 expression in CD4+ T cells. |
| 2565 | 19828627 | Here we show that Ikaros, a zinc finger DNA-binding protein, plays an important role in the regulation of Il10 in murine CD4(+) T cells. |
| 2566 | 19828627 | Here we show that Ikaros, a zinc finger DNA-binding protein, plays an important role in the regulation of Il10 in murine CD4(+) T cells. |
| 2567 | 19828627 | Upon initial stimulation of the TCR, T cells deficient in Ikaros express significantly lower levels of IL-10 compared with wild-type T cells. |
| 2568 | 19828627 | Upon initial stimulation of the TCR, T cells deficient in Ikaros express significantly lower levels of IL-10 compared with wild-type T cells. |
| 2569 | 19828627 | In addition, under Th2 skewing conditions, which induce IL-10 production by wild-type T cells, Ikaros null T cells are unable to properly differentiate, producing only low levels of IL-10. |
| 2570 | 19828627 | In addition, under Th2 skewing conditions, which induce IL-10 production by wild-type T cells, Ikaros null T cells are unable to properly differentiate, producing only low levels of IL-10. |
| 2571 | 19828627 | Expression of a dominant-negative isoform of Ikaros in wild-type Th2 cells represses IL-10 production but does not significantly alter expression levels of the genes encoding the transcription factors GATA-3 and T-bet. |
| 2572 | 19828627 | Expression of a dominant-negative isoform of Ikaros in wild-type Th2 cells represses IL-10 production but does not significantly alter expression levels of the genes encoding the transcription factors GATA-3 and T-bet. |
| 2573 | 19828627 | Furthermore, expression of Ikaros in Ikaros null T cells restores expression of the Th2 cytokines IL-10 and IL-4 while reducing production of the Th1 cytokine, IFN-gamma. |
| 2574 | 19828627 | Furthermore, expression of Ikaros in Ikaros null T cells restores expression of the Th2 cytokines IL-10 and IL-4 while reducing production of the Th1 cytokine, IFN-gamma. |
| 2575 | 19828627 | Coexpression of Ikaros and GATA-3 further increases IL-10 production, showing that these two factors have an additive effect on activating Il10 expression. |
| 2576 | 19828627 | Coexpression of Ikaros and GATA-3 further increases IL-10 production, showing that these two factors have an additive effect on activating Il10 expression. |
| 2577 | 19828627 | Finally, we show that Ikaros binds to conserved regulatory regions of the Il10 gene locus in Th2 cells, supporting a direct role for Ikaros in Il10 expression. |
| 2578 | 19828627 | Finally, we show that Ikaros binds to conserved regulatory regions of the Il10 gene locus in Th2 cells, supporting a direct role for Ikaros in Il10 expression. |
| 2579 | 19828627 | Thus, we provide evidence for Ikaros as a regulator of Il10 and Ifng gene expression and suggest a role for Ikaros in directing lineage-specific cytokine gene activation and repression. |
| 2580 | 19828627 | Thus, we provide evidence for Ikaros as a regulator of Il10 and Ifng gene expression and suggest a role for Ikaros in directing lineage-specific cytokine gene activation and repression. |
| 2581 | 19757192 | In contrast to B lymphocytes, T cells of B-CLL patients characterise with the increased production of interferon-gamma (IFN-gamma) and this cytokine has been indicated to prevent malignant cells from entering apoptosis including the slowly expanding population of CD5+ B cells that characterizes chronic lymphocytic leukemia. |
| 2582 | 19747638 | Interferon gamma 13-CA-repeat homozygous genotype and a low proportion of CD4(+) lymphocytes are independent risk factors for cytomegalovirus reactivation with a high number of copies in hematopoietic stem cell transplantation recipients. |
| 2583 | 19747638 | Interferon gamma 13-CA-repeat homozygous genotype and a low proportion of CD4(+) lymphocytes are independent risk factors for cytomegalovirus reactivation with a high number of copies in hematopoietic stem cell transplantation recipients. |
| 2584 | 19747638 | Interferon gamma 13-CA-repeat homozygous genotype and a low proportion of CD4(+) lymphocytes are independent risk factors for cytomegalovirus reactivation with a high number of copies in hematopoietic stem cell transplantation recipients. |
| 2585 | 19747638 | Cytomegalovirus (CMV) reactivation was analyzed in 92 recipients of allogeneic hematopoietic stem cell transplantation (HSCT) in relation to the proportion of CD4(+) lymphocytes in blood and a microsatellite polymorphism within the first intron of the interferon-gamma (IFNG) gene. |
| 2586 | 19747638 | Cytomegalovirus (CMV) reactivation was analyzed in 92 recipients of allogeneic hematopoietic stem cell transplantation (HSCT) in relation to the proportion of CD4(+) lymphocytes in blood and a microsatellite polymorphism within the first intron of the interferon-gamma (IFNG) gene. |
| 2587 | 19747638 | Cytomegalovirus (CMV) reactivation was analyzed in 92 recipients of allogeneic hematopoietic stem cell transplantation (HSCT) in relation to the proportion of CD4(+) lymphocytes in blood and a microsatellite polymorphism within the first intron of the interferon-gamma (IFNG) gene. |
| 2588 | 19747638 | Multivariate analysis demonstrated that the IFNG 13-CA-repeat homozygous genotype (odds ratio [OR] = 0.221; P = .044), a low proportion of CD4(+) lymphocytes (OR = 0.276; P = .050), and a lack of optimal (10/10 alleles) donor-recipient HLA match (OR = 15.19; P = .006) were independent risk factors for CMV reactivation with a high number of copies. |
| 2589 | 19747638 | Multivariate analysis demonstrated that the IFNG 13-CA-repeat homozygous genotype (odds ratio [OR] = 0.221; P = .044), a low proportion of CD4(+) lymphocytes (OR = 0.276; P = .050), and a lack of optimal (10/10 alleles) donor-recipient HLA match (OR = 15.19; P = .006) were independent risk factors for CMV reactivation with a high number of copies. |
| 2590 | 19747638 | Multivariate analysis demonstrated that the IFNG 13-CA-repeat homozygous genotype (odds ratio [OR] = 0.221; P = .044), a low proportion of CD4(+) lymphocytes (OR = 0.276; P = .050), and a lack of optimal (10/10 alleles) donor-recipient HLA match (OR = 15.19; P = .006) were independent risk factors for CMV reactivation with a high number of copies. |
| 2591 | 19689734 | A continuous T-bet expression is required to silence the interleukin-4-producing potential in T helper type 1 cells. |
| 2592 | 19689734 | A continuous T-bet expression is required to silence the interleukin-4-producing potential in T helper type 1 cells. |
| 2593 | 19689734 | To develop into committed T helper type 1 (Th1) cells, naive CD4(+) T cells not only need to acquire the capacity to produce interferon-gamma (IFN-gamma), but they also need to gain the ability to silence their interleukin-4 (IL-4) -producing potential. |
| 2594 | 19689734 | To develop into committed T helper type 1 (Th1) cells, naive CD4(+) T cells not only need to acquire the capacity to produce interferon-gamma (IFN-gamma), but they also need to gain the ability to silence their interleukin-4 (IL-4) -producing potential. |
| 2595 | 19689734 | We found that a lack of IL-4 stimulation was not sufficient to silence the IL-4-producing potential in activated CD4(+) T cells and that Th1-promoting factor was required. |
| 2596 | 19689734 | We found that a lack of IL-4 stimulation was not sufficient to silence the IL-4-producing potential in activated CD4(+) T cells and that Th1-promoting factor was required. |
| 2597 | 19689734 | Although it has been shown that T-bet is a crucial factor in suppressing Il4 gene expression, it is unclear whether a continuous presence of T-bet is required to silence the Il4 gene in Th1 cells. |
| 2598 | 19689734 | Although it has been shown that T-bet is a crucial factor in suppressing Il4 gene expression, it is unclear whether a continuous presence of T-bet is required to silence the Il4 gene in Th1 cells. |
| 2599 | 19689734 | To address this problem, we used an inducible form of T-bet - a T-bet-oestrogen receptor fusion molecule (T-bet-ER). |
| 2600 | 19689734 | To address this problem, we used an inducible form of T-bet - a T-bet-oestrogen receptor fusion molecule (T-bet-ER). |
| 2601 | 19689734 | We found that the activation of T-bet during primary or secondary culture was sufficient to silence IL-4-producing potential. |
| 2602 | 19689734 | We found that the activation of T-bet during primary or secondary culture was sufficient to silence IL-4-producing potential. |
| 2603 | 19689734 | On the other hand, the inactivation of T-bet after naïve CD4(+) T cells had differentiated into Th1 cells resulted in derepression of Il4 gene transcription. |
| 2604 | 19689734 | On the other hand, the inactivation of T-bet after naïve CD4(+) T cells had differentiated into Th1 cells resulted in derepression of Il4 gene transcription. |
| 2605 | 19689734 | Additionally, we found that T-bet is required to maintain Ifng expression. |
| 2606 | 19689734 | Additionally, we found that T-bet is required to maintain Ifng expression. |
| 2607 | 19689734 | Our data demonstrate that the continuous expression of T-bet is required for Th1 cells to silence their IL-4-producing potential. |
| 2608 | 19689734 | Our data demonstrate that the continuous expression of T-bet is required for Th1 cells to silence their IL-4-producing potential. |
| 2609 | 19632728 | Transient increases of proinflammatory cytokine (IL6 and IFNG) and chemokine (IL8 and K60) genes increased as early as 6h in response to S. |
| 2610 | 19625655 | DNA methyltransferase 3a (DNMT3a) is a de novo methyltransferase important to the epigenetic control of cell fate. |
| 2611 | 19625655 | DNA methyltransferase 3a (DNMT3a) is a de novo methyltransferase important to the epigenetic control of cell fate. |
| 2612 | 19625655 | T cells lacking DNMT3a simultaneously express IFN-gamma and IL-4 after expansion under nonbiasing conditions. |
| 2613 | 19625655 | T cells lacking DNMT3a simultaneously express IFN-gamma and IL-4 after expansion under nonbiasing conditions. |
| 2614 | 19625655 | While global methylation of DNA from wild-type and knockout T cells is similar, DNMT3a-null T cells demonstrate selective hypomethylation of both the Il4 and Ifng loci after activation. |
| 2615 | 19625655 | While global methylation of DNA from wild-type and knockout T cells is similar, DNMT3a-null T cells demonstrate selective hypomethylation of both the Il4 and Ifng loci after activation. |
| 2616 | 19574556 | Interferon-gamma induces prolyl hydroxylase (PHD)3 through a STAT1-dependent mechanism in human endothelial cells. |
| 2617 | 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. |
| 2618 | 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. |
| 2619 | 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). |
| 2620 | 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). |
| 2621 | 19494038 | Here, we present a comprehensive analysis of differential DNA methylation in human conventional CD4(+) T cells (Tconv) and CD4(+)CD25(+) regulatory T cells (Treg), cell types whose differentiation and function are known to be controlled by epigenetic mechanisms. |
| 2622 | 19494038 | More than 100 differentially methylated regions (DMRs) were identified that are present mainly in cell type-specific genes (e.g., FOXP3, IL2RA, CTLA4, CD40LG, and IFNG) and show differential patterns of histone H3 lysine 4 methylation. |
| 2623 | 19464989 | In this issue of Immunity, Schulz et al. (2009) use mathematical modeling to elucidate a signaling network controlling Ifng gene expression, thereby showing the importance of an Interleukin-12-dependent, Interferon-gamma-independent second phase of inducing the transcription factor T-bet. |
| 2624 | 19384057 | Recently, we reported a novel mechanism by which the T-box transcription factor T-bet interacts with JMJD3, an H3K27-demethylase, and Set7/9, an H3K4-methyltransferase (Genes Dev. 2008. 22: 2980-2993). |
| 2625 | 19384057 | Therefore, studies examining the molecular mechanisms that account for the ability of T-bet to regulate Ifng and Cxcr3, prototypic CD4+ Th1 genes, have provided novel insight into essential regulatory events that occur at diverse developmental transitions. |
| 2626 | 19375805 | The objective was to search for an association between spontaneous preterm birth (sPTB) and single and/or combined polymorphisms in genes TNFA -308 G>A, IL10 -1082 G>A, IL10 -819 C>T, IL10 -592 C>A, IL6 -174 G>C, and IFNG +874 A>T. |
| 2627 | 19375805 | The objective was to search for an association between spontaneous preterm birth (sPTB) and single and/or combined polymorphisms in genes TNFA -308 G>A, IL10 -1082 G>A, IL10 -819 C>T, IL10 -592 C>A, IL6 -174 G>C, and IFNG +874 A>T. |
| 2628 | 19375805 | The objective was to search for an association between spontaneous preterm birth (sPTB) and single and/or combined polymorphisms in genes TNFA -308 G>A, IL10 -1082 G>A, IL10 -819 C>T, IL10 -592 C>A, IL6 -174 G>C, and IFNG +874 A>T. |
| 2629 | 19375805 | The multi-locus analysis revealed a significant association between sPTB and the TNFA(GG)/IL6(GG)/IFNG(AA) genotype combination (p=0.002), confirmed by logistic regression. |
| 2630 | 19375805 | The multi-locus analysis revealed a significant association between sPTB and the TNFA(GG)/IL6(GG)/IFNG(AA) genotype combination (p=0.002), confirmed by logistic regression. |
| 2631 | 19375805 | The multi-locus analysis revealed a significant association between sPTB and the TNFA(GG)/IL6(GG)/IFNG(AA) genotype combination (p=0.002), confirmed by logistic regression. |
| 2632 | 19375805 | Our data suggest that the combination of TNF-alpha, IFN-gamma, and IL-6 maternal gene polymorphisms might contribute to susceptibility to sPTB. |
| 2633 | 19375805 | Our data suggest that the combination of TNF-alpha, IFN-gamma, and IL-6 maternal gene polymorphisms might contribute to susceptibility to sPTB. |
| 2634 | 19375805 | Our data suggest that the combination of TNF-alpha, IFN-gamma, and IL-6 maternal gene polymorphisms might contribute to susceptibility to sPTB. |
| 2635 | 19332534 | Ascaris-infected pigs had increased levels of liver mRNA for T-helper-2 (Th2)-associated cytokines, mast cell markers, and T regulatory (Treg) cells, while infected pigs given ATRA had higher IL4, IL13, CCL11, CCL26, CCL17, CCL22, and TPSB1 expression. |
| 2636 | 19332534 | Gene expression for Th1-associated markers (IFNG, IL12B, and TBX21), the CXCR3 ligand (CXCL9), IL1B, and the putative Treg marker TNFRSF18 was also increased. |
| 2637 | 19332534 | Expression of IL4, IL13, IL1B, IL6, CCL11, and CCL26 was increased in the lungs of infected pigs treated with ATRA. |
| 2638 | 19332534 | IL4 induced CCL11, CCL17, CCL22, and CCL26 mRNA, and ATRA increased the basal and IL4-stimulated expression of CCL17 and CCL22. |
| 2639 | 19302234 | K562/A02 cells showed a 65-fold higher IC(50) to adriamycin and less intracellular accumulation of adriamycin than K562. cDNA microarray showed marked increases in binding of collagen and cell proliferation-related genes (CD44, DLL3, IL17B, NUMB, and NUMBL) and decreases in signal transduction and transcription factor activity related genes (FZD9, GBP2, GLI1, GLI2, IFNG, KRT5, Notch2, and Notch3). |
| 2640 | 19234226 | End-organ damage in a mouse model of fulminant liver inflammation requires CD4+ T cell production of IFN-gamma but is independent of Fas. |
| 2641 | 19234226 | End-organ damage in a mouse model of fulminant liver inflammation requires CD4+ T cell production of IFN-gamma but is independent of Fas. |
| 2642 | 19234226 | End-organ damage in a mouse model of fulminant liver inflammation requires CD4+ T cell production of IFN-gamma but is independent of Fas. |
| 2643 | 19234226 | End-organ damage in a mouse model of fulminant liver inflammation requires CD4+ T cell production of IFN-gamma but is independent of Fas. |
| 2644 | 19234226 | End-organ damage in a mouse model of fulminant liver inflammation requires CD4+ T cell production of IFN-gamma but is independent of Fas. |
| 2645 | 19234226 | End-organ damage in a mouse model of fulminant liver inflammation requires CD4+ T cell production of IFN-gamma but is independent of Fas. |
| 2646 | 19234226 | The BALB/c-Tgfb1(-/-) mouse exhibits extensive, spontaneously developing necroinflammation in the liver, accompanied by the accumulation of IFN-gamma-producing CD4(+) and CD8(+) T cells. |
| 2647 | 19234226 | The BALB/c-Tgfb1(-/-) mouse exhibits extensive, spontaneously developing necroinflammation in the liver, accompanied by the accumulation of IFN-gamma-producing CD4(+) and CD8(+) T cells. |
| 2648 | 19234226 | The BALB/c-Tgfb1(-/-) mouse exhibits extensive, spontaneously developing necroinflammation in the liver, accompanied by the accumulation of IFN-gamma-producing CD4(+) and CD8(+) T cells. |
| 2649 | 19234226 | The BALB/c-Tgfb1(-/-) mouse exhibits extensive, spontaneously developing necroinflammation in the liver, accompanied by the accumulation of IFN-gamma-producing CD4(+) and CD8(+) T cells. |
| 2650 | 19234226 | The BALB/c-Tgfb1(-/-) mouse exhibits extensive, spontaneously developing necroinflammation in the liver, accompanied by the accumulation of IFN-gamma-producing CD4(+) and CD8(+) T cells. |
| 2651 | 19234226 | The BALB/c-Tgfb1(-/-) mouse exhibits extensive, spontaneously developing necroinflammation in the liver, accompanied by the accumulation of IFN-gamma-producing CD4(+) and CD8(+) T cells. |
| 2652 | 19234226 | In Tgfb1(-/-) liver, CD4(+) T cells were more numerous than CD8(+) T cells and NK cells, and produced more IFN-gamma. |
| 2653 | 19234226 | In Tgfb1(-/-) liver, CD4(+) T cells were more numerous than CD8(+) T cells and NK cells, and produced more IFN-gamma. |
| 2654 | 19234226 | In Tgfb1(-/-) liver, CD4(+) T cells were more numerous than CD8(+) T cells and NK cells, and produced more IFN-gamma. |
| 2655 | 19234226 | In Tgfb1(-/-) liver, CD4(+) T cells were more numerous than CD8(+) T cells and NK cells, and produced more IFN-gamma. |
| 2656 | 19234226 | In Tgfb1(-/-) liver, CD4(+) T cells were more numerous than CD8(+) T cells and NK cells, and produced more IFN-gamma. |
| 2657 | 19234226 | In Tgfb1(-/-) liver, CD4(+) T cells were more numerous than CD8(+) T cells and NK cells, and produced more IFN-gamma. |
| 2658 | 19234226 | Depletion of CD4(+) T cells eliminated both the elevation in plasma IFN-gamma and aspartate aminotransferase, whereas depletion of CD8(+) T cells did not. |
| 2659 | 19234226 | Depletion of CD4(+) T cells eliminated both the elevation in plasma IFN-gamma and aspartate aminotransferase, whereas depletion of CD8(+) T cells did not. |
| 2660 | 19234226 | Depletion of CD4(+) T cells eliminated both the elevation in plasma IFN-gamma and aspartate aminotransferase, whereas depletion of CD8(+) T cells did not. |
| 2661 | 19234226 | Depletion of CD4(+) T cells eliminated both the elevation in plasma IFN-gamma and aspartate aminotransferase, whereas depletion of CD8(+) T cells did not. |
| 2662 | 19234226 | Depletion of CD4(+) T cells eliminated both the elevation in plasma IFN-gamma and aspartate aminotransferase, whereas depletion of CD8(+) T cells did not. |
| 2663 | 19234226 | Depletion of CD4(+) T cells eliminated both the elevation in plasma IFN-gamma and aspartate aminotransferase, whereas depletion of CD8(+) T cells did not. |
| 2664 | 19234226 | Rag1(-/-)Tgfb1(-/-) mice exhibited neither IFN-gamma elevation nor tissue damage, indicating that NK cells are not sufficient. |
| 2665 | 19234226 | Rag1(-/-)Tgfb1(-/-) mice exhibited neither IFN-gamma elevation nor tissue damage, indicating that NK cells are not sufficient. |
| 2666 | 19234226 | Rag1(-/-)Tgfb1(-/-) mice exhibited neither IFN-gamma elevation nor tissue damage, indicating that NK cells are not sufficient. |
| 2667 | 19234226 | Rag1(-/-)Tgfb1(-/-) mice exhibited neither IFN-gamma elevation nor tissue damage, indicating that NK cells are not sufficient. |
| 2668 | 19234226 | Rag1(-/-)Tgfb1(-/-) mice exhibited neither IFN-gamma elevation nor tissue damage, indicating that NK cells are not sufficient. |
| 2669 | 19234226 | Rag1(-/-)Tgfb1(-/-) mice exhibited neither IFN-gamma elevation nor tissue damage, indicating that NK cells are not sufficient. |
| 2670 | 19234226 | IFN-gamma was required for strong overexpression of class II genes but not for CD4(+) T cell activation, oligoclonal expansion, or accumulation in the liver. |
| 2671 | 19234226 | IFN-gamma was required for strong overexpression of class II genes but not for CD4(+) T cell activation, oligoclonal expansion, or accumulation in the liver. |
| 2672 | 19234226 | IFN-gamma was required for strong overexpression of class II genes but not for CD4(+) T cell activation, oligoclonal expansion, or accumulation in the liver. |
| 2673 | 19234226 | IFN-gamma was required for strong overexpression of class II genes but not for CD4(+) T cell activation, oligoclonal expansion, or accumulation in the liver. |
| 2674 | 19234226 | IFN-gamma was required for strong overexpression of class II genes but not for CD4(+) T cell activation, oligoclonal expansion, or accumulation in the liver. |
| 2675 | 19234226 | IFN-gamma was required for strong overexpression of class II genes but not for CD4(+) T cell activation, oligoclonal expansion, or accumulation in the liver. |
| 2676 | 19234226 | Finally, whereas Tgfb1(-/-) CD4(+) T cells overexpressed Fas ligand, hepatocellular damage was observed in Fas(lpr/lpr)Tgfb1(-/-) mice, indicating that liver pathology is Fas independent. |
| 2677 | 19234226 | Finally, whereas Tgfb1(-/-) CD4(+) T cells overexpressed Fas ligand, hepatocellular damage was observed in Fas(lpr/lpr)Tgfb1(-/-) mice, indicating that liver pathology is Fas independent. |
| 2678 | 19234226 | Finally, whereas Tgfb1(-/-) CD4(+) T cells overexpressed Fas ligand, hepatocellular damage was observed in Fas(lpr/lpr)Tgfb1(-/-) mice, indicating that liver pathology is Fas independent. |
| 2679 | 19234226 | Finally, whereas Tgfb1(-/-) CD4(+) T cells overexpressed Fas ligand, hepatocellular damage was observed in Fas(lpr/lpr)Tgfb1(-/-) mice, indicating that liver pathology is Fas independent. |
| 2680 | 19234226 | Finally, whereas Tgfb1(-/-) CD4(+) T cells overexpressed Fas ligand, hepatocellular damage was observed in Fas(lpr/lpr)Tgfb1(-/-) mice, indicating that liver pathology is Fas independent. |
| 2681 | 19234226 | Finally, whereas Tgfb1(-/-) CD4(+) T cells overexpressed Fas ligand, hepatocellular damage was observed in Fas(lpr/lpr)Tgfb1(-/-) mice, indicating that liver pathology is Fas independent. |
| 2682 | 19234226 | We conclude that liver damage in this model of fulminant autoimmune hepatitis is driven by CD4(+) T cell production of IFN-gamma, is independent of both CD8(+) T cells and the Fas ligand/Fas pathway, and is not explained by a lack of PD-L1 expression. |
| 2683 | 19234226 | We conclude that liver damage in this model of fulminant autoimmune hepatitis is driven by CD4(+) T cell production of IFN-gamma, is independent of both CD8(+) T cells and the Fas ligand/Fas pathway, and is not explained by a lack of PD-L1 expression. |
| 2684 | 19234226 | We conclude that liver damage in this model of fulminant autoimmune hepatitis is driven by CD4(+) T cell production of IFN-gamma, is independent of both CD8(+) T cells and the Fas ligand/Fas pathway, and is not explained by a lack of PD-L1 expression. |
| 2685 | 19234226 | We conclude that liver damage in this model of fulminant autoimmune hepatitis is driven by CD4(+) T cell production of IFN-gamma, is independent of both CD8(+) T cells and the Fas ligand/Fas pathway, and is not explained by a lack of PD-L1 expression. |
| 2686 | 19234226 | We conclude that liver damage in this model of fulminant autoimmune hepatitis is driven by CD4(+) T cell production of IFN-gamma, is independent of both CD8(+) T cells and the Fas ligand/Fas pathway, and is not explained by a lack of PD-L1 expression. |
| 2687 | 19234226 | We conclude that liver damage in this model of fulminant autoimmune hepatitis is driven by CD4(+) T cell production of IFN-gamma, is independent of both CD8(+) T cells and the Fas ligand/Fas pathway, and is not explained by a lack of PD-L1 expression. |
| 2688 | 19189859 | Interleukin 8 -251T>A and Interferon gamma +874A>T polymorphism: potential predictors of allograft outcome in renal transplant recipients from north India. |
| 2689 | 19164174 | Despite this, rodent and human trophoblast cells show dampened responses to IFNG that reflect the resistance of these cells to IFNG-mediated activation of major histocompatibility complex (MHC) class II transplantation antigen expression. |
| 2690 | 19139386 | Interferon-gamma and the interferon-inducible chemokine CXCL10 protect against aneurysm formation and rupture. |
| 2691 | 19129516 | The present study was conducted to explore the source of acetylcholine (ACH) in the corpus luteum (CL) and to test our hypothesis of an antiapoptotic role of ACH in the bovine CL and, further, to investigate whether nerve growth factor (NGF), insulin-like growth factor 1 (IGF1), and transforming growth factor beta1 (TGFB1) influence the expression of choline acetyltransferase (CHAT), the biosynthetic enzyme of ACH, in cultured bovine luteal cells. |
| 2692 | 19129516 | The present study was conducted to explore the source of acetylcholine (ACH) in the corpus luteum (CL) and to test our hypothesis of an antiapoptotic role of ACH in the bovine CL and, further, to investigate whether nerve growth factor (NGF), insulin-like growth factor 1 (IGF1), and transforming growth factor beta1 (TGFB1) influence the expression of choline acetyltransferase (CHAT), the biosynthetic enzyme of ACH, in cultured bovine luteal cells. |
| 2693 | 19129516 | The present study was conducted to explore the source of acetylcholine (ACH) in the corpus luteum (CL) and to test our hypothesis of an antiapoptotic role of ACH in the bovine CL and, further, to investigate whether nerve growth factor (NGF), insulin-like growth factor 1 (IGF1), and transforming growth factor beta1 (TGFB1) influence the expression of choline acetyltransferase (CHAT), the biosynthetic enzyme of ACH, in cultured bovine luteal cells. |
| 2694 | 19129516 | Cell viability and TUNEL assays were performed on cultured midluteal cells treated with or without tumor necrosis factor alpha (TNF)/interferon gamma (IFNG) in the presence of ACH and its muscarinic (atropine) and nicotinic (mecamylamine) receptor antagonists. |
| 2695 | 19129516 | Cell viability and TUNEL assays were performed on cultured midluteal cells treated with or without tumor necrosis factor alpha (TNF)/interferon gamma (IFNG) in the presence of ACH and its muscarinic (atropine) and nicotinic (mecamylamine) receptor antagonists. |
| 2696 | 19129516 | Cell viability and TUNEL assays were performed on cultured midluteal cells treated with or without tumor necrosis factor alpha (TNF)/interferon gamma (IFNG) in the presence of ACH and its muscarinic (atropine) and nicotinic (mecamylamine) receptor antagonists. |
| 2697 | 19129516 | ACH increased cell viability and prevented cell death induced by TNF/IFNG. |
| 2698 | 19129516 | ACH increased cell viability and prevented cell death induced by TNF/IFNG. |
| 2699 | 19129516 | ACH increased cell viability and prevented cell death induced by TNF/IFNG. |
| 2700 | 19129516 | TNF/IFNG treatment downregulated CHAT expression, whereas NGF, IGF1, and TGFB1 upregulated CHAT expression, in cultured luteal cells. |
| 2701 | 19129516 | TNF/IFNG treatment downregulated CHAT expression, whereas NGF, IGF1, and TGFB1 upregulated CHAT expression, in cultured luteal cells. |
| 2702 | 19129516 | TNF/IFNG treatment downregulated CHAT expression, whereas NGF, IGF1, and TGFB1 upregulated CHAT expression, in cultured luteal cells. |
| 2703 | 19129516 | Locally produced ACH appears to be regulated by NGF, IGF1, and TGFB1. |
| 2704 | 19129516 | Locally produced ACH appears to be regulated by NGF, IGF1, and TGFB1. |
| 2705 | 19129516 | Locally produced ACH appears to be regulated by NGF, IGF1, and TGFB1. |
| 2706 | 19075734 | Three major cytokines, namely, tumor necrosis factor (TNF-alpha), interleukin (IL)-1, and IL-6 are produced by cultured brain cells after various stimuli such as ischemia. |
| 2707 | 19075734 | TNF-alpha expression after stroke stimulates expression of tissue factor and adhesion molecules for leukocytes, release of interleukin-1 (IL-1), nitric oxide, factor VIII/von Willebrand factor, platelet-activating factor and endothelin, suppression of the thrombomodulin-protein C-protein S system, reduction of tissue-plasminogen activator and release of plasminogen activator inhibitor-1. |
| 2708 | 19075734 | IL-6 can be induced by a variety of molecules including IL-1, TNF-alpha, transforming growth factor-beta and prostaglandins (PGs), and many other mediators such as b-amyloid, interferon-g (IFNg) and IL-4 can potentiate these primary inducers, highlighting the complex nature of IL-6 modulation. |
| 2709 | 19075734 | Several studies reported that plasma levels of TNF-alpha and IL-6 are associated with prognosis after ischemic stroke and our group showed that plasma levels of cytokines such as TNF-alpha, IL-1beta are different in every diagnostic subtype of ischemic stroke, and how plasma levels of some immunoinflammatory markers and thrombotic-phybrinolitic markers are predictive of acute ischemic stroke diagnosis in the acute setting. |
| 2710 | 19031096 | Association of IL-18 gene polymorphism (-137C) with arthritis manifestations in SLE: combined effect with IFN gamma gene polymorphism (+874A). |
| 2711 | 19031096 | Association of IL-18 gene polymorphism (-137C) with arthritis manifestations in SLE: combined effect with IFN gamma gene polymorphism (+874A). |
| 2712 | 19031096 | We analyzed the association between single nucleotide polymorphisms in IL-12 and IL-18 genes in disease susceptibility and severity of SLE in Thais. |
| 2713 | 19031096 | We analyzed the association between single nucleotide polymorphisms in IL-12 and IL-18 genes in disease susceptibility and severity of SLE in Thais. |
| 2714 | 19031096 | Interestingly, we found the combined effect between the G/C genotype of IL-18 (-137) and the A/A genotype of IFNG (+874) gene causing susceptibility of arthritis in SLE patients (OR = 13.22, 95% CI = 1.56-291.66, P = 0.004). |
| 2715 | 19031096 | Interestingly, we found the combined effect between the G/C genotype of IL-18 (-137) and the A/A genotype of IFNG (+874) gene causing susceptibility of arthritis in SLE patients (OR = 13.22, 95% CI = 1.56-291.66, P = 0.004). |
| 2716 | 19017962 | Self-antigen prevents CD8 T cell effector differentiation by CD134 and CD137 dual costimulation. |
| 2717 | 19017962 | Enforced dual costimulation through OX40 and 4-1BB redirected CD8 cells encountering soluble exogenous peptide to expand and differentiate into IFN-gamma and TNF-alpha double-producing effectors rather than becoming tolerant. |
| 2718 | 19017962 | Thus, the ability of enforced OX40 plus 4-1BB dual costimulation to redirect CD8 cells to undergo effector differentiation was unexpectedly influenced by the source of tolerizing Ag and help was selectively required to facilitate CD8 cell effector differentiation when the tolerizing Ag derived from self. |
| 2719 | 19007808 | In this study, we demonstrate distinct expression patterns of innate immune genes including - Toll-like receptors (TLRs) (TLR2, TLR15 and TLR21, but not TLR4), the complete repertoire of AvBDs, CTHLs and both pro- and anti-inflammatory cytokines (IL1B, IL8, IFNG and IL10) during early chicken embryonic development. |
| 2720 | 18849521 | Classical MHC genes are expressed in a cell type-specific pattern and can be induced by cytokines such as interferon-gamma (IFNG). |
| 2721 | 18715881 | Interferon-gamma inhibits cellular proliferation and ACTH production in corticotroph tumor cells through a novel janus kinases-signal transducer and activator of transcription 1/nuclear factor-kappa B inhibitory signaling pathway. |
| 2722 | 18715881 | Interferon-gamma inhibits cellular proliferation and ACTH production in corticotroph tumor cells through a novel janus kinases-signal transducer and activator of transcription 1/nuclear factor-kappa B inhibitory signaling pathway. |
| 2723 | 18715881 | Interferon-gamma inhibits cellular proliferation and ACTH production in corticotroph tumor cells through a novel janus kinases-signal transducer and activator of transcription 1/nuclear factor-kappa B inhibitory signaling pathway. |
| 2724 | 18715881 | Interferon-gamma inhibits cellular proliferation and ACTH production in corticotroph tumor cells through a novel janus kinases-signal transducer and activator of transcription 1/nuclear factor-kappa B inhibitory signaling pathway. |
| 2725 | 18715881 | Interferon-gamma inhibits cellular proliferation and ACTH production in corticotroph tumor cells through a novel janus kinases-signal transducer and activator of transcription 1/nuclear factor-kappa B inhibitory signaling pathway. |
| 2726 | 18715881 | Interferon-gamma inhibits cellular proliferation and ACTH production in corticotroph tumor cells through a novel janus kinases-signal transducer and activator of transcription 1/nuclear factor-kappa B inhibitory signaling pathway. |
| 2727 | 18715881 | Moreover, IFNG modulates normal pituitary hormone secretion, and was shown to inhibit the expression of the ACTH precursor POMC in murine ACTH-secreting AtT-2010/21/2008 tumor cells. |
| 2728 | 18715881 | Moreover, IFNG modulates normal pituitary hormone secretion, and was shown to inhibit the expression of the ACTH precursor POMC in murine ACTH-secreting AtT-2010/21/2008 tumor cells. |
| 2729 | 18715881 | Moreover, IFNG modulates normal pituitary hormone secretion, and was shown to inhibit the expression of the ACTH precursor POMC in murine ACTH-secreting AtT-2010/21/2008 tumor cells. |
| 2730 | 18715881 | Moreover, IFNG modulates normal pituitary hormone secretion, and was shown to inhibit the expression of the ACTH precursor POMC in murine ACTH-secreting AtT-2010/21/2008 tumor cells. |
| 2731 | 18715881 | Moreover, IFNG modulates normal pituitary hormone secretion, and was shown to inhibit the expression of the ACTH precursor POMC in murine ACTH-secreting AtT-2010/21/2008 tumor cells. |
| 2732 | 18715881 | Moreover, IFNG modulates normal pituitary hormone secretion, and was shown to inhibit the expression of the ACTH precursor POMC in murine ACTH-secreting AtT-2010/21/2008 tumor cells. |
| 2733 | 18715881 | We have studied the functional role of IFNG on pituitary tumor cells, focusing on the involvement of IFNG in the molecular events leading to the control of POMC transcriptional repression. |
| 2734 | 18715881 | We have studied the functional role of IFNG on pituitary tumor cells, focusing on the involvement of IFNG in the molecular events leading to the control of POMC transcriptional repression. |
| 2735 | 18715881 | We have studied the functional role of IFNG on pituitary tumor cells, focusing on the involvement of IFNG in the molecular events leading to the control of POMC transcriptional repression. |
| 2736 | 18715881 | We have studied the functional role of IFNG on pituitary tumor cells, focusing on the involvement of IFNG in the molecular events leading to the control of POMC transcriptional repression. |
| 2737 | 18715881 | We have studied the functional role of IFNG on pituitary tumor cells, focusing on the involvement of IFNG in the molecular events leading to the control of POMC transcriptional repression. |
| 2738 | 18715881 | We have studied the functional role of IFNG on pituitary tumor cells, focusing on the involvement of IFNG in the molecular events leading to the control of POMC transcriptional repression. |
| 2739 | 18715881 | Unexpectedly, an activated janus kinases-signal transducer and activator of transcription (JAK-STAT1) cascade is required for IFNG inhibitory action on POMC promoter activity. |
| 2740 | 18715881 | Unexpectedly, an activated janus kinases-signal transducer and activator of transcription (JAK-STAT1) cascade is required for IFNG inhibitory action on POMC promoter activity. |
| 2741 | 18715881 | Unexpectedly, an activated janus kinases-signal transducer and activator of transcription (JAK-STAT1) cascade is required for IFNG inhibitory action on POMC promoter activity. |
| 2742 | 18715881 | Unexpectedly, an activated janus kinases-signal transducer and activator of transcription (JAK-STAT1) cascade is required for IFNG inhibitory action on POMC promoter activity. |
| 2743 | 18715881 | Unexpectedly, an activated janus kinases-signal transducer and activator of transcription (JAK-STAT1) cascade is required for IFNG inhibitory action on POMC promoter activity. |
| 2744 | 18715881 | Unexpectedly, an activated janus kinases-signal transducer and activator of transcription (JAK-STAT1) cascade is required for IFNG inhibitory action on POMC promoter activity. |
| 2745 | 18715881 | Factor-kappa B (NF-kappaB) is necessary for the inhibitory action of IFNG on Pomc transcription, since loss of NF-kappaB activity with IkappaB super-repressor abolishes this effect. |
| 2746 | 18715881 | Factor-kappa B (NF-kappaB) is necessary for the inhibitory action of IFNG on Pomc transcription, since loss of NF-kappaB activity with IkappaB super-repressor abolishes this effect. |
| 2747 | 18715881 | Factor-kappa B (NF-kappaB) is necessary for the inhibitory action of IFNG on Pomc transcription, since loss of NF-kappaB activity with IkappaB super-repressor abolishes this effect. |
| 2748 | 18715881 | Factor-kappa B (NF-kappaB) is necessary for the inhibitory action of IFNG on Pomc transcription, since loss of NF-kappaB activity with IkappaB super-repressor abolishes this effect. |
| 2749 | 18715881 | Factor-kappa B (NF-kappaB) is necessary for the inhibitory action of IFNG on Pomc transcription, since loss of NF-kappaB activity with IkappaB super-repressor abolishes this effect. |
| 2750 | 18715881 | Factor-kappa B (NF-kappaB) is necessary for the inhibitory action of IFNG on Pomc transcription, since loss of NF-kappaB activity with IkappaB super-repressor abolishes this effect. |
| 2751 | 18715881 | Interestingly, IFNG inhibits ACTH production from these cells in primary cell culture, without affecting basal ACTH biosynthesis in normal non-tumoral pituitary cells. |
| 2752 | 18715881 | Interestingly, IFNG inhibits ACTH production from these cells in primary cell culture, without affecting basal ACTH biosynthesis in normal non-tumoral pituitary cells. |
| 2753 | 18715881 | Interestingly, IFNG inhibits ACTH production from these cells in primary cell culture, without affecting basal ACTH biosynthesis in normal non-tumoral pituitary cells. |
| 2754 | 18715881 | Interestingly, IFNG inhibits ACTH production from these cells in primary cell culture, without affecting basal ACTH biosynthesis in normal non-tumoral pituitary cells. |
| 2755 | 18715881 | Interestingly, IFNG inhibits ACTH production from these cells in primary cell culture, without affecting basal ACTH biosynthesis in normal non-tumoral pituitary cells. |
| 2756 | 18715881 | Interestingly, IFNG inhibits ACTH production from these cells in primary cell culture, without affecting basal ACTH biosynthesis in normal non-tumoral pituitary cells. |
| 2757 | 18715881 | In conclusion, our data show for the first time that POMC transcription can be negatively regulated by a JAK-STAT1 and NF-kappaB-dependent pathway. |
| 2758 | 18715881 | In conclusion, our data show for the first time that POMC transcription can be negatively regulated by a JAK-STAT1 and NF-kappaB-dependent pathway. |
| 2759 | 18715881 | In conclusion, our data show for the first time that POMC transcription can be negatively regulated by a JAK-STAT1 and NF-kappaB-dependent pathway. |
| 2760 | 18715881 | In conclusion, our data show for the first time that POMC transcription can be negatively regulated by a JAK-STAT1 and NF-kappaB-dependent pathway. |
| 2761 | 18715881 | In conclusion, our data show for the first time that POMC transcription can be negatively regulated by a JAK-STAT1 and NF-kappaB-dependent pathway. |
| 2762 | 18715881 | In conclusion, our data show for the first time that POMC transcription can be negatively regulated by a JAK-STAT1 and NF-kappaB-dependent pathway. |
| 2763 | 18684979 | Surprisingly, human naive CD4(+) T lymphocytes displayed hypermethylation at the IFNG promoter region, which is in sharp contrast to the completely demethylated status of this region in mice. |
| 2764 | 18684979 | Surprisingly, human naive CD4(+) T lymphocytes displayed hypermethylation at the IFNG promoter region, which is in sharp contrast to the completely demethylated status of this region in mice. |
| 2765 | 18684979 | Surprisingly, human naive CD4(+) T lymphocytes displayed hypermethylation at the IFNG promoter region, which is in sharp contrast to the completely demethylated status of this region in mice. |
| 2766 | 18684979 | Furthermore, CD19(+) B lymphocytes displayed hypomethylation at the IFNG promoter region with a similar pattern to Th1 effector cells. |
| 2767 | 18684979 | Furthermore, CD19(+) B lymphocytes displayed hypomethylation at the IFNG promoter region with a similar pattern to Th1 effector cells. |
| 2768 | 18684979 | Furthermore, CD19(+) B lymphocytes displayed hypomethylation at the IFNG promoter region with a similar pattern to Th1 effector cells. |
| 2769 | 18684979 | We conclude that there are obvious interspecies differences in the methylation status of the IFNG gene in naive CD4(+) T lymphocytes, where Th1 commitment in human lymphocytes involves demethylation before IFNG expression. |
| 2770 | 18684979 | We conclude that there are obvious interspecies differences in the methylation status of the IFNG gene in naive CD4(+) T lymphocytes, where Th1 commitment in human lymphocytes involves demethylation before IFNG expression. |
| 2771 | 18684979 | We conclude that there are obvious interspecies differences in the methylation status of the IFNG gene in naive CD4(+) T lymphocytes, where Th1 commitment in human lymphocytes involves demethylation before IFNG expression. |
| 2772 | 18653623 | Insulin-like growth factor-1 delays Fas-mediated apoptosis in human neutrophils through the phosphatidylinositol-3 kinase pathway. |
| 2773 | 18653623 | We previously showed that insulin-like growth factor-1 (IGF1) delays spontaneous neutrophil apoptosis without influencing the secretion of cytokines by these cells. |
| 2774 | 18653623 | We show that IGF1 delays neutrophil apoptosis triggered by the agonistic anti-Fas antibody CH11 and that the effect of IGF1 is comparable in magnitude to that of the acknowledged anti-apoptotic cytokines interferon-gamma (IFNG) and granulocyte-macrophage colony-stimulating factor (GM-CSF; now known as CSF2). |
| 2775 | 18653623 | IGF1 did not affect Fas expression or activation by anti-Fas of caspase-8, but inhibited the depolarization of the mitochondrial membrane. |
| 2776 | 18653623 | Inhibitor studies indicate that the phosphatidylinositol-3 kinase (PI3K) pathway, but not the MEK-ERK pathway, mediates the effects of IGF1. |
| 2777 | 18653623 | However, in contrast to CSF2, IGF1 did not induce phosphorylation and translocation to the membrane of AKT, the canonical downstream target of PI3K. |
| 2778 | 18653623 | We therefore speculate that other downstream targets of PI3K are involved in the delay of neutrophil apoptosis by IGF1, possibly through stabilization of the mitochondrial membrane. |
| 2779 | 18632870 | Interestingly, in SARS-CoV-infected aged mice, a subset of genes, including Tnfa, Il6, Ccl2, Ccl3, Cxcl10, and Ifng, was induced in a biphasic pattern that correlated with peak viral replication and a subsequent influx of lymphocytes and severe histopathologic changes in the lungs. |
| 2780 | 18549798 | Janus-kinase-3-dependent signals induce chromatin remodeling at the Ifng locus during T helper 1 cell differentiation. |
| 2781 | 18549798 | Janus-kinase-3-dependent signals induce chromatin remodeling at the Ifng locus during T helper 1 cell differentiation. |
| 2782 | 18549798 | Janus-kinase-3-dependent signals induce chromatin remodeling at the Ifng locus during T helper 1 cell differentiation. |
| 2783 | 18549798 | Janus-kinase-3-dependent signals induce chromatin remodeling at the Ifng locus during T helper 1 cell differentiation. |
| 2784 | 18549798 | Janus-kinase-3-dependent signals induce chromatin remodeling at the Ifng locus during T helper 1 cell differentiation. |
| 2785 | 18549798 | Differentiation of naive CD4+ T cells into T helper type 1 (Th1) effector cells requires both T cell receptor (TCR) signaling and cytokines such as interleukin-12 and interferon gamma (IFN-gamma). |
| 2786 | 18549798 | Differentiation of naive CD4+ T cells into T helper type 1 (Th1) effector cells requires both T cell receptor (TCR) signaling and cytokines such as interleukin-12 and interferon gamma (IFN-gamma). |
| 2787 | 18549798 | Differentiation of naive CD4+ T cells into T helper type 1 (Th1) effector cells requires both T cell receptor (TCR) signaling and cytokines such as interleukin-12 and interferon gamma (IFN-gamma). |
| 2788 | 18549798 | Differentiation of naive CD4+ T cells into T helper type 1 (Th1) effector cells requires both T cell receptor (TCR) signaling and cytokines such as interleukin-12 and interferon gamma (IFN-gamma). |
| 2789 | 18549798 | Differentiation of naive CD4+ T cells into T helper type 1 (Th1) effector cells requires both T cell receptor (TCR) signaling and cytokines such as interleukin-12 and interferon gamma (IFN-gamma). |
| 2790 | 18549798 | Here, we report that a third cytokine signal, mediated by the Janus family tyrosine kinase 3 (Jak3) and signal transducer and activator of transcription 5 (STAT5) pathway, is also required for Th1 cell differentiation. |
| 2791 | 18549798 | Here, we report that a third cytokine signal, mediated by the Janus family tyrosine kinase 3 (Jak3) and signal transducer and activator of transcription 5 (STAT5) pathway, is also required for Th1 cell differentiation. |
| 2792 | 18549798 | Here, we report that a third cytokine signal, mediated by the Janus family tyrosine kinase 3 (Jak3) and signal transducer and activator of transcription 5 (STAT5) pathway, is also required for Th1 cell differentiation. |
| 2793 | 18549798 | Here, we report that a third cytokine signal, mediated by the Janus family tyrosine kinase 3 (Jak3) and signal transducer and activator of transcription 5 (STAT5) pathway, is also required for Th1 cell differentiation. |
| 2794 | 18549798 | Here, we report that a third cytokine signal, mediated by the Janus family tyrosine kinase 3 (Jak3) and signal transducer and activator of transcription 5 (STAT5) pathway, is also required for Th1 cell differentiation. |
| 2795 | 18549798 | In the absence of Jak3-dependent signals, naive CD4+ T cells proliferate robustly but produce little IFN-gamma after Th1 cell polarization in vitro. |
| 2796 | 18549798 | In the absence of Jak3-dependent signals, naive CD4+ T cells proliferate robustly but produce little IFN-gamma after Th1 cell polarization in vitro. |
| 2797 | 18549798 | In the absence of Jak3-dependent signals, naive CD4+ T cells proliferate robustly but produce little IFN-gamma after Th1 cell polarization in vitro. |
| 2798 | 18549798 | In the absence of Jak3-dependent signals, naive CD4+ T cells proliferate robustly but produce little IFN-gamma after Th1 cell polarization in vitro. |
| 2799 | 18549798 | In the absence of Jak3-dependent signals, naive CD4+ T cells proliferate robustly but produce little IFN-gamma after Th1 cell polarization in vitro. |
| 2800 | 18549798 | This defect is not due to reduced activation of STAT1 or STAT4 or to impaired upregulation of the transcription factor T-bet. |
| 2801 | 18549798 | This defect is not due to reduced activation of STAT1 or STAT4 or to impaired upregulation of the transcription factor T-bet. |
| 2802 | 18549798 | This defect is not due to reduced activation of STAT1 or STAT4 or to impaired upregulation of the transcription factor T-bet. |
| 2803 | 18549798 | This defect is not due to reduced activation of STAT1 or STAT4 or to impaired upregulation of the transcription factor T-bet. |
| 2804 | 18549798 | This defect is not due to reduced activation of STAT1 or STAT4 or to impaired upregulation of the transcription factor T-bet. |
| 2805 | 18549798 | Instead, we find that T-bet binding to the Ifng promoter is greatly diminished in the absence of Jak3-dependent signals, correlating with a decrease in Ifng promoter accessibility and histone acetylation. |
| 2806 | 18549798 | Instead, we find that T-bet binding to the Ifng promoter is greatly diminished in the absence of Jak3-dependent signals, correlating with a decrease in Ifng promoter accessibility and histone acetylation. |
| 2807 | 18549798 | Instead, we find that T-bet binding to the Ifng promoter is greatly diminished in the absence of Jak3-dependent signals, correlating with a decrease in Ifng promoter accessibility and histone acetylation. |
| 2808 | 18549798 | Instead, we find that T-bet binding to the Ifng promoter is greatly diminished in the absence of Jak3-dependent signals, correlating with a decrease in Ifng promoter accessibility and histone acetylation. |
| 2809 | 18549798 | Instead, we find that T-bet binding to the Ifng promoter is greatly diminished in the absence of Jak3-dependent signals, correlating with a decrease in Ifng promoter accessibility and histone acetylation. |
| 2810 | 18549798 | These data indicate that Jak3 regulates epigenetic modification and chromatin remodeling of the Ifng locus during Th1 cell differentiation. |
| 2811 | 18549798 | These data indicate that Jak3 regulates epigenetic modification and chromatin remodeling of the Ifng locus during Th1 cell differentiation. |
| 2812 | 18549798 | These data indicate that Jak3 regulates epigenetic modification and chromatin remodeling of the Ifng locus during Th1 cell differentiation. |
| 2813 | 18549798 | These data indicate that Jak3 regulates epigenetic modification and chromatin remodeling of the Ifng locus during Th1 cell differentiation. |
| 2814 | 18549798 | These data indicate that Jak3 regulates epigenetic modification and chromatin remodeling of the Ifng locus during Th1 cell differentiation. |
| 2815 | 18463360 | Prostaglandin E2 (1 microM) and PGF2alpha (1 microM) significantly stimulated progesterone (P4) production and reduced the levels of cell death in the cells cultured with or without tumor necrosis factor alpha (TNF)/interferon gamma (IFNG), in the presence and absence of FAS ligand (P < 0.05). |
| 2816 | 18463360 | Prostaglandin E2 (1 microM) and PGF2alpha (1 microM) significantly stimulated progesterone (P4) production and reduced the levels of cell death in the cells cultured with or without tumor necrosis factor alpha (TNF)/interferon gamma (IFNG), in the presence and absence of FAS ligand (P < 0.05). |
| 2817 | 18463360 | Prostaglandin E2 (1 microM) and PGF2alpha (1 microM) significantly stimulated progesterone (P4) production and reduced the levels of cell death in the cells cultured with or without tumor necrosis factor alpha (TNF)/interferon gamma (IFNG), in the presence and absence of FAS ligand (P < 0.05). |
| 2818 | 18463360 | Prostaglandin E2 (1 microM) and PGF2alpha (1 microM) significantly stimulated progesterone (P4) production and reduced the levels of cell death in the cells cultured with or without tumor necrosis factor alpha (TNF)/interferon gamma (IFNG), in the presence and absence of FAS ligand (P < 0.05). |
| 2819 | 18463360 | Furthermore, DNA fragmentation induced by TNF/IFNG was observed to be suppressed by PGE2 and PGF2alpha. |
| 2820 | 18463360 | Furthermore, DNA fragmentation induced by TNF/IFNG was observed to be suppressed by PGE2 and PGF2alpha. |
| 2821 | 18463360 | Furthermore, DNA fragmentation induced by TNF/IFNG was observed to be suppressed by PGE2 and PGF2alpha. |
| 2822 | 18463360 | Furthermore, DNA fragmentation induced by TNF/IFNG was observed to be suppressed by PGE2 and PGF2alpha. |
| 2823 | 18463360 | Prostaglandin E2 and PGF2alpha also attenuated mRNA expression of caspase 3 and caspase 8, as well as caspase 3 activity (P < 0.05) in TNF/IFNG-treated cells. |
| 2824 | 18463360 | Prostaglandin E2 and PGF2alpha also attenuated mRNA expression of caspase 3 and caspase 8, as well as caspase 3 activity (P < 0.05) in TNF/IFNG-treated cells. |
| 2825 | 18463360 | Prostaglandin E2 and PGF2alpha also attenuated mRNA expression of caspase 3 and caspase 8, as well as caspase 3 activity (P < 0.05) in TNF/IFNG-treated cells. |
| 2826 | 18463360 | Prostaglandin E2 and PGF2alpha also attenuated mRNA expression of caspase 3 and caspase 8, as well as caspase 3 activity (P < 0.05) in TNF/IFNG-treated cells. |
| 2827 | 18463360 | A specific P4 receptor antagonist (onapristone) attenuated the apoptosis-inhibitory effects of PGE2 and PGF2alpha in the absence of TNF/IFNG (P < 0.05). |
| 2828 | 18463360 | A specific P4 receptor antagonist (onapristone) attenuated the apoptosis-inhibitory effects of PGE2 and PGF2alpha in the absence of TNF/IFNG (P < 0.05). |
| 2829 | 18463360 | A specific P4 receptor antagonist (onapristone) attenuated the apoptosis-inhibitory effects of PGE2 and PGF2alpha in the absence of TNF/IFNG (P < 0.05). |
| 2830 | 18463360 | A specific P4 receptor antagonist (onapristone) attenuated the apoptosis-inhibitory effects of PGE2 and PGF2alpha in the absence of TNF/IFNG (P < 0.05). |
| 2831 | 18414898 | IFNG +874T/A, IL10 -1082G/A and TNF -308G/A polymorphisms in association with tuberculosis susceptibility: a meta-analysis study. |
| 2832 | 18414898 | IFNG +874T/A, IL10 -1082G/A and TNF -308G/A polymorphisms in association with tuberculosis susceptibility: a meta-analysis study. |
| 2833 | 18414898 | IFNG +874T/A, IL10 -1082G/A and TNF -308G/A polymorphisms in association with tuberculosis susceptibility: a meta-analysis study. |
| 2834 | 18414898 | IFNG +874T/A, IL10 -1082G/A and TNF -308G/A polymorphisms in association with tuberculosis susceptibility: a meta-analysis study. |
| 2835 | 18414898 | IFNG +874T/A, IL10 -1082G/A and TNF -308G/A polymorphisms in association with tuberculosis susceptibility: a meta-analysis study. |
| 2836 | 18414898 | In tuberculosis (TB), interferon-gamma (IFNgamma) is crucial to control intracellular growth of Mycobacterium tuberculosis while interleukin-10 (IL-10) has an antagonistic role. |
| 2837 | 18414898 | In tuberculosis (TB), interferon-gamma (IFNgamma) is crucial to control intracellular growth of Mycobacterium tuberculosis while interleukin-10 (IL-10) has an antagonistic role. |
| 2838 | 18414898 | In tuberculosis (TB), interferon-gamma (IFNgamma) is crucial to control intracellular growth of Mycobacterium tuberculosis while interleukin-10 (IL-10) has an antagonistic role. |
| 2839 | 18414898 | In tuberculosis (TB), interferon-gamma (IFNgamma) is crucial to control intracellular growth of Mycobacterium tuberculosis while interleukin-10 (IL-10) has an antagonistic role. |
| 2840 | 18414898 | In tuberculosis (TB), interferon-gamma (IFNgamma) is crucial to control intracellular growth of Mycobacterium tuberculosis while interleukin-10 (IL-10) has an antagonistic role. |
| 2841 | 18414898 | Tumor necrosis factor (TNF) is a central mediator of granuloma formation and control of bacilli spread synergizing with IFNgamma to hamper M. tuberculosis infection. |
| 2842 | 18414898 | Tumor necrosis factor (TNF) is a central mediator of granuloma formation and control of bacilli spread synergizing with IFNgamma to hamper M. tuberculosis infection. |
| 2843 | 18414898 | Tumor necrosis factor (TNF) is a central mediator of granuloma formation and control of bacilli spread synergizing with IFNgamma to hamper M. tuberculosis infection. |
| 2844 | 18414898 | Tumor necrosis factor (TNF) is a central mediator of granuloma formation and control of bacilli spread synergizing with IFNgamma to hamper M. tuberculosis infection. |
| 2845 | 18414898 | Tumor necrosis factor (TNF) is a central mediator of granuloma formation and control of bacilli spread synergizing with IFNgamma to hamper M. tuberculosis infection. |
| 2846 | 18414898 | The aim of this study was to determine the association of the interferon-gamma gene (IFNG) +874T/A, interleukin-10 gene (IL10) -1082G/A and tumor necrosis factor gene (TNF) -308G/A SNPs with TB in several populations using meta-analysis. |
| 2847 | 18414898 | The aim of this study was to determine the association of the interferon-gamma gene (IFNG) +874T/A, interleukin-10 gene (IL10) -1082G/A and tumor necrosis factor gene (TNF) -308G/A SNPs with TB in several populations using meta-analysis. |
| 2848 | 18414898 | The aim of this study was to determine the association of the interferon-gamma gene (IFNG) +874T/A, interleukin-10 gene (IL10) -1082G/A and tumor necrosis factor gene (TNF) -308G/A SNPs with TB in several populations using meta-analysis. |
| 2849 | 18414898 | The aim of this study was to determine the association of the interferon-gamma gene (IFNG) +874T/A, interleukin-10 gene (IL10) -1082G/A and tumor necrosis factor gene (TNF) -308G/A SNPs with TB in several populations using meta-analysis. |
| 2850 | 18414898 | The aim of this study was to determine the association of the interferon-gamma gene (IFNG) +874T/A, interleukin-10 gene (IL10) -1082G/A and tumor necrosis factor gene (TNF) -308G/A SNPs with TB in several populations using meta-analysis. |
| 2851 | 18414898 | Eleven studies were included in the IFNG +874T/A meta-analysis, while eight were used for the IL10 -1082G/A, and 10 were employed for TNF -308G/A. |
| 2852 | 18414898 | Eleven studies were included in the IFNG +874T/A meta-analysis, while eight were used for the IL10 -1082G/A, and 10 were employed for TNF -308G/A. |
| 2853 | 18414898 | Eleven studies were included in the IFNG +874T/A meta-analysis, while eight were used for the IL10 -1082G/A, and 10 were employed for TNF -308G/A. |
| 2854 | 18414898 | Eleven studies were included in the IFNG +874T/A meta-analysis, while eight were used for the IL10 -1082G/A, and 10 were employed for TNF -308G/A. |
| 2855 | 18414898 | Eleven studies were included in the IFNG +874T/A meta-analysis, while eight were used for the IL10 -1082G/A, and 10 were employed for TNF -308G/A. |
| 2856 | 18413324 | Interleukin-12 is required for Th1 cell differentiation, which is characterized by the production of interferon-gamma. |
| 2857 | 18413324 | Interleukin-12 is required for Th1 cell differentiation, which is characterized by the production of interferon-gamma. |
| 2858 | 18413324 | We investigated 21 markers in IL12-related genes, including IL12A and IL12B encoding the two IL-12 (IL12p70) subunits, IL12p35 and IL12p40. |
| 2859 | 18413324 | We investigated 21 markers in IL12-related genes, including IL12A and IL12B encoding the two IL-12 (IL12p70) subunits, IL12p35 and IL12p40. |
| 2860 | 18413324 | These results, together with the findings from immunological studies of low interferon-gamma and IL-12 levels in CM, support a protective role for the Th1 pathway in CM. |
| 2861 | 18413324 | These results, together with the findings from immunological studies of low interferon-gamma and IL-12 levels in CM, support a protective role for the Th1 pathway in CM. |
| 2862 | 18345012 | Fibrous tissue formation is regulated by the balance between plasminogen activator inhibitor type 1 (PAI-1) and tissue-type plasminogen activator (tPA), which reciprocally regulate fibrin deposition. |
| 2863 | 18345012 | Fibrous tissue formation is regulated by the balance between plasminogen activator inhibitor type 1 (PAI-1) and tissue-type plasminogen activator (tPA), which reciprocally regulate fibrin deposition. |
| 2864 | 18345012 | Fibrous tissue formation is regulated by the balance between plasminogen activator inhibitor type 1 (PAI-1) and tissue-type plasminogen activator (tPA), which reciprocally regulate fibrin deposition. |
| 2865 | 18345012 | Adhesion development depended upon the interferon-gamma (IFN-gamma) and signal transducer and activator of transcription-1 (STAT1) system. |
| 2866 | 18345012 | Adhesion development depended upon the interferon-gamma (IFN-gamma) and signal transducer and activator of transcription-1 (STAT1) system. |
| 2867 | 18345012 | Adhesion development depended upon the interferon-gamma (IFN-gamma) and signal transducer and activator of transcription-1 (STAT1) system. |
| 2868 | 18345012 | This response does not depend on STAT4, STAT6, interleukin-12 (IL-12), IL-18, tumor necrosis factor-alpha, Toll-like receptor 4 or myeloid differentiation factor-88-mediated signals. |
| 2869 | 18345012 | This response does not depend on STAT4, STAT6, interleukin-12 (IL-12), IL-18, tumor necrosis factor-alpha, Toll-like receptor 4 or myeloid differentiation factor-88-mediated signals. |
| 2870 | 18345012 | This response does not depend on STAT4, STAT6, interleukin-12 (IL-12), IL-18, tumor necrosis factor-alpha, Toll-like receptor 4 or myeloid differentiation factor-88-mediated signals. |
| 2871 | 18345012 | Wild-type mice increased the ratio of PAI-1 to tPA after cecal cauterization, whereas Ifng(-/-) or Stat1(-/-) mice did not, suggesting that IFN-gamma has a crucial role in the differential regulation of PAI-1 and tPA. |
| 2872 | 18345012 | Wild-type mice increased the ratio of PAI-1 to tPA after cecal cauterization, whereas Ifng(-/-) or Stat1(-/-) mice did not, suggesting that IFN-gamma has a crucial role in the differential regulation of PAI-1 and tPA. |
| 2873 | 18345012 | Wild-type mice increased the ratio of PAI-1 to tPA after cecal cauterization, whereas Ifng(-/-) or Stat1(-/-) mice did not, suggesting that IFN-gamma has a crucial role in the differential regulation of PAI-1 and tPA. |
| 2874 | 18345012 | Additionally, hepatocyte growth factor, a potent mitogenic factor for hepatocytes, strongly inhibited intestinal adhesion by diminishing IFN-gamma production, providing a potential new way to prevent postoperative adhesions. |
| 2875 | 18345012 | Additionally, hepatocyte growth factor, a potent mitogenic factor for hepatocytes, strongly inhibited intestinal adhesion by diminishing IFN-gamma production, providing a potential new way to prevent postoperative adhesions. |
| 2876 | 18345012 | Additionally, hepatocyte growth factor, a potent mitogenic factor for hepatocytes, strongly inhibited intestinal adhesion by diminishing IFN-gamma production, providing a potential new way to prevent postoperative adhesions. |
| 2877 | 18337305 | New approach reveals CD28 and IFNG gene interaction in the susceptibility to cervical cancer. |
| 2878 | 18337305 | New approach reveals CD28 and IFNG gene interaction in the susceptibility to cervical cancer. |
| 2879 | 18337305 | New approach reveals CD28 and IFNG gene interaction in the susceptibility to cervical cancer. |
| 2880 | 18337305 | New approach reveals CD28 and IFNG gene interaction in the susceptibility to cervical cancer. |
| 2881 | 18337305 | New approach reveals CD28 and IFNG gene interaction in the susceptibility to cervical cancer. |
| 2882 | 18337305 | New approach reveals CD28 and IFNG gene interaction in the susceptibility to cervical cancer. |
| 2883 | 18337305 | New approach reveals CD28 and IFNG gene interaction in the susceptibility to cervical cancer. |
| 2884 | 18337305 | A total of 14 single nucleotide polymorphisms (SNPs) distributed in CD28, CTLA4, ICOS, PDCD1, FAS, TNFA, IL6, IFNG, TGFB1 and IL10 genes were determined in patients and healthy individuals from three independent case/control sets. |
| 2885 | 18337305 | A total of 14 single nucleotide polymorphisms (SNPs) distributed in CD28, CTLA4, ICOS, PDCD1, FAS, TNFA, IL6, IFNG, TGFB1 and IL10 genes were determined in patients and healthy individuals from three independent case/control sets. |
| 2886 | 18337305 | A total of 14 single nucleotide polymorphisms (SNPs) distributed in CD28, CTLA4, ICOS, PDCD1, FAS, TNFA, IL6, IFNG, TGFB1 and IL10 genes were determined in patients and healthy individuals from three independent case/control sets. |
| 2887 | 18337305 | A total of 14 single nucleotide polymorphisms (SNPs) distributed in CD28, CTLA4, ICOS, PDCD1, FAS, TNFA, IL6, IFNG, TGFB1 and IL10 genes were determined in patients and healthy individuals from three independent case/control sets. |
| 2888 | 18337305 | A total of 14 single nucleotide polymorphisms (SNPs) distributed in CD28, CTLA4, ICOS, PDCD1, FAS, TNFA, IL6, IFNG, TGFB1 and IL10 genes were determined in patients and healthy individuals from three independent case/control sets. |
| 2889 | 18337305 | A total of 14 single nucleotide polymorphisms (SNPs) distributed in CD28, CTLA4, ICOS, PDCD1, FAS, TNFA, IL6, IFNG, TGFB1 and IL10 genes were determined in patients and healthy individuals from three independent case/control sets. |
| 2890 | 18337305 | A total of 14 single nucleotide polymorphisms (SNPs) distributed in CD28, CTLA4, ICOS, PDCD1, FAS, TNFA, IL6, IFNG, TGFB1 and IL10 genes were determined in patients and healthy individuals from three independent case/control sets. |
| 2891 | 18337305 | The multi-locus analysis revealed higher frequencies in cancer patients of three three-genotype combinations [CD28+17(TT)/IFNG+874(AA)/TNFA-308(GG), CD28+17(TT)/IFN+847(AA)/PDCD1+7785(CT), and CD28 +17(TT)/IFNG+874(AA)/ICOS+1564(TT)] (P < 0.01, Monte Carlo simulation). |
| 2892 | 18337305 | The multi-locus analysis revealed higher frequencies in cancer patients of three three-genotype combinations [CD28+17(TT)/IFNG+874(AA)/TNFA-308(GG), CD28+17(TT)/IFN+847(AA)/PDCD1+7785(CT), and CD28 +17(TT)/IFNG+874(AA)/ICOS+1564(TT)] (P < 0.01, Monte Carlo simulation). |
| 2893 | 18337305 | The multi-locus analysis revealed higher frequencies in cancer patients of three three-genotype combinations [CD28+17(TT)/IFNG+874(AA)/TNFA-308(GG), CD28+17(TT)/IFN+847(AA)/PDCD1+7785(CT), and CD28 +17(TT)/IFNG+874(AA)/ICOS+1564(TT)] (P < 0.01, Monte Carlo simulation). |
| 2894 | 18337305 | The multi-locus analysis revealed higher frequencies in cancer patients of three three-genotype combinations [CD28+17(TT)/IFNG+874(AA)/TNFA-308(GG), CD28+17(TT)/IFN+847(AA)/PDCD1+7785(CT), and CD28 +17(TT)/IFNG+874(AA)/ICOS+1564(TT)] (P < 0.01, Monte Carlo simulation). |
| 2895 | 18337305 | The multi-locus analysis revealed higher frequencies in cancer patients of three three-genotype combinations [CD28+17(TT)/IFNG+874(AA)/TNFA-308(GG), CD28+17(TT)/IFN+847(AA)/PDCD1+7785(CT), and CD28 +17(TT)/IFNG+874(AA)/ICOS+1564(TT)] (P < 0.01, Monte Carlo simulation). |
| 2896 | 18337305 | The multi-locus analysis revealed higher frequencies in cancer patients of three three-genotype combinations [CD28+17(TT)/IFNG+874(AA)/TNFA-308(GG), CD28+17(TT)/IFN+847(AA)/PDCD1+7785(CT), and CD28 +17(TT)/IFNG+874(AA)/ICOS+1564(TT)] (P < 0.01, Monte Carlo simulation). |
| 2897 | 18337305 | The multi-locus analysis revealed higher frequencies in cancer patients of three three-genotype combinations [CD28+17(TT)/IFNG+874(AA)/TNFA-308(GG), CD28+17(TT)/IFN+847(AA)/PDCD1+7785(CT), and CD28 +17(TT)/IFNG+874(AA)/ICOS+1564(TT)] (P < 0.01, Monte Carlo simulation). |
| 2898 | 18337305 | We hypothesized that this two-genotype [CD28(TT) and IFNG(AA)] combination could have a major contribution to the observed association. |
| 2899 | 18337305 | We hypothesized that this two-genotype [CD28(TT) and IFNG(AA)] combination could have a major contribution to the observed association. |
| 2900 | 18337305 | We hypothesized that this two-genotype [CD28(TT) and IFNG(AA)] combination could have a major contribution to the observed association. |
| 2901 | 18337305 | We hypothesized that this two-genotype [CD28(TT) and IFNG(AA)] combination could have a major contribution to the observed association. |
| 2902 | 18337305 | We hypothesized that this two-genotype [CD28(TT) and IFNG(AA)] combination could have a major contribution to the observed association. |
| 2903 | 18337305 | We hypothesized that this two-genotype [CD28(TT) and IFNG(AA)] combination could have a major contribution to the observed association. |
| 2904 | 18337305 | We hypothesized that this two-genotype [CD28(TT) and IFNG(AA)] combination could have a major contribution to the observed association. |
| 2905 | 18337305 | To address this question, we analyzed the frequency of the CD28(TT), IFNG(AA) genotype combination in the three groups combined, and observed its increase in patients (P = 0.0011 by Fisher's exact test). |
| 2906 | 18337305 | To address this question, we analyzed the frequency of the CD28(TT), IFNG(AA) genotype combination in the three groups combined, and observed its increase in patients (P = 0.0011 by Fisher's exact test). |
| 2907 | 18337305 | To address this question, we analyzed the frequency of the CD28(TT), IFNG(AA) genotype combination in the three groups combined, and observed its increase in patients (P = 0.0011 by Fisher's exact test). |
| 2908 | 18337305 | To address this question, we analyzed the frequency of the CD28(TT), IFNG(AA) genotype combination in the three groups combined, and observed its increase in patients (P = 0.0011 by Fisher's exact test). |
| 2909 | 18337305 | To address this question, we analyzed the frequency of the CD28(TT), IFNG(AA) genotype combination in the three groups combined, and observed its increase in patients (P = 0.0011 by Fisher's exact test). |
| 2910 | 18337305 | To address this question, we analyzed the frequency of the CD28(TT), IFNG(AA) genotype combination in the three groups combined, and observed its increase in patients (P = 0.0011 by Fisher's exact test). |
| 2911 | 18337305 | To address this question, we analyzed the frequency of the CD28(TT), IFNG(AA) genotype combination in the three groups combined, and observed its increase in patients (P = 0.0011 by Fisher's exact test). |
| 2912 | 18337305 | Further analysis suggested that gene-gene interaction between CD28 and IFNG might contribute to susceptibility to cervical cancer. |
| 2913 | 18337305 | Further analysis suggested that gene-gene interaction between CD28 and IFNG might contribute to susceptibility to cervical cancer. |
| 2914 | 18337305 | Further analysis suggested that gene-gene interaction between CD28 and IFNG might contribute to susceptibility to cervical cancer. |
| 2915 | 18337305 | Further analysis suggested that gene-gene interaction between CD28 and IFNG might contribute to susceptibility to cervical cancer. |
| 2916 | 18337305 | Further analysis suggested that gene-gene interaction between CD28 and IFNG might contribute to susceptibility to cervical cancer. |
| 2917 | 18337305 | Further analysis suggested that gene-gene interaction between CD28 and IFNG might contribute to susceptibility to cervical cancer. |
| 2918 | 18337305 | Further analysis suggested that gene-gene interaction between CD28 and IFNG might contribute to susceptibility to cervical cancer. |
| 2919 | 18337305 | Our results showed an epistatic effect between CD28 and IFNG genes in susceptibility to cervical cancer, a finding that might be relevant for a better understanding of the disease pathogenesis. |
| 2920 | 18337305 | Our results showed an epistatic effect between CD28 and IFNG genes in susceptibility to cervical cancer, a finding that might be relevant for a better understanding of the disease pathogenesis. |
| 2921 | 18337305 | Our results showed an epistatic effect between CD28 and IFNG genes in susceptibility to cervical cancer, a finding that might be relevant for a better understanding of the disease pathogenesis. |
| 2922 | 18337305 | Our results showed an epistatic effect between CD28 and IFNG genes in susceptibility to cervical cancer, a finding that might be relevant for a better understanding of the disease pathogenesis. |
| 2923 | 18337305 | Our results showed an epistatic effect between CD28 and IFNG genes in susceptibility to cervical cancer, a finding that might be relevant for a better understanding of the disease pathogenesis. |
| 2924 | 18337305 | Our results showed an epistatic effect between CD28 and IFNG genes in susceptibility to cervical cancer, a finding that might be relevant for a better understanding of the disease pathogenesis. |
| 2925 | 18337305 | Our results showed an epistatic effect between CD28 and IFNG genes in susceptibility to cervical cancer, a finding that might be relevant for a better understanding of the disease pathogenesis. |
| 2926 | 18296866 | The CLENDOs were also exposed to cytokines to assess differences in activation of nuclear factor kappa B signaling (NF-kappaB), induction of the transcription factor interferon regulatory factor 1 (IRF1), cytokine production, and cytokine-induced cell death. |
| 2927 | 18296866 | In response to TNF, for instance, both types of CLENDOs exhibited a rapid, 5-fold decrease in NF-kappaB inhibitor alpha (NFKBIA) protein expression (P<0.05), and a 4-fold increase in IRF1 expression (P<0.05), that did not differ with phenotype (P>0.05). |
| 2928 | 18296866 | Similarly, both types of CLENDOs produced tumor necrosis factor alpha and chemokine ligand 2 in response to IFNG stimulation (P<0.05) that did not differ with phenotype (P>0.05). |
| 2929 | 18287876 | We studied the associations between single nucleotide polymorphisms (SNPs) in cyclooxygenase 1 and 2 (PTGS1 and PTGS2), inducible nitric oxide synthase (NOS2A), interferon gamma (IFNG) and its receptor (IFNGR1), and risk of gastric precancerous lesions in a Venezuelan population characterized by high rates of H. pylori infection. |
| 2930 | 18287876 | A nonsynonymous SNP of NOS2A (Ser608Leu) and an SNP located in the promoter of IFNGR1 (C-56T) were associated with higher risk of atrophic gastritis [odds ratio (OR)=1.37, 95% confidence interval (CI)=1.01-1.86, and OR=1.49, 95% CI=1.01-2.19, respectively]. |
| 2931 | 18285333 | Nevertheless, the polycomb proteins, YY1, Mel-18, Ring1A, Ezh2, and Eed, bound to the Il4 and Ifng loci in a differential pattern. |
| 2932 | 18285333 | The recruitment of the polycomb proteins Mel-18 and Ezh2 to the cytokine promoters was inhibited in the presence of cyclosporine A, suggesting the involvement of NFAT. |
| 2933 | 18218610 | Cortisol (an active GC) reduced the mRNA expression of caspase 8 (CASP8) and caspase 3 (CASP3) and reduced the enzymatic activity of CASP3 and cell death induced by tumor necrosis factor (TNF) and interferon gamma (IFNG) in cultured bovine luteal cells. mRNAs and proteins of GC receptor (NR3C1), 11beta-hydroxysteroid dehydrogenase type 1 (HSD11B1), and HSD11B2 were expressed in CL throughout the estrous cycle. |
| 2934 | 18218610 | These results suggest that cortisol suppresses TNF-IFNG-induced apoptosis in vitro by reducing apoptosis signals via CASP8 and CASP3 in bovine CL and that the local increase in cortisol production resulting from increased HSD11B1 at the early and midluteal stages helps to maintain CL function by suppressing apoptosis of luteal cells. |
| 2935 | 18216180 | In this study, we compare the intensity of lipid peroxidation (estimated as malondialdehyde (MDA) serum levels), the antioxidant status, (measured as glutathione peroxidase (GPX) and superoxide dismutase (SOD) activities in red blood cells), and levels of cytokines derived from Th1 cells (such as interferon gamma (IFNG)), Th2 cells (such as interleukin (IL)-4), Th3 cells (such as transforming growth factor beta (TGF-beta)), and IL-6, IL-8, and tumor necrosis factor (TNF)-alpha in patients affected by chronic hepatitis C virus infection, 26 drinkers of alcohol and 40 nondrinkers of alcohol. |
| 2936 | 18216180 | In this study, we compare the intensity of lipid peroxidation (estimated as malondialdehyde (MDA) serum levels), the antioxidant status, (measured as glutathione peroxidase (GPX) and superoxide dismutase (SOD) activities in red blood cells), and levels of cytokines derived from Th1 cells (such as interferon gamma (IFNG)), Th2 cells (such as interleukin (IL)-4), Th3 cells (such as transforming growth factor beta (TGF-beta)), and IL-6, IL-8, and tumor necrosis factor (TNF)-alpha in patients affected by chronic hepatitis C virus infection, 26 drinkers of alcohol and 40 nondrinkers of alcohol. |
| 2937 | 18216180 | Patients showed significantly higher TNF-alpha (Z = 4.92, P < 0.001), IL-8 (Z = 4.95, P < 0.001), IFNG (Z = 2.81, P = 0.005), TGF-beta (t = 2.12, P = 0.037), MDA (Z = 5, P < 0.001), but lower IL-6 (Z = 3.61, P < 0.001) and GPX (F = 4.30, P < 0.05) than controls, whereas no differences were observed regarding IL-4 (Z = 0.35, P = 0.72), GPX and SOD activities. |
| 2938 | 18216180 | Patients showed significantly higher TNF-alpha (Z = 4.92, P < 0.001), IL-8 (Z = 4.95, P < 0.001), IFNG (Z = 2.81, P = 0.005), TGF-beta (t = 2.12, P = 0.037), MDA (Z = 5, P < 0.001), but lower IL-6 (Z = 3.61, P < 0.001) and GPX (F = 4.30, P < 0.05) than controls, whereas no differences were observed regarding IL-4 (Z = 0.35, P = 0.72), GPX and SOD activities. |
| 2939 | 18216180 | Alcoholics showed significantly higher TNF-alpha, but lower IL-4, MDA, and GPX, than nonalcoholics. |
| 2940 | 18216180 | Alcoholics showed significantly higher TNF-alpha, but lower IL-4, MDA, and GPX, than nonalcoholics. |
| 2941 | 18216180 | TNF-alpha was significantly related to albumin and prothrombin activity, whereas TGF-beta was significantly related to MDA levels. |
| 2942 | 18216180 | TNF-alpha was significantly related to albumin and prothrombin activity, whereas TGF-beta was significantly related to MDA levels. |
| 2943 | 19578489 | We identified 7 proteins that significantly differentiate HCC patients from hepatitis patients (p < 0.05) (AFP, CTNNB, CSF1, SELL, IGFBP6, IL6R, and VCAM1). |
| 2944 | 19578489 | Importantly, we also identified 8 proteins that significantly differentiate HCC patients with 'normal' levels of AFP (< 20 ng/ml) from hepatitis patients (p < 0.05) (IL1RN, IFNG, CDKN1A, RETN, CXCL14, CTNNB, FGF2, and SELL). |
| 2945 | 18158121 | Cytokine gene polymorphism in kidney transplantation--impact of TGF-beta 1, TNF-alpha and IL-6 on graft outcome. |
| 2946 | 18158121 | Eight single nucleotide polymorphisms (SNPs) including TNFA (-308), TGFB1 (cdns10, 25), IL-10 (-1082, -819, -592), IL-6 (-174) and IFNG (+874) were analyzed in 56 patients with stable graft function (SGF), 10 with CAN and 28 kidney donors by PCR-SSP method. |
| 2947 | 18158121 | No statistically significant differences in distribution of IL-10, IL-6 and IFNG genotypes between recipients with SGF and CAN were found. |
| 2948 | 18158121 | In conclusion our data suggest that the high producer genotype of profibrogenetic TGF-beta1, pro-inflammatory TNF-alpha and genetically determined low production of immunoregulatory IL-6 cytokine might be risk factors for CAN development. |
| 2949 | 18068529 | To determine ancestral allele in possible cancer-associated polymorphisms, DNA samples from 10 chimpanzees (Pan troglodytes) were sequenced for alleles corresponding to 17 polymorphisms: 8 short tandem repeats [IL1RN (alias IL-1RA) variable number tandem repeat (VNTR); TYMS (previously TS) VNTR; AR CAG repeat; dinucleotide repeats of UGT1A1, IGF1, IFNG (alias IFN-gamma), ESR1 (alias ER-alpha), and EGFR] and 9 single nucleotide polymorphisms (MMP1-1607 1G/2G, MMP3-1171 5A/6A, OGG1 Ser326Cys, ALDH2 Gly487Lys, TP53 Arg72Pro, ABCG2 Gln141Lys, MGMT Leu84Phe, SOD2 Ala-9Val, and MTHFR Ala222Val). |
| 2950 | 18068529 | To determine ancestral allele in possible cancer-associated polymorphisms, DNA samples from 10 chimpanzees (Pan troglodytes) were sequenced for alleles corresponding to 17 polymorphisms: 8 short tandem repeats [IL1RN (alias IL-1RA) variable number tandem repeat (VNTR); TYMS (previously TS) VNTR; AR CAG repeat; dinucleotide repeats of UGT1A1, IGF1, IFNG (alias IFN-gamma), ESR1 (alias ER-alpha), and EGFR] and 9 single nucleotide polymorphisms (MMP1-1607 1G/2G, MMP3-1171 5A/6A, OGG1 Ser326Cys, ALDH2 Gly487Lys, TP53 Arg72Pro, ABCG2 Gln141Lys, MGMT Leu84Phe, SOD2 Ala-9Val, and MTHFR Ala222Val). |
| 2951 | 18068529 | Dinucleotide repeat polymorphisms of IGF1, IFNG, ESR1, and EGFR were shared by chimpanzees, but the length of repeats tended to be longer in humans than in chimpanzees. |
| 2952 | 18068529 | Dinucleotide repeat polymorphisms of IGF1, IFNG, ESR1, and EGFR were shared by chimpanzees, but the length of repeats tended to be longer in humans than in chimpanzees. |
| 2953 | 18068529 | Thus, all of the possible cancer-associated polymorphisms tested have human-specific alleles, and the ancestral allele is lost in three polymorphisms (IL1RN VNTR, UGT1A1 CA repeat, and MMP3-1171 5A/6A), suggesting a possible involvement of human-specific alleles in cancer susceptibility. |
| 2954 | 18068529 | Thus, all of the possible cancer-associated polymorphisms tested have human-specific alleles, and the ancestral allele is lost in three polymorphisms (IL1RN VNTR, UGT1A1 CA repeat, and MMP3-1171 5A/6A), suggesting a possible involvement of human-specific alleles in cancer susceptibility. |
| 2955 | 18068331 | Low Sociable animals also showed alterations in lymph node expression of the immunoregulatory cytokine genes IFNG and IL4, and lower secondary IgG responses to tetanus vaccination. |
| 2956 | 18062835 | Single nucleotide polymorphisms (SNPs) in the TLR4 (rs4986790), IFNG (rs2430561 and rs1861493), STAT1 (rs1914408), IL1B (rs16944), NRAMP (SLC11A1 rs2276631), JUN (rs11688) and VDR (rs10735810) genes were determined. |
| 2957 | 18056971 | We identified four genetic risk sets for acute myocardial infarction (AMI) from information on functional gene variants that favor inflammation or modulate cholesterol metabolism: IL6 -174 G/C, TNF -308 G/A, IL10 -1082 G/A, SERPINA3 -51 G/T, IFNG +874 T/A, HMGCR -911 C/A, and APOE epsilon2/3/4; 316 patients and 461 healthy subjects, all Italian. |
| 2958 | 18056971 | The 'low intrinsic risk' set had alleles that downregulate inflammation and cholesterol synthesis (IL6, TNF, ILl0, HMGCR). |
| 2959 | 18056971 | 'AMI across a broad age range' carried multiple proinflammatory alleles (IL6, TNF, IL10, SERPINA3): All 72 persons like this set were affected yet had relatively low plasma cholesterol levels. |
| 2960 | 18056971 | 'A subset of AMI in middle age' had numerous proinflammatory alleles (IL6, TNF, SERPINA3, IFNG, HMGCR). |
| 2961 | 18056971 | 'AMI after age 80' had a reduced risk set (IL6, IL10, IFNG). |
| 2962 | 18026101 | The LPS hypersensitivity phenotype is not suppressed by mutations in Myd88, Trif, Tnf, Tnfrsf1a, Ifnb, Ifng or Stat1, genes contributing to LPS responses, and results from an abnormality extrinsic to hematopoietic cells. |
| 2963 | 18006399 | Gene expression of RANKL, OPG, TGFB2, IFNG and CSF-1 was analyzed after no mechanical stimulation (control), exposure to compression or exposure to micromotions. |
| 2964 | 18006399 | Gene expression of RANKL, OPG, TGFB2, IFNG and CSF-1 was analyzed after no mechanical stimulation (control), exposure to compression or exposure to micromotions. |
| 2965 | 18006399 | We observed an 8-fold upregulation of RANKL after exposure to micromotions, and downregulation of OPG, IFNG and TGFB2. |
| 2966 | 18006399 | We observed an 8-fold upregulation of RANKL after exposure to micromotions, and downregulation of OPG, IFNG and TGFB2. |
| 2967 | 18006399 | The RANKL:OPG ratio was upregulated 24-fold after micromotions. |
| 2968 | 18006399 | The RANKL:OPG ratio was upregulated 24-fold after micromotions. |
| 2969 | 17994425 | Interleukin (IL)-12, IL-2, interferon-gamma gene polymorphisms in subacute sclerosing panencephalitis patients. |
| 2970 | 17994425 | Interleukin (IL)-12, IL-2, interferon-gamma gene polymorphisms in subacute sclerosing panencephalitis patients. |
| 2971 | 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. |
| 2972 | 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. |
| 2973 | 17989360 | We have found that, in response to interferon gamma (IFNG), mouse Sertoli cells strongly up-regulate the negative co-stimulatory ligand B7-H1 but remain devoid of positive co-stimulatory molecules. |
| 2974 | 17989360 | We have found that, in response to interferon gamma (IFNG), mouse Sertoli cells strongly up-regulate the negative co-stimulatory ligand B7-H1 but remain devoid of positive co-stimulatory molecules. |
| 2975 | 17989360 | Blockade of B7-H1 on the Sertoli cell surface resulted in enhanced proliferation of CD8(+) T cells cocultured with Sertoli cells. |
| 2976 | 17989360 | Blockade of B7-H1 on the Sertoli cell surface resulted in enhanced proliferation of CD8(+) T cells cocultured with Sertoli cells. |
| 2977 | 17989360 | Moreover, IFNG-stimulated Sertoli cells were found to express, concurrent with B7-H1, MHC class II. |
| 2978 | 17989360 | Moreover, IFNG-stimulated Sertoli cells were found to express, concurrent with B7-H1, MHC class II. |
| 2979 | 17989360 | Interestingly, we found that coculturing T cells with Sertoli cells can indeed induce an increase in CD4(+)CD25(+)(officially known as IL2RA)FOXP3(+) Tregs and a decrease in CD4(+)CD25(-) T cells, suggesting Sertoli cell-mediated Treg conversion; this process was found to be B7-H1-independent. |
| 2980 | 17989360 | Interestingly, we found that coculturing T cells with Sertoli cells can indeed induce an increase in CD4(+)CD25(+)(officially known as IL2RA)FOXP3(+) Tregs and a decrease in CD4(+)CD25(-) T cells, suggesting Sertoli cell-mediated Treg conversion; this process was found to be B7-H1-independent. |
| 2981 | 17989360 | Altogether these data show that Sertoli cells are potentially capable of down-regulating the local immune response, on one hand by directly inhibiting CD8(+) T cell proliferation through B7-H1 and, on the other hand, by inducing an increase in Tregs that might suppress other bystander T cells. |
| 2982 | 17989360 | Altogether these data show that Sertoli cells are potentially capable of down-regulating the local immune response, on one hand by directly inhibiting CD8(+) T cell proliferation through B7-H1 and, on the other hand, by inducing an increase in Tregs that might suppress other bystander T cells. |
| 2983 | 17982583 | In situ hybridization analysis of LPS/IFNg and experimental autoimmune encephalomyelitis (EAE)-induced CNS inflammation revealed that only a subset of CNS macrophages express Golli-MBP. |
| 2984 | 17981204 | This cytokine is produced predominantly by natural killer (NK) and natural killer T (NKT) cells as part of the innate immune response, and by Th1 CD4 and CD8 cytotoxic T lymphocyte (CTL) effector T cells once antigen-specific immunity develops. |
| 2985 | 17981204 | The epigenetic modifications and three-dimensional structure of the Ifng locus in naive CD4 T cells, and the modifications they undergo as these cells differentiate into effector T cells, suggest a model whereby the chromatin architecture of Ifng is poised to facilitate either rapid opening or silencing during Th1 or Th2 differentiation, respectively. |
| 2986 | 17715431 | The proportions of CD4(+) and CD8(+) cells were unchanged, but the number of gamma delta T cells was increased by coculture with luteal cells. |
| 2987 | 17715431 | The concentrations of interferon-gamma (IFNG) and interleukin 10 (IL10) were increased in luteal cell-T cell cocultures, whereas IL4 was undetectable, and IL12 was barely detectable in culture medium. |
| 2988 | 17675500 | IL-10 is excluded from the functional cytokine memory of human CD4+ memory T lymphocytes. |
| 2989 | 17675500 | IL-10 is excluded from the functional cytokine memory of human CD4+ memory T lymphocytes. |
| 2990 | 17675500 | Memory Th cells secreting IL-10 or IFN-gamma were directly isolated ex vivo from peripheral blood of healthy volunteers, and the DNA methylation status of IL10 and IFNG was assessed. |
| 2991 | 17675500 | Memory Th cells secreting IL-10 or IFN-gamma were directly isolated ex vivo from peripheral blood of healthy volunteers, and the DNA methylation status of IL10 and IFNG was assessed. |
| 2992 | 17675500 | Our data indicate that IL10 does not become epigenetically marked in human memory Th cells unlike effector cytokine genes such as IFNG. |
| 2993 | 17675500 | Our data indicate that IL10 does not become epigenetically marked in human memory Th cells unlike effector cytokine genes such as IFNG. |
| 2994 | 17675500 | The exclusion of IL-10, but not effector cytokines, from the functional memory of human CD4(+) T lymphocytes ex vivo may reflect the need for appropriate regulation of IL-10 secretion, due to its potent immunoregulatory potential. |
| 2995 | 17675500 | The exclusion of IL-10, but not effector cytokines, from the functional memory of human CD4(+) T lymphocytes ex vivo may reflect the need for appropriate regulation of IL-10 secretion, due to its potent immunoregulatory potential. |
| 2996 | 17611223 | The IL-4/IL-13/Stat6 signalling pathway promotes luminal mammary epithelial cell development. |
| 2997 | 17611223 | The Th1/Th2 cytokine milieu is a key paradigm in lineage commitment, and IL-4 (Il4), IL-13 (Il13) and Stat6 are important mediators of Th2 development. |
| 2998 | 17611223 | Thus, the Th1 cytokines IL-12 (Il12), interferon gamma (INFgamma; also known as Ifng) and Tnfalpha are downregulated concomitantly with the upregulation of the Th2 cytokines IL-4, IL-13 and IL-5 (Il5) as epithelial cells commit to the luminal lineage. |
| 2999 | 17611223 | Moreover, we show that Th2 cytokines play a crucial role in mammary gland development in vivo, because differentiation and alveolar morphogenesis are reduced in both Stat6 and IL-4/IL-13 doubly deficient mice during pregnancy. |
| 3000 | 17583733 | Recruitment of the RNA polymerase II transcription complex to the promoter of the Ifng gene has been studied by chromatin immunoprecipitation (ChIP) in activated functionally different CD4+ T helper (Th) cell subsets. |
| 3001 | 17546034 | Here we explored the formation of marks of repressive methylation of histone 3 at lysine 9 (H3-K9) and of H3-K27 at the locus encoding interferon-gamma (Ifng locus) during the commitment of naive T cells to the T helper type 1 (TH1) and TH2 lineages. |
| 3002 | 17546034 | In contrast, TH2 differentiation caused loss of methylation of H3-K9 and gain of methylation of H3-K27 by mechanisms dependent on the transcription factors GATA-3 and STAT6. |
| 3003 | 17546033 | Here our evolutionary analysis showed that the mouse Ifng locus diverged from the ancestral locus as a result of structural rearrangements producing deletion of the neighboring gene encoding interleukin 26 and disrupting synteny 57 kilobases upstream of Ifng. |
| 3004 | 17509455 | Polymorphisms of interferon-gamma, interleukin-10, and interleukin-12 genes in myasthenia gravis. |
| 3005 | 17509455 | Polymorphisms of interferon-gamma, interleukin-10, and interleukin-12 genes in myasthenia gravis. |
| 3006 | 17509455 | Polymorphisms of interferon-gamma, interleukin-10, and interleukin-12 genes in myasthenia gravis. |
| 3007 | 17509455 | Polymorphisms of interferon-gamma, interleukin-10, and interleukin-12 genes in myasthenia gravis. |
| 3008 | 17509455 | To assess the involvement of polymorphisms in genetic susceptibility to myasthenia gravis (MG), this study analyzed four polymorphisms of interferon (IFN)-gamma, interleukin (IL)-10, and IL-12 genes in 115 patients and 204 healthy controls (HC). |
| 3009 | 17509455 | To assess the involvement of polymorphisms in genetic susceptibility to myasthenia gravis (MG), this study analyzed four polymorphisms of interferon (IFN)-gamma, interleukin (IL)-10, and IL-12 genes in 115 patients and 204 healthy controls (HC). |
| 3010 | 17509455 | To assess the involvement of polymorphisms in genetic susceptibility to myasthenia gravis (MG), this study analyzed four polymorphisms of interferon (IFN)-gamma, interleukin (IL)-10, and IL-12 genes in 115 patients and 204 healthy controls (HC). |
| 3011 | 17509455 | To assess the involvement of polymorphisms in genetic susceptibility to myasthenia gravis (MG), this study analyzed four polymorphisms of interferon (IFN)-gamma, interleukin (IL)-10, and IL-12 genes in 115 patients and 204 healthy controls (HC). |
| 3012 | 17509455 | IFNG +874T carriers were less frequent in MG, in patients with anti-acetylcholine receptor (AChR) (63%) and anti-titin (56.2%) antibodies compared with HC (p = 0.01 for all, OR: 0.5, 0.5, and 0.4, respectively). |
| 3013 | 17509455 | IFNG +874T carriers were less frequent in MG, in patients with anti-acetylcholine receptor (AChR) (63%) and anti-titin (56.2%) antibodies compared with HC (p = 0.01 for all, OR: 0.5, 0.5, and 0.4, respectively). |
| 3014 | 17509455 | IFNG +874T carriers were less frequent in MG, in patients with anti-acetylcholine receptor (AChR) (63%) and anti-titin (56.2%) antibodies compared with HC (p = 0.01 for all, OR: 0.5, 0.5, and 0.4, respectively). |
| 3015 | 17509455 | IFNG +874T carriers were less frequent in MG, in patients with anti-acetylcholine receptor (AChR) (63%) and anti-titin (56.2%) antibodies compared with HC (p = 0.01 for all, OR: 0.5, 0.5, and 0.4, respectively). |
| 3016 | 17509455 | The presence of thymoma was also associated with lower frequency of IFNG +874T allele (p = 0.018, OR = 0.34). |
| 3017 | 17509455 | The presence of thymoma was also associated with lower frequency of IFNG +874T allele (p = 0.018, OR = 0.34). |
| 3018 | 17509455 | The presence of thymoma was also associated with lower frequency of IFNG +874T allele (p = 0.018, OR = 0.34). |
| 3019 | 17509455 | The presence of thymoma was also associated with lower frequency of IFNG +874T allele (p = 0.018, OR = 0.34). |
| 3020 | 17505015 | Furthermore, lipopolysaccharide (LPS) stimulation of dendritic cells prompts Gata1 up-regulation, which is accompanied by increased levels of BclX and Ifng. |
| 3021 | 17392024 | Association of polymorphisms in IL-12/IFN-gamma pathway genes with susceptibility to pulmonary tuberculosis in Indonesia. |
| 3022 | 17392024 | Association of polymorphisms in IL-12/IFN-gamma pathway genes with susceptibility to pulmonary tuberculosis in Indonesia. |
| 3023 | 17392024 | Association of polymorphisms in IL-12/IFN-gamma pathway genes with susceptibility to pulmonary tuberculosis in Indonesia. |
| 3024 | 17392024 | Association of polymorphisms in IL-12/IFN-gamma pathway genes with susceptibility to pulmonary tuberculosis in Indonesia. |
| 3025 | 17392024 | Association of polymorphisms in IL-12/IFN-gamma pathway genes with susceptibility to pulmonary tuberculosis in Indonesia. |
| 3026 | 17392024 | Upon infection with mycobacteria the IL-12/IFN-gamma axis plays an essential role in the activation of cell-mediated immunity required for the elimination of pathogens. |
| 3027 | 17392024 | Upon infection with mycobacteria the IL-12/IFN-gamma axis plays an essential role in the activation of cell-mediated immunity required for the elimination of pathogens. |
| 3028 | 17392024 | Upon infection with mycobacteria the IL-12/IFN-gamma axis plays an essential role in the activation of cell-mediated immunity required for the elimination of pathogens. |
| 3029 | 17392024 | Upon infection with mycobacteria the IL-12/IFN-gamma axis plays an essential role in the activation of cell-mediated immunity required for the elimination of pathogens. |
| 3030 | 17392024 | Upon infection with mycobacteria the IL-12/IFN-gamma axis plays an essential role in the activation of cell-mediated immunity required for the elimination of pathogens. |
| 3031 | 17392024 | Mutations in genes of the IL-12/IFN-gamma axis are known to cause extreme susceptibility to infection with environmental mycobacteria, and subtle variations in these genes may influence susceptibility to more virulent mycobacteria. |
| 3032 | 17392024 | Mutations in genes of the IL-12/IFN-gamma axis are known to cause extreme susceptibility to infection with environmental mycobacteria, and subtle variations in these genes may influence susceptibility to more virulent mycobacteria. |
| 3033 | 17392024 | Mutations in genes of the IL-12/IFN-gamma axis are known to cause extreme susceptibility to infection with environmental mycobacteria, and subtle variations in these genes may influence susceptibility to more virulent mycobacteria. |
| 3034 | 17392024 | Mutations in genes of the IL-12/IFN-gamma axis are known to cause extreme susceptibility to infection with environmental mycobacteria, and subtle variations in these genes may influence susceptibility to more virulent mycobacteria. |
| 3035 | 17392024 | Mutations in genes of the IL-12/IFN-gamma axis are known to cause extreme susceptibility to infection with environmental mycobacteria, and subtle variations in these genes may influence susceptibility to more virulent mycobacteria. |
| 3036 | 17392024 | We analyzed the distribution of polymorphisms in four essential genes from the IL-12/IFN-gamma axis, IL12B, IL12RB1, IFNG and IFNGR1, in 382 pulmonary tuberculosis patients and 437 healthy controls from an endemic region in Jakarta, Indonesia. |
| 3037 | 17392024 | We analyzed the distribution of polymorphisms in four essential genes from the IL-12/IFN-gamma axis, IL12B, IL12RB1, IFNG and IFNGR1, in 382 pulmonary tuberculosis patients and 437 healthy controls from an endemic region in Jakarta, Indonesia. |
| 3038 | 17392024 | We analyzed the distribution of polymorphisms in four essential genes from the IL-12/IFN-gamma axis, IL12B, IL12RB1, IFNG and IFNGR1, in 382 pulmonary tuberculosis patients and 437 healthy controls from an endemic region in Jakarta, Indonesia. |
| 3039 | 17392024 | We analyzed the distribution of polymorphisms in four essential genes from the IL-12/IFN-gamma axis, IL12B, IL12RB1, IFNG and IFNGR1, in 382 pulmonary tuberculosis patients and 437 healthy controls from an endemic region in Jakarta, Indonesia. |
| 3040 | 17392024 | We analyzed the distribution of polymorphisms in four essential genes from the IL-12/IFN-gamma axis, IL12B, IL12RB1, IFNG and IFNGR1, in 382 pulmonary tuberculosis patients and 437 healthy controls from an endemic region in Jakarta, Indonesia. |
| 3041 | 17392024 | Six functional SNPs (-2C>T, 467G>A, 641A>G, 1312C>T, 1573G>A, 1781G>A) in IL12RB1, an IL12B promoter insertion/deletion polymorphism and CA repeats in IFNG and IFNGR1 were analyzed in the cohort. |
| 3042 | 17392024 | Six functional SNPs (-2C>T, 467G>A, 641A>G, 1312C>T, 1573G>A, 1781G>A) in IL12RB1, an IL12B promoter insertion/deletion polymorphism and CA repeats in IFNG and IFNGR1 were analyzed in the cohort. |
| 3043 | 17392024 | Six functional SNPs (-2C>T, 467G>A, 641A>G, 1312C>T, 1573G>A, 1781G>A) in IL12RB1, an IL12B promoter insertion/deletion polymorphism and CA repeats in IFNG and IFNGR1 were analyzed in the cohort. |
| 3044 | 17392024 | Six functional SNPs (-2C>T, 467G>A, 641A>G, 1312C>T, 1573G>A, 1781G>A) in IL12RB1, an IL12B promoter insertion/deletion polymorphism and CA repeats in IFNG and IFNGR1 were analyzed in the cohort. |
| 3045 | 17392024 | Six functional SNPs (-2C>T, 467G>A, 641A>G, 1312C>T, 1573G>A, 1781G>A) in IL12RB1, an IL12B promoter insertion/deletion polymorphism and CA repeats in IFNG and IFNGR1 were analyzed in the cohort. |
| 3046 | 17392024 | The IFNGR1 allele CA(12) (p=0.004) and genotype CA(12)/CA(12) (p=0.01; OR 0.5) were associated with protection from pulmonary tuberculosis. |
| 3047 | 17392024 | The IFNGR1 allele CA(12) (p=0.004) and genotype CA(12)/CA(12) (p=0.01; OR 0.5) were associated with protection from pulmonary tuberculosis. |
| 3048 | 17392024 | The IFNGR1 allele CA(12) (p=0.004) and genotype CA(12)/CA(12) (p=0.01; OR 0.5) were associated with protection from pulmonary tuberculosis. |
| 3049 | 17392024 | The IFNGR1 allele CA(12) (p=0.004) and genotype CA(12)/CA(12) (p=0.01; OR 0.5) were associated with protection from pulmonary tuberculosis. |
| 3050 | 17392024 | The IFNGR1 allele CA(12) (p=0.004) and genotype CA(12)/CA(12) (p=0.01; OR 0.5) were associated with protection from pulmonary tuberculosis. |
| 3051 | 17337057 | Seven genes identified by suppression subtractive hybridization as up-regulated in the mesenteric lymph nodes at 24h (h) post-inoculation (p.i.) in serovar Choleraesuis-infected pigs (ARPC2, CCT7, HSPH1, LCP1, PTMA, SDCBP, VCP) and three genes in serovar Typhimurium-infected pigs (CD47/IAP, CXCL10, SCARB2) were analyzed by real-time PCR at 8h, 24 h, 48 h, 7 days (d) and 21 d p.i. |
| 3052 | 17337057 | Seven genes identified by suppression subtractive hybridization as up-regulated in the mesenteric lymph nodes at 24h (h) post-inoculation (p.i.) in serovar Choleraesuis-infected pigs (ARPC2, CCT7, HSPH1, LCP1, PTMA, SDCBP, VCP) and three genes in serovar Typhimurium-infected pigs (CD47/IAP, CXCL10, SCARB2) were analyzed by real-time PCR at 8h, 24 h, 48 h, 7 days (d) and 21 d p.i. |
| 3053 | 17337057 | (IFNG, IL12A, IL4, IL8, CSF2) coincided with extended transcriptional activation throughout the 21 d infection (IFNG, INDO, SOCS1, STAT1, IL1B, IL6, IL8, SLC11A1). |
| 3054 | 17337057 | (IFNG, IL12A, IL4, IL8, CSF2) coincided with extended transcriptional activation throughout the 21 d infection (IFNG, INDO, SOCS1, STAT1, IL1B, IL6, IL8, SLC11A1). |
| 3055 | 17337057 | The serovar Typhimurium-infected swine presented a more transient induction of immune-related genes (IFNG, INDO, IRF1, SOCS1, STAT1, IL1B, IL8, SLC11A1) early in the infection (24-48 h) followed by a significant repression of IL12A, IL12B, IL4, IL8 and CSF2. |
| 3056 | 17337057 | The serovar Typhimurium-infected swine presented a more transient induction of immune-related genes (IFNG, INDO, IRF1, SOCS1, STAT1, IL1B, IL8, SLC11A1) early in the infection (24-48 h) followed by a significant repression of IL12A, IL12B, IL4, IL8 and CSF2. |
| 3057 | 17215490 | After LPS administration, inflammatory cytokines tumor necrosis factor-alpha (TNFA) and IL6 were markedly increased in serum, uterine, and conceptus tissues in Il10(-/-) mice compared with Il10(+/+) mice, with elevated local synthesis of Tnfa and Il6 mRNAs in the gestational tissues. |
| 3058 | 17215490 | IL1A and IL12p40 were similarly elevated in serum and gestational tissues, whereas interferon gamma (IFNG) and soluble TNFRII content were unchanged in the absence of IL10. |
| 3059 | 17215490 | IL10 genotype also influenced the responsiveness of mice to a TNFA antagonist, etanercept. |
| 3060 | 17215490 | Fetal loss in Il10(-/-) mice was partly alleviated by moderate or high doses of etanercept, whereas Il10(+/+) mice were refractory to high-dose etanercept, consistent with attenuation by IL10 status of TNFA bioavailability after etanercept treatment. |
| 3061 | 17215490 | These data show that IL10 modulates resistance to inflammatory stimuli by downregulating expression of proinflammatory cytokines TNFA, IL6, IL1A, and IL12, acting to protect against inflammation-induced pathology in the implantation site. |
| 3062 | 17195845 | Transcription factors T-bet and Runx3 cooperate to activate Ifng and silence Il4 in T helper type 1 cells. |
| 3063 | 17195845 | Transcription factors T-bet and Runx3 cooperate to activate Ifng and silence Il4 in T helper type 1 cells. |
| 3064 | 17195845 | Transcription factors T-bet and Runx3 cooperate to activate Ifng and silence Il4 in T helper type 1 cells. |
| 3065 | 17195845 | Here we show that the transcription factor Runx3 is induced in T helper type 1 (T(H)1) cells in a T-bet-dependent manner, and that both transcription factors T-bet and Runx3 are required for maximal production of interferon-gamma (IFN-gamma) and silencing of the gene encoding interleukin 4 (Il4) in T(H)1 cells. |
| 3066 | 17195845 | Here we show that the transcription factor Runx3 is induced in T helper type 1 (T(H)1) cells in a T-bet-dependent manner, and that both transcription factors T-bet and Runx3 are required for maximal production of interferon-gamma (IFN-gamma) and silencing of the gene encoding interleukin 4 (Il4) in T(H)1 cells. |
| 3067 | 17195845 | Here we show that the transcription factor Runx3 is induced in T helper type 1 (T(H)1) cells in a T-bet-dependent manner, and that both transcription factors T-bet and Runx3 are required for maximal production of interferon-gamma (IFN-gamma) and silencing of the gene encoding interleukin 4 (Il4) in T(H)1 cells. |
| 3068 | 17195845 | T-bet does not repress Il4 in Runx3-deficient T(H)2 cells, but coexpression of Runx3 and T-bet induces potent repression in those cells. |
| 3069 | 17195845 | T-bet does not repress Il4 in Runx3-deficient T(H)2 cells, but coexpression of Runx3 and T-bet induces potent repression in those cells. |
| 3070 | 17195845 | T-bet does not repress Il4 in Runx3-deficient T(H)2 cells, but coexpression of Runx3 and T-bet induces potent repression in those cells. |
| 3071 | 17195845 | Both T-bet and Runx3 bind to the Ifng promoter and the Il4 silencer, and deletion of the silencer decreases the sensitivity of Il4 to repression by either factor. |
| 3072 | 17195845 | Both T-bet and Runx3 bind to the Ifng promoter and the Il4 silencer, and deletion of the silencer decreases the sensitivity of Il4 to repression by either factor. |
| 3073 | 17195845 | Both T-bet and Runx3 bind to the Ifng promoter and the Il4 silencer, and deletion of the silencer decreases the sensitivity of Il4 to repression by either factor. |
| 3074 | 17195845 | Our data indicate that cytokine gene expression in T(H)1 cells may be controlled by a feed-forward regulatory circuit in which T-bet induces Runx3 and then 'partners' with Runx3 to direct lineage-specific gene activation and silencing. |
| 3075 | 17195845 | Our data indicate that cytokine gene expression in T(H)1 cells may be controlled by a feed-forward regulatory circuit in which T-bet induces Runx3 and then 'partners' with Runx3 to direct lineage-specific gene activation and silencing. |
| 3076 | 17195845 | Our data indicate that cytokine gene expression in T(H)1 cells may be controlled by a feed-forward regulatory circuit in which T-bet induces Runx3 and then 'partners' with Runx3 to direct lineage-specific gene activation and silencing. |
| 3077 | 17138064 | Effects of IL10, IL6 and IFNG gene polymorphisms, known to affect CMV infectivity, were investigated in 71 CMV seronegative recipients of grafts from CMV seropositive cadaver donors. |
| 3078 | 17136124 | IFNG and IFNGR1 gene polymorphisms and susceptibility to post-kala-azar dermal leishmaniasis in Sudan. |
| 3079 | 17136124 | IFNG and IFNGR1 gene polymorphisms and susceptibility to post-kala-azar dermal leishmaniasis in Sudan. |
| 3080 | 17136124 | IFNG and IFNGR1 gene polymorphisms and susceptibility to post-kala-azar dermal leishmaniasis in Sudan. |
| 3081 | 17136124 | IFNG and IFNGR1 gene polymorphisms and susceptibility to post-kala-azar dermal leishmaniasis in Sudan. |
| 3082 | 17136124 | Post-kala-azar dermal leishmanaisis (PKDL) in Sudan is associated with elevated interferon-gamma (IFN-gamma). |
| 3083 | 17136124 | Post-kala-azar dermal leishmanaisis (PKDL) in Sudan is associated with elevated interferon-gamma (IFN-gamma). |
| 3084 | 17136124 | Post-kala-azar dermal leishmanaisis (PKDL) in Sudan is associated with elevated interferon-gamma (IFN-gamma). |
| 3085 | 17136124 | Post-kala-azar dermal leishmanaisis (PKDL) in Sudan is associated with elevated interferon-gamma (IFN-gamma). |
| 3086 | 17136124 | To study interferon-gamma pathways in PKDL, we genotyped 80 trios from the Masalit ethnic group for polymorphisms at -470 ins/delTT, -270T/C, -56T/C and +95T/C in IFNGR1 and at -179G/A and +874T/A in IFNG. |
| 3087 | 17136124 | To study interferon-gamma pathways in PKDL, we genotyped 80 trios from the Masalit ethnic group for polymorphisms at -470 ins/delTT, -270T/C, -56T/C and +95T/C in IFNGR1 and at -179G/A and +874T/A in IFNG. |
| 3088 | 17136124 | To study interferon-gamma pathways in PKDL, we genotyped 80 trios from the Masalit ethnic group for polymorphisms at -470 ins/delTT, -270T/C, -56T/C and +95T/C in IFNGR1 and at -179G/A and +874T/A in IFNG. |
| 3089 | 17136124 | To study interferon-gamma pathways in PKDL, we genotyped 80 trios from the Masalit ethnic group for polymorphisms at -470 ins/delTT, -270T/C, -56T/C and +95T/C in IFNGR1 and at -179G/A and +874T/A in IFNG. |
| 3090 | 17136124 | When compared with data on malaria associations from Gambia, the results suggest a complex pattern of haplotypic variation at the IFNGR1 promoter locus associated with different infectious disease in African populations that reflect the complex roles of IFN-gamma in parasite killing versus inflammation and pathogenesis. |
| 3091 | 17136124 | When compared with data on malaria associations from Gambia, the results suggest a complex pattern of haplotypic variation at the IFNGR1 promoter locus associated with different infectious disease in African populations that reflect the complex roles of IFN-gamma in parasite killing versus inflammation and pathogenesis. |
| 3092 | 17136124 | When compared with data on malaria associations from Gambia, the results suggest a complex pattern of haplotypic variation at the IFNGR1 promoter locus associated with different infectious disease in African populations that reflect the complex roles of IFN-gamma in parasite killing versus inflammation and pathogenesis. |
| 3093 | 17136124 | When compared with data on malaria associations from Gambia, the results suggest a complex pattern of haplotypic variation at the IFNGR1 promoter locus associated with different infectious disease in African populations that reflect the complex roles of IFN-gamma in parasite killing versus inflammation and pathogenesis. |
| 3094 | 17093503 | Here, we analyzed nuclear matrix attachment regions (MARs) in the Ifng gene by DNA array technique in unactivated and activated CD4+ Th cells. |
| 3095 | 17093503 | Here, we analyzed nuclear matrix attachment regions (MARs) in the Ifng gene by DNA array technique in unactivated and activated CD4+ Th cells. |
| 3096 | 17093503 | The data suggest that such structural dynamics provide the means for transcriptional regulation of the Ifng gene in the course of activation and differentiation of CD4+Th cells. |
| 3097 | 17093503 | The data suggest that such structural dynamics provide the means for transcriptional regulation of the Ifng gene in the course of activation and differentiation of CD4+Th cells. |
| 3098 | 16988213 | These HY-specific CD8+ T cells produced interferon gamma (IFNG) following peptide stimulation, demonstrating their functional capacity. |
| 3099 | 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. |
| 3100 | 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. |
| 3101 | 16934001 | The previously reported L706S, like the novel Q463H and E320Q alleles, are intrinsically deleterious for both interferon gamma (IFNG)-induced gamma-activating factor-mediated immunity and interferon alpha (IFNA)-induced interferon-stimulated genes factor 3-mediated immunity, as shown in STAT1-deficient cells transfected with the corresponding alleles. |
| 3102 | 16934001 | The previously reported L706S, like the novel Q463H and E320Q alleles, are intrinsically deleterious for both interferon gamma (IFNG)-induced gamma-activating factor-mediated immunity and interferon alpha (IFNA)-induced interferon-stimulated genes factor 3-mediated immunity, as shown in STAT1-deficient cells transfected with the corresponding alleles. |
| 3103 | 16934001 | Indeed, IFNA-induced interferon-stimulated genes factor 3-mediated immunity is not affected, and these patients are not particularly susceptible to viral disease, unlike patients homozygous for other, equally deleterious STAT1 mutations recessive for both phenotypes. |
| 3104 | 16934001 | Indeed, IFNA-induced interferon-stimulated genes factor 3-mediated immunity is not affected, and these patients are not particularly susceptible to viral disease, unlike patients homozygous for other, equally deleterious STAT1 mutations recessive for both phenotypes. |
| 3105 | 16934001 | The three STAT1 alleles are therefore dominant for IFNG-mediated antimycobacterial immunity but recessive for IFNA-mediated antiviral immunity at the cellular and clinical levels. |
| 3106 | 16934001 | The three STAT1 alleles are therefore dominant for IFNG-mediated antimycobacterial immunity but recessive for IFNA-mediated antiviral immunity at the cellular and clinical levels. |
| 3107 | 16930709 | Network analysis indicates that TNF and NFKB1 are key regulators of gene expression at this early time point. |
| 3108 | 16930709 | At 4h, IL1B in addition to TNF and NFKB1 play dominant roles in the up-regulation of immune gene expression, whereas by 8h this function is mediated by TNF, IFNG, and MYC. |
| 3109 | 16845603 | A novel finding was that two transglutaminase family genes (TGM1 and TGM3) showed dramatic increases in expression postinoculation; combined with several other apoptotic genes, they indicated the induction of apoptotic pathways during SC infection. |
| 3110 | 16845603 | Genes induced by IFNs (GBP1, GBP2, C1S, C1R, MHC2TA, PSMB8, TAP1, TAP2) showed increased expression during porcine lung infection. |
| 3111 | 16835788 | The polymorphic positions studied were: TNFA -1031, -863, -857, -851, -574, -376, -308, -238, +488; TGFB1 -988, -800, -509, +869, +915, +652, +673, +713, +788; IL10 -1082, -819, -592; IL6 -174; IFNG -333, +874. |
| 3112 | 16835788 | The polymorphic positions studied were: TNFA -1031, -863, -857, -851, -574, -376, -308, -238, +488; TGFB1 -988, -800, -509, +869, +915, +652, +673, +713, +788; IL10 -1082, -819, -592; IL6 -174; IFNG -333, +874. |
| 3113 | 16835788 | The polymorphic positions studied were: TNFA -1031, -863, -857, -851, -574, -376, -308, -238, +488; TGFB1 -988, -800, -509, +869, +915, +652, +673, +713, +788; IL10 -1082, -819, -592; IL6 -174; IFNG -333, +874. |
| 3114 | 16835788 | It was found that TNFA -238 GA, TGFB1 -509 CT, -800 GG, IFNG +874 AT, IL6 -174 GG, IL10 -1082 GA genotypes were significantly decreased, while TNFA -238 AA, -857 CC, TGFB1 -509 TT, IFNG +874 AA, IL6 -174 CC, IL10 -1082 AA, -819 TT, -592 AA genotypes were significantly increased, in MM. |
| 3115 | 16835788 | It was found that TNFA -238 GA, TGFB1 -509 CT, -800 GG, IFNG +874 AT, IL6 -174 GG, IL10 -1082 GA genotypes were significantly decreased, while TNFA -238 AA, -857 CC, TGFB1 -509 TT, IFNG +874 AA, IL6 -174 CC, IL10 -1082 AA, -819 TT, -592 AA genotypes were significantly increased, in MM. |
| 3116 | 16835788 | It was found that TNFA -238 GA, TGFB1 -509 CT, -800 GG, IFNG +874 AT, IL6 -174 GG, IL10 -1082 GA genotypes were significantly decreased, while TNFA -238 AA, -857 CC, TGFB1 -509 TT, IFNG +874 AA, IL6 -174 CC, IL10 -1082 AA, -819 TT, -592 AA genotypes were significantly increased, in MM. |
| 3117 | 16835788 | This suggests that genotypes provisionally associated with low expression of pro-inflammatory and immunomodulatory TNF-alpha, IFN-gamma and IL-6 and anti-inflammatory IL-10 and TGF-beta1 could be involved in the mechanisms of cancer progression and escape from immunosurveillance. |
| 3118 | 16835788 | This suggests that genotypes provisionally associated with low expression of pro-inflammatory and immunomodulatory TNF-alpha, IFN-gamma and IL-6 and anti-inflammatory IL-10 and TGF-beta1 could be involved in the mechanisms of cancer progression and escape from immunosurveillance. |
| 3119 | 16835788 | This suggests that genotypes provisionally associated with low expression of pro-inflammatory and immunomodulatory TNF-alpha, IFN-gamma and IL-6 and anti-inflammatory IL-10 and TGF-beta1 could be involved in the mechanisms of cancer progression and escape from immunosurveillance. |
| 3120 | 16792541 | Interferon gamma-secreting HCV-specific CD8+ T cells in the liver of patients with chronic C hepatitis: relation to liver fibrosis--ANRS HC EP07 study. |
| 3121 | 16792541 | Interferon gamma-secreting HCV-specific CD8+ T cells in the liver of patients with chronic C hepatitis: relation to liver fibrosis--ANRS HC EP07 study. |
| 3122 | 16792541 | An IFNg-specific CD8+ T-cell response was detected in the liver samples of 47% of patients which was significantly related to a lower stage of fibrosis (P = 0.02) and a lower progression rate of fibrosis (P = 0.01). |
| 3123 | 16792541 | An IFNg-specific CD8+ T-cell response was detected in the liver samples of 47% of patients which was significantly related to a lower stage of fibrosis (P = 0.02) and a lower progression rate of fibrosis (P = 0.01). |
| 3124 | 16750565 | The clone secreted GM-CSF, TNFa, and IFNg when stimulated with AML blasts from 3 of 11 patients or cell lines tested, but not with K562 or autologous B-LCL. |
| 3125 | 16728393 | There was no functional difference in the signal transducers and activators of transcription (STAT) pathways between progenitors and mature oligodendrocytes as determined by induction of IRF1 mRNA in response to IFNG. |
| 3126 | 16728393 | There was no functional difference in the signal transducers and activators of transcription (STAT) pathways between progenitors and mature oligodendrocytes as determined by induction of IRF1 mRNA in response to IFNG. |
| 3127 | 16728393 | Therefore, we concluded that simultaneous activation of the STAT pathway by IFNG and of the ERK pathway by exogenous trophic factors played a role in the stage-specific IFNG-induced cytotoxicity in oligodendroglial progenitors. |
| 3128 | 16728393 | Therefore, we concluded that simultaneous activation of the STAT pathway by IFNG and of the ERK pathway by exogenous trophic factors played a role in the stage-specific IFNG-induced cytotoxicity in oligodendroglial progenitors. |
| 3129 | 16724074 | Previous studies identified mucosa-specific CD2 cis-elements within the -204 to -108 bp IFNG promoter. |
| 3130 | 16724074 | Previous studies identified mucosa-specific CD2 cis-elements within the -204 to -108 bp IFNG promoter. |
| 3131 | 16724074 | Within this region, a single-site nucleotide polymorphism, -179G/T, imparts tumor necrosis factor-alpha stimulation of IFNG in peripheral blood lymphocytes, and is linked with accelerated AIDS progression. |
| 3132 | 16724074 | Within this region, a single-site nucleotide polymorphism, -179G/T, imparts tumor necrosis factor-alpha stimulation of IFNG in peripheral blood lymphocytes, and is linked with accelerated AIDS progression. |
| 3133 | 16627761 | Interleukin 12 (IL-12) is a major inducer of interferon gamma (IFN-gamma) and the principal mediator of T helper 1 (Th1) differentiation. |
| 3134 | 16627761 | Interleukin 12 (IL-12) is a major inducer of interferon gamma (IFN-gamma) and the principal mediator of T helper 1 (Th1) differentiation. |
| 3135 | 16627761 | Interleukin 12 (IL-12) is a major inducer of interferon gamma (IFN-gamma) and the principal mediator of T helper 1 (Th1) differentiation. |
| 3136 | 16627761 | To identify IL-12-regulated genes, which might contribute to Th1 differentiation and IFNG regulation, we employed microarray analysis. |
| 3137 | 16627761 | To identify IL-12-regulated genes, which might contribute to Th1 differentiation and IFNG regulation, we employed microarray analysis. |
| 3138 | 16627761 | To identify IL-12-regulated genes, which might contribute to Th1 differentiation and IFNG regulation, we employed microarray analysis. |
| 3139 | 16627761 | Thus, we conclude that IL-12 induction of furin might represent a new aspect of IFN-gamma regulation and control of Th1 differentiation. |
| 3140 | 16627761 | Thus, we conclude that IL-12 induction of furin might represent a new aspect of IFN-gamma regulation and control of Th1 differentiation. |
| 3141 | 16627761 | Thus, we conclude that IL-12 induction of furin might represent a new aspect of IFN-gamma regulation and control of Th1 differentiation. |
| 3142 | 16622216 | Previous studies have determined that Slc11a1 was an excellent candidate gene for Ses1. |
| 3143 | 16622216 | Quantitative reverse transcription-PCR revealed an increase in Th1 cytokine (Ifng and Il12) and Th1-specific transcription factor Tbx21 expression during infection in both the 129S6 and 129S6-Slc11a1(tm1Mcg) strains. |
| 3144 | 16622216 | However, the expression of Gata3, a transcription factor involved in Th2 polarization, Cd28, and Il4 was markedly increased in Slc11a1-deficient mice during infection, suggesting a predominant Th2 phenotype in 129S6-Slc11a1(tm1Mcg) animals following S. enterica serovar Enteritidis infection. |
| 3145 | 16520391 | T-bet regulates Th1 responses through essential effects on GATA-3 function rather than on IFNG gene acetylation and transcription. |
| 3146 | 16520391 | T-bet regulates Th1 responses through essential effects on GATA-3 function rather than on IFNG gene acetylation and transcription. |
| 3147 | 16520391 | T-bet regulates Th1 responses through essential effects on GATA-3 function rather than on IFNG gene acetylation and transcription. |
| 3148 | 16520391 | T helper type 1 (Th1) development is facilitated by interrelated changes in key intracellular factors, particularly signal transducer and activator of transcription (STAT)4, T-bet, and GATA-3. |
| 3149 | 16520391 | T helper type 1 (Th1) development is facilitated by interrelated changes in key intracellular factors, particularly signal transducer and activator of transcription (STAT)4, T-bet, and GATA-3. |
| 3150 | 16520391 | T helper type 1 (Th1) development is facilitated by interrelated changes in key intracellular factors, particularly signal transducer and activator of transcription (STAT)4, T-bet, and GATA-3. |
| 3151 | 16520391 | Here we show that CD4+ cells from T-bet-/- mice are skewed toward Th2 differentiation by high endogenous GATA-3 levels but exhibit virtually normal Th1 differentiation provided that GATA-3 levels are regulated at an early stage by anti-interleukin (IL)-4 blockade of IL-4 receptor (R) signaling. |
| 3152 | 16520391 | Here we show that CD4+ cells from T-bet-/- mice are skewed toward Th2 differentiation by high endogenous GATA-3 levels but exhibit virtually normal Th1 differentiation provided that GATA-3 levels are regulated at an early stage by anti-interleukin (IL)-4 blockade of IL-4 receptor (R) signaling. |
| 3153 | 16520391 | Here we show that CD4+ cells from T-bet-/- mice are skewed toward Th2 differentiation by high endogenous GATA-3 levels but exhibit virtually normal Th1 differentiation provided that GATA-3 levels are regulated at an early stage by anti-interleukin (IL)-4 blockade of IL-4 receptor (R) signaling. |
| 3154 | 16520391 | In addition, under these conditions, Th1 cells from T-bet-/- mice manifest IFNG promotor accessibility as detected by histone acetylation and deoxyribonuclease I hypersensitivity. |
| 3155 | 16520391 | In addition, under these conditions, Th1 cells from T-bet-/- mice manifest IFNG promotor accessibility as detected by histone acetylation and deoxyribonuclease I hypersensitivity. |
| 3156 | 16520391 | In addition, under these conditions, Th1 cells from T-bet-/- mice manifest IFNG promotor accessibility as detected by histone acetylation and deoxyribonuclease I hypersensitivity. |
| 3157 | 16520391 | In related studies, we show that the negative effect of GATA-3 on Th1 differentiation in T-bet-/- cells arises from its ability to suppress STAT4 levels, because if this is prevented by a STAT4-expressing retrovirus, normal Th1 differentiation is observed. |
| 3158 | 16520391 | In related studies, we show that the negative effect of GATA-3 on Th1 differentiation in T-bet-/- cells arises from its ability to suppress STAT4 levels, because if this is prevented by a STAT4-expressing retrovirus, normal Th1 differentiation is observed. |
| 3159 | 16520391 | In related studies, we show that the negative effect of GATA-3 on Th1 differentiation in T-bet-/- cells arises from its ability to suppress STAT4 levels, because if this is prevented by a STAT4-expressing retrovirus, normal Th1 differentiation is observed. |
| 3160 | 16520391 | Finally, we show that retroviral T-bet expression in developing and established Th2 cells leads to down-regulation of GATA-3 levels. |
| 3161 | 16520391 | Finally, we show that retroviral T-bet expression in developing and established Th2 cells leads to down-regulation of GATA-3 levels. |
| 3162 | 16520391 | Finally, we show that retroviral T-bet expression in developing and established Th2 cells leads to down-regulation of GATA-3 levels. |
| 3163 | 16520391 | These findings lead to a model of T cell differentiation that holds that naive T cells tend toward Th2 differentiation through induction of GATA-3 and subsequent down-regulation of STAT4/IL-12Rbeta2 chain unless GATA-3 levels or function is regulated by T-bet. |
| 3164 | 16520391 | These findings lead to a model of T cell differentiation that holds that naive T cells tend toward Th2 differentiation through induction of GATA-3 and subsequent down-regulation of STAT4/IL-12Rbeta2 chain unless GATA-3 levels or function is regulated by T-bet. |
| 3165 | 16520391 | These findings lead to a model of T cell differentiation that holds that naive T cells tend toward Th2 differentiation through induction of GATA-3 and subsequent down-regulation of STAT4/IL-12Rbeta2 chain unless GATA-3 levels or function is regulated by T-bet. |
| 3166 | 16520391 | Thus, the principal function of T-bet in developing Th1 cells is to negatively regulate GATA-3 rather than to positively regulate the IFNG gene. |
| 3167 | 16520391 | Thus, the principal function of T-bet in developing Th1 cells is to negatively regulate GATA-3 rather than to positively regulate the IFNG gene. |
| 3168 | 16520391 | Thus, the principal function of T-bet in developing Th1 cells is to negatively regulate GATA-3 rather than to positively regulate the IFNG gene. |
| 3169 | 16499690 | Here we test for evidence of selection in three genes involved in vertebrate immune function - the major histocompatibility complex (MHC), interferon gamma (IFNG) and natural resistance associated macrophage polymorphism (NRAMP) - in highly structured populations of wild thinhorn sheep (Ovis dalli). |
| 3170 | 16499690 | Here we test for evidence of selection in three genes involved in vertebrate immune function - the major histocompatibility complex (MHC), interferon gamma (IFNG) and natural resistance associated macrophage polymorphism (NRAMP) - in highly structured populations of wild thinhorn sheep (Ovis dalli). |
| 3171 | 16499690 | The translated coding sequences of thinhorn IFNG and NRAMP are fixed and identical to those of domestic sheep (Ovis aries). |
| 3172 | 16499690 | The translated coding sequences of thinhorn IFNG and NRAMP are fixed and identical to those of domestic sheep (Ovis aries). |
| 3173 | 16476014 | Interferon-gamma receptor-1 gene promoter polymorphisms (G-611A; T-56C) and susceptibility to tuberculosis. |
| 3174 | 16476014 | Interferon-gamma receptor-1 gene promoter polymorphisms (G-611A; T-56C) and susceptibility to tuberculosis. |
| 3175 | 16476014 | Interferon-gamma receptor-1 gene promoter polymorphisms (G-611A; T-56C) and susceptibility to tuberculosis. |
| 3176 | 16476014 | We analysed frequencies of two single-nucleotide polymorphisms (SNP) in the interferon-gamma (IFN-gamma) receptor-1 (IFNGR1) gene promoter (G-611A, T-56C) in tuberculosis patients (n = 244) and compared them with controls (n = 521). |
| 3177 | 16476014 | We analysed frequencies of two single-nucleotide polymorphisms (SNP) in the interferon-gamma (IFN-gamma) receptor-1 (IFNGR1) gene promoter (G-611A, T-56C) in tuberculosis patients (n = 244) and compared them with controls (n = 521). |
| 3178 | 16476014 | We analysed frequencies of two single-nucleotide polymorphisms (SNP) in the interferon-gamma (IFN-gamma) receptor-1 (IFNGR1) gene promoter (G-611A, T-56C) in tuberculosis patients (n = 244) and compared them with controls (n = 521). |
| 3179 | 16476014 | Further analysis revealed a significant association between the protective (CA)(n) polymorphism (22 repeats, 192 FA(1)), located in the fifth intron of the IFNGR1 gene (+16682), and GT promoter haplotype (-611; -56) that showed the strongest expression capacity. |
| 3180 | 16476014 | Further analysis revealed a significant association between the protective (CA)(n) polymorphism (22 repeats, 192 FA(1)), located in the fifth intron of the IFNGR1 gene (+16682), and GT promoter haplotype (-611; -56) that showed the strongest expression capacity. |
| 3181 | 16476014 | Further analysis revealed a significant association between the protective (CA)(n) polymorphism (22 repeats, 192 FA(1)), located in the fifth intron of the IFNGR1 gene (+16682), and GT promoter haplotype (-611; -56) that showed the strongest expression capacity. |
| 3182 | 16476014 | These results suggest that a particular combination of IFNG and IFNGR1 SNP might offer a better protection against tuberculosis in this population. |
| 3183 | 16476014 | These results suggest that a particular combination of IFNG and IFNGR1 SNP might offer a better protection against tuberculosis in this population. |
| 3184 | 16476014 | These results suggest that a particular combination of IFNG and IFNGR1 SNP might offer a better protection against tuberculosis in this population. |
| 3185 | 16474934 | We studied four SNPs in IFNG in 585 non-Hispanic whites (NHW) who had the fastest (n =280) or the slowest (n=305) decline of FEV(1)% predicted selected from among continuous smokers followed for 5 years in the NHLBI Lung Health Study. |
| 3186 | 16319288 | Indoleamine 2,3-dioxygenase participates in the interferon-gamma-induced cell death process in cultured bovine luteal cells. |
| 3187 | 16319288 | Indoleamine 2,3-dioxygenase participates in the interferon-gamma-induced cell death process in cultured bovine luteal cells. |
| 3188 | 16319288 | Indoleamine 2,3-dioxygenase participates in the interferon-gamma-induced cell death process in cultured bovine luteal cells. |
| 3189 | 16319288 | Indoleamine 2,3-dioxygenase participates in the interferon-gamma-induced cell death process in cultured bovine luteal cells. |
| 3190 | 16319288 | Indoleamine 2,3-dioxygenase participates in the interferon-gamma-induced cell death process in cultured bovine luteal cells. |
| 3191 | 16319288 | The IFNG-inducible enzyme indoleamine 2,3-dioxygenase (INDO) catalyzes the first step in a metabolic pathway that degrades tryptophan. |
| 3192 | 16319288 | The IFNG-inducible enzyme indoleamine 2,3-dioxygenase (INDO) catalyzes the first step in a metabolic pathway that degrades tryptophan. |
| 3193 | 16319288 | The IFNG-inducible enzyme indoleamine 2,3-dioxygenase (INDO) catalyzes the first step in a metabolic pathway that degrades tryptophan. |
| 3194 | 16319288 | The IFNG-inducible enzyme indoleamine 2,3-dioxygenase (INDO) catalyzes the first step in a metabolic pathway that degrades tryptophan. |
| 3195 | 16319288 | The IFNG-inducible enzyme indoleamine 2,3-dioxygenase (INDO) catalyzes the first step in a metabolic pathway that degrades tryptophan. |
| 3196 | 16319288 | In the first experiment, RT-PCR revealed the presence of INDO mRNA in luteal cells treated with IFNG, but not in untreated cells. |
| 3197 | 16319288 | In the first experiment, RT-PCR revealed the presence of INDO mRNA in luteal cells treated with IFNG, but not in untreated cells. |
| 3198 | 16319288 | In the first experiment, RT-PCR revealed the presence of INDO mRNA in luteal cells treated with IFNG, but not in untreated cells. |
| 3199 | 16319288 | In the first experiment, RT-PCR revealed the presence of INDO mRNA in luteal cells treated with IFNG, but not in untreated cells. |
| 3200 | 16319288 | In the first experiment, RT-PCR revealed the presence of INDO mRNA in luteal cells treated with IFNG, but not in untreated cells. |
| 3201 | 16319288 | To determine whether INDO participates in IFNG-induced death of bovine luteal cells, an experiment was performed to test the effect of 1-methyl-D-tryptophan (1-MT), an inhibitor of INDO, on IFNG-induced DNA fragmentation in luteal cells. |
| 3202 | 16319288 | To determine whether INDO participates in IFNG-induced death of bovine luteal cells, an experiment was performed to test the effect of 1-methyl-D-tryptophan (1-MT), an inhibitor of INDO, on IFNG-induced DNA fragmentation in luteal cells. |
| 3203 | 16319288 | To determine whether INDO participates in IFNG-induced death of bovine luteal cells, an experiment was performed to test the effect of 1-methyl-D-tryptophan (1-MT), an inhibitor of INDO, on IFNG-induced DNA fragmentation in luteal cells. |
| 3204 | 16319288 | To determine whether INDO participates in IFNG-induced death of bovine luteal cells, an experiment was performed to test the effect of 1-methyl-D-tryptophan (1-MT), an inhibitor of INDO, on IFNG-induced DNA fragmentation in luteal cells. |
| 3205 | 16319288 | To determine whether INDO participates in IFNG-induced death of bovine luteal cells, an experiment was performed to test the effect of 1-methyl-D-tryptophan (1-MT), an inhibitor of INDO, on IFNG-induced DNA fragmentation in luteal cells. |
| 3206 | 16319288 | We conclude that INDO participates in IFNG-induced death of bovine luteal cells, through a mechanism that involves degradation of tryptophan, thereby reducing tryptophan concentrations to a point insufficient to meet luteal cells needs. |
| 3207 | 16319288 | We conclude that INDO participates in IFNG-induced death of bovine luteal cells, through a mechanism that involves degradation of tryptophan, thereby reducing tryptophan concentrations to a point insufficient to meet luteal cells needs. |
| 3208 | 16319288 | We conclude that INDO participates in IFNG-induced death of bovine luteal cells, through a mechanism that involves degradation of tryptophan, thereby reducing tryptophan concentrations to a point insufficient to meet luteal cells needs. |
| 3209 | 16319288 | We conclude that INDO participates in IFNG-induced death of bovine luteal cells, through a mechanism that involves degradation of tryptophan, thereby reducing tryptophan concentrations to a point insufficient to meet luteal cells needs. |
| 3210 | 16319288 | We conclude that INDO participates in IFNG-induced death of bovine luteal cells, through a mechanism that involves degradation of tryptophan, thereby reducing tryptophan concentrations to a point insufficient to meet luteal cells needs. |
| 3211 | 16293125 | Chromosomal locations of 19 horse immunity-related loci (CASP1, CD14, EIF5A, FCER1A, IFNG, IL12A, IL12B, IL12RB2, IL1A, IL23A, IL4, IL6, MMP7, MS4A2, MYD88, NOS2A, PTGS2, TFRC and TLR2) were determined by fluorescence in situ hybridization. |
| 3212 | 16293125 | Chromosomal locations of 19 horse immunity-related loci (CASP1, CD14, EIF5A, FCER1A, IFNG, IL12A, IL12B, IL12RB2, IL1A, IL23A, IL4, IL6, MMP7, MS4A2, MYD88, NOS2A, PTGS2, TFRC and TLR2) were determined by fluorescence in situ hybridization. |
| 3213 | 16293125 | For IFNG and PTGS2, this study is a confirmation of their previously reported position. |
| 3214 | 16293125 | For IFNG and PTGS2, this study is a confirmation of their previously reported position. |
| 3215 | 16237092 | Using conditional introduction of dominant-negative factors, we now show that T-bet and GATA-3 are far more critical in establishment than maintenance of IFN-gamma and IL-4 activity during Th1 and Th2 maturation, respectively. |
| 3216 | 16237092 | T-bet plus Hlx can disrupt ifng silencing when introduced into developing Th2 cells, but they fail to perturb ifng silencing in mature Th2 cells. |
| 3217 | 16223768 | NK-cell activation by LIGHT triggers tumor-specific CD8+ T-cell immunity to reject established tumors. |
| 3218 | 16223768 | NK-cell activation by LIGHT triggers tumor-specific CD8+ T-cell immunity to reject established tumors. |
| 3219 | 16223768 | NK-cell activation by LIGHT triggers tumor-specific CD8+ T-cell immunity to reject established tumors. |
| 3220 | 16223768 | We now demonstrate that the TNF superfamily member, LIGHT, known as TNFSF14 and a T-cell costimulatory molecule, is a critical ligand for the activation of NK cells. |
| 3221 | 16223768 | We now demonstrate that the TNF superfamily member, LIGHT, known as TNFSF14 and a T-cell costimulatory molecule, is a critical ligand for the activation of NK cells. |
| 3222 | 16223768 | We now demonstrate that the TNF superfamily member, LIGHT, known as TNFSF14 and a T-cell costimulatory molecule, is a critical ligand for the activation of NK cells. |
| 3223 | 16223768 | Herpesvirus entry mediator (HVEM) is expressed on NK cells, and its engagement with LIGHT mediates NK-cell activation. |
| 3224 | 16223768 | Herpesvirus entry mediator (HVEM) is expressed on NK cells, and its engagement with LIGHT mediates NK-cell activation. |
| 3225 | 16223768 | Herpesvirus entry mediator (HVEM) is expressed on NK cells, and its engagement with LIGHT mediates NK-cell activation. |
| 3226 | 16223768 | Interestingly, activated NK cells do not kill tumors directly but can facilitate the priming of tumor-specific CD8+ T cells in an IFN-gamma-dependent manner. |
| 3227 | 16223768 | Interestingly, activated NK cells do not kill tumors directly but can facilitate the priming of tumor-specific CD8+ T cells in an IFN-gamma-dependent manner. |
| 3228 | 16223768 | Interestingly, activated NK cells do not kill tumors directly but can facilitate the priming of tumor-specific CD8+ T cells in an IFN-gamma-dependent manner. |
| 3229 | 16223768 | Conversely, intratumor depletion of either NK cells or IFN-gamma during tumor progression disrupts CD8+ cell-mediated tumor rejection, suggesting that the tumor is the essential site for the crosstalk between NK and CD8+ cells. |
| 3230 | 16223768 | Conversely, intratumor depletion of either NK cells or IFN-gamma during tumor progression disrupts CD8+ cell-mediated tumor rejection, suggesting that the tumor is the essential site for the crosstalk between NK and CD8+ cells. |
| 3231 | 16223768 | Conversely, intratumor depletion of either NK cells or IFN-gamma during tumor progression disrupts CD8+ cell-mediated tumor rejection, suggesting that the tumor is the essential site for the crosstalk between NK and CD8+ cells. |
| 3232 | 16223768 | Furthermore, IFNG-deficient NK cells fail to effectively activate CD8+ T cells, suggesting IFN-gamma plays an important role in NK-mediated activation of cytotoxic T lymphocytes (CTLs). |
| 3233 | 16223768 | Furthermore, IFNG-deficient NK cells fail to effectively activate CD8+ T cells, suggesting IFN-gamma plays an important role in NK-mediated activation of cytotoxic T lymphocytes (CTLs). |
| 3234 | 16223768 | Furthermore, IFNG-deficient NK cells fail to effectively activate CD8+ T cells, suggesting IFN-gamma plays an important role in NK-mediated activation of cytotoxic T lymphocytes (CTLs). |
| 3235 | 16223768 | Our findings establish a direct role for LIGHT in NK activation/expansion and a critical helper role of activated NK cells in priming CD8+ T cells and breaking T-cell tolerance at the tumor site. |
| 3236 | 16223768 | Our findings establish a direct role for LIGHT in NK activation/expansion and a critical helper role of activated NK cells in priming CD8+ T cells and breaking T-cell tolerance at the tumor site. |
| 3237 | 16223768 | Our findings establish a direct role for LIGHT in NK activation/expansion and a critical helper role of activated NK cells in priming CD8+ T cells and breaking T-cell tolerance at the tumor site. |
| 3238 | 16216674 | Several polymorphisms in regions where Th1 cytokines (IL12B and IFNG genes) are located were analyzed in 303 Spanish subjects with type 1 diabetes and compared with a control cohort (n = 548). |
| 3239 | 16216674 | Several polymorphisms in regions where Th1 cytokines (IL12B and IFNG genes) are located were analyzed in 303 Spanish subjects with type 1 diabetes and compared with a control cohort (n = 548). |
| 3240 | 16216674 | No association was found for any of IL12B and IFNG markers individually. |
| 3241 | 16216674 | No association was found for any of IL12B and IFNG markers individually. |
| 3242 | 16115485 | Interferon-gamma and interferon-gamma receptor 1 and 2 gene polymorphisms and restenosis following coronary stenting. |
| 3243 | 16115485 | Interferon-gamma and interferon-gamma receptor 1 and 2 gene polymorphisms and restenosis following coronary stenting. |
| 3244 | 16115485 | Interferon-gamma and interferon-gamma receptor 1 and 2 gene polymorphisms and restenosis following coronary stenting. |
| 3245 | 16115485 | Interferon-gamma and interferon-gamma receptor 1 and 2 gene polymorphisms and restenosis following coronary stenting. |
| 3246 | 16115485 | Interferon-gamma and interferon-gamma receptor 1 and 2 gene polymorphisms and restenosis following coronary stenting. |
| 3247 | 16115485 | Polymorphisms in the genes encoding for IFN-gamma (IFNG T874A) and its receptors 1 (IFNGR1 C-56T) and 2 (IFNGR2 A839G) were tested for their association with restenosis. |
| 3248 | 16115485 | Polymorphisms in the genes encoding for IFN-gamma (IFNG T874A) and its receptors 1 (IFNGR1 C-56T) and 2 (IFNGR2 A839G) were tested for their association with restenosis. |
| 3249 | 16115485 | Polymorphisms in the genes encoding for IFN-gamma (IFNG T874A) and its receptors 1 (IFNGR1 C-56T) and 2 (IFNGR2 A839G) were tested for their association with restenosis. |
| 3250 | 16115485 | Polymorphisms in the genes encoding for IFN-gamma (IFNG T874A) and its receptors 1 (IFNGR1 C-56T) and 2 (IFNGR2 A839G) were tested for their association with restenosis. |
| 3251 | 16115485 | Polymorphisms in the genes encoding for IFN-gamma (IFNG T874A) and its receptors 1 (IFNGR1 C-56T) and 2 (IFNGR2 A839G) were tested for their association with restenosis. |
| 3252 | 16115485 | IFNG T874A, IFNGR1 C-56T and IFNGR2 A839G genotypes were determined in a consecutive series of patients (n=2591) that had been treated with coronary stents. |
| 3253 | 16115485 | IFNG T874A, IFNGR1 C-56T and IFNGR2 A839G genotypes were determined in a consecutive series of patients (n=2591) that had been treated with coronary stents. |
| 3254 | 16115485 | IFNG T874A, IFNGR1 C-56T and IFNGR2 A839G genotypes were determined in a consecutive series of patients (n=2591) that had been treated with coronary stents. |
| 3255 | 16115485 | IFNG T874A, IFNGR1 C-56T and IFNGR2 A839G genotypes were determined in a consecutive series of patients (n=2591) that had been treated with coronary stents. |
| 3256 | 16115485 | IFNG T874A, IFNGR1 C-56T and IFNGR2 A839G genotypes were determined in a consecutive series of patients (n=2591) that had been treated with coronary stents. |
| 3257 | 16115485 | IFNG T874A, IFNGR1 C-56T and IFNGR2 A839G genotypes were not associated with the incidence of angiographic and clinical restenosis (P>0.23). |
| 3258 | 16115485 | IFNG T874A, IFNGR1 C-56T and IFNGR2 A839G genotypes were not associated with the incidence of angiographic and clinical restenosis (P>0.23). |
| 3259 | 16115485 | IFNG T874A, IFNGR1 C-56T and IFNGR2 A839G genotypes were not associated with the incidence of angiographic and clinical restenosis (P>0.23). |
| 3260 | 16115485 | IFNG T874A, IFNGR1 C-56T and IFNGR2 A839G genotypes were not associated with the incidence of angiographic and clinical restenosis (P>0.23). |
| 3261 | 16115485 | IFNG T874A, IFNGR1 C-56T and IFNGR2 A839G genotypes were not associated with the incidence of angiographic and clinical restenosis (P>0.23). |
| 3262 | 16115485 | Moreover, there was no association between IFNG, IFNGR1 and IFNGR2 genotypes and the combined incidence of death form any cause and non-fatal myocardial infarction during the first 12 months following the intervention (P>0.61). |
| 3263 | 16115485 | Moreover, there was no association between IFNG, IFNGR1 and IFNGR2 genotypes and the combined incidence of death form any cause and non-fatal myocardial infarction during the first 12 months following the intervention (P>0.61). |
| 3264 | 16115485 | Moreover, there was no association between IFNG, IFNGR1 and IFNGR2 genotypes and the combined incidence of death form any cause and non-fatal myocardial infarction during the first 12 months following the intervention (P>0.61). |
| 3265 | 16115485 | Moreover, there was no association between IFNG, IFNGR1 and IFNGR2 genotypes and the combined incidence of death form any cause and non-fatal myocardial infarction during the first 12 months following the intervention (P>0.61). |
| 3266 | 16115485 | Moreover, there was no association between IFNG, IFNGR1 and IFNGR2 genotypes and the combined incidence of death form any cause and non-fatal myocardial infarction during the first 12 months following the intervention (P>0.61). |
| 3267 | 15932407 | In this study, nine microsatellite loci (SW1897, SW2427, SW489, SW957, TNFB, IFNG, SW2410, SW2019 and S0215) were analysed using DNA samples of pigs from Vietnam (Indigenous breeds Co, Meo, Muong Khuong, Tap Na) and Germany (European Wild Boar, Pietrain). |
| 3268 | 15893066 | Groups of 2-5 interferon gamma gene knockout (IFN-gamma-KO) (BALB/c-Ifng), inducible nitric oxide synthase (NOS) gene knockout (iNOS-KO) (C57BL/6), B-cell-deficient (microMT) (C57BL/6), and BALB/c mice were intravenously (i.v.) or subcutaneously (s.c.) inoculated with various doses of promastigotes of the LIVT-1 strain of L. infantum. |
| 3269 | 15858598 | Investigation of malaria susceptibility determinants in the IFNG/IL26/IL22 genomic region. |
| 3270 | 15858598 | Investigation of malaria susceptibility determinants in the IFNG/IL26/IL22 genomic region. |
| 3271 | 15858598 | Investigation of malaria susceptibility determinants in the IFNG/IL26/IL22 genomic region. |
| 3272 | 15858598 | We began by analysing West African and European haplotype structure and patterns of linkage disequilibrium across a 100 kb genomic region encompassing IFNG and its immediate neighbours IL22 and IL26. |
| 3273 | 15858598 | We began by analysing West African and European haplotype structure and patterns of linkage disequilibrium across a 100 kb genomic region encompassing IFNG and its immediate neighbours IL22 and IL26. |
| 3274 | 15858598 | We began by analysing West African and European haplotype structure and patterns of linkage disequilibrium across a 100 kb genomic region encompassing IFNG and its immediate neighbours IL22 and IL26. |
| 3275 | 15858598 | A large case-control study of severe malaria in a West Africa population identified several weak associations with individual single-nucleotide polymorphisms in the IFNG and IL22 genes, and defined two IL22 haplotypes that are, respectively, associated with resistance and susceptibility. |
| 3276 | 15858598 | A large case-control study of severe malaria in a West Africa population identified several weak associations with individual single-nucleotide polymorphisms in the IFNG and IL22 genes, and defined two IL22 haplotypes that are, respectively, associated with resistance and susceptibility. |
| 3277 | 15858598 | A large case-control study of severe malaria in a West Africa population identified several weak associations with individual single-nucleotide polymorphisms in the IFNG and IL22 genes, and defined two IL22 haplotypes that are, respectively, associated with resistance and susceptibility. |
| 3278 | 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. |
| 3279 | 15799696 | The mRNA expression of Il2 and Il4 decreased from day 5 to day 14 after irradiation. |
| 3280 | 15799696 | Thereafter, the expression level of Il2 mRNA recovered to normal control levels; however, the expression of Il4 mRNA tended toward significantly low levels. |
| 3281 | 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. |
| 3282 | 15733644 | No disease-causing mutations were identified in IL1A, IL1B, IL6 or TNFA. |
| 3283 | 15710911 | IFN-gamma gene expression is controlled by the architectural transcription factor HMGA1. |
| 3284 | 15710911 | IFN-gamma gene expression is controlled by the architectural transcription factor HMGA1. |
| 3285 | 15710911 | IFN-gamma gene expression is controlled by the architectural transcription factor HMGA1. |
| 3286 | 15710911 | IFN-gamma gene expression is controlled by the architectural transcription factor HMGA1. |
| 3287 | 15710911 | This finding is supported by our direct studies of T cells isolated from the HMGA1-transgenic mice displaying an up-regulation of IFN-gamma production and of HMGA1-deficient mice exhibited a decreased IFN-gamma induction. |
| 3288 | 15710911 | This finding is supported by our direct studies of T cells isolated from the HMGA1-transgenic mice displaying an up-regulation of IFN-gamma production and of HMGA1-deficient mice exhibited a decreased IFN-gamma induction. |
| 3289 | 15710911 | This finding is supported by our direct studies of T cells isolated from the HMGA1-transgenic mice displaying an up-regulation of IFN-gamma production and of HMGA1-deficient mice exhibited a decreased IFN-gamma induction. |
| 3290 | 15710911 | This finding is supported by our direct studies of T cells isolated from the HMGA1-transgenic mice displaying an up-regulation of IFN-gamma production and of HMGA1-deficient mice exhibited a decreased IFN-gamma induction. |
| 3291 | 15710911 | In parallel transfection studies in EL4 cells, we observed elevated IFNG gene promoter activity in cells stably over-expressing HMGA1 and a reduction of such activity in cells expressing dominant-negative HMGA1. |
| 3292 | 15710911 | In parallel transfection studies in EL4 cells, we observed elevated IFNG gene promoter activity in cells stably over-expressing HMGA1 and a reduction of such activity in cells expressing dominant-negative HMGA1. |
| 3293 | 15710911 | In parallel transfection studies in EL4 cells, we observed elevated IFNG gene promoter activity in cells stably over-expressing HMGA1 and a reduction of such activity in cells expressing dominant-negative HMGA1. |
| 3294 | 15710911 | In parallel transfection studies in EL4 cells, we observed elevated IFNG gene promoter activity in cells stably over-expressing HMGA1 and a reduction of such activity in cells expressing dominant-negative HMGA1. |
| 3295 | 15710911 | In vitro binding assays further demonstrated a specific interaction of HMGA1 to defined regions of the IFNG gene proximal promoter. |
| 3296 | 15710911 | In vitro binding assays further demonstrated a specific interaction of HMGA1 to defined regions of the IFNG gene proximal promoter. |
| 3297 | 15710911 | In vitro binding assays further demonstrated a specific interaction of HMGA1 to defined regions of the IFNG gene proximal promoter. |
| 3298 | 15710911 | In vitro binding assays further demonstrated a specific interaction of HMGA1 to defined regions of the IFNG gene proximal promoter. |
| 3299 | 15661146 | The most noteworthy changes in gene expression mainly affected the transcriptional network regulated by interferons (IFNs), including both IFN-alpha/beta-inducible genes (STAT1, STAT2, ISGF3G/IRF9, IFI27, G1P3, G1P2, OAS2, MX1) and IFN-gamma-inducible genes (CXCL9, CXCL10, CXCL11). |
| 3300 | 15661146 | The most noteworthy changes in gene expression mainly affected the transcriptional network regulated by interferons (IFNs), including both IFN-alpha/beta-inducible genes (STAT1, STAT2, ISGF3G/IRF9, IFI27, G1P3, G1P2, OAS2, MX1) and IFN-gamma-inducible genes (CXCL9, CXCL10, CXCL11). |
| 3301 | 15661146 | The most noteworthy changes in gene expression mainly affected the transcriptional network regulated by interferons (IFNs), including both IFN-alpha/beta-inducible genes (STAT1, STAT2, ISGF3G/IRF9, IFI27, G1P3, G1P2, OAS2, MX1) and IFN-gamma-inducible genes (CXCL9, CXCL10, CXCL11). |
| 3302 | 15661146 | Interesting, upregulation of IFN-alpha/beta-inducible genes (but not IFN-gamma-inducible genes) was independent of histological scores (grade and stage of fibrosis) and HCV characteristics (hepatic HCV mRNA levels and the HCV genotype), and was specific to HCV (as compared to hepatitis B virus (HBV)). |
| 3303 | 15661146 | Interesting, upregulation of IFN-alpha/beta-inducible genes (but not IFN-gamma-inducible genes) was independent of histological scores (grade and stage of fibrosis) and HCV characteristics (hepatic HCV mRNA levels and the HCV genotype), and was specific to HCV (as compared to hepatitis B virus (HBV)). |
| 3304 | 15661146 | Interesting, upregulation of IFN-alpha/beta-inducible genes (but not IFN-gamma-inducible genes) was independent of histological scores (grade and stage of fibrosis) and HCV characteristics (hepatic HCV mRNA levels and the HCV genotype), and was specific to HCV (as compared to hepatitis B virus (HBV)). |
| 3305 | 15661146 | Other genes dysregulated in F1-CH-C, albeit less markedly than IFN-alpha/beta- and IFN-gamma-inducible genes, were mainly involved in the activation of lymphocytes infiltrating the liver (IFNG, TNF, CXCL6, IL6, CCL8, CXCR3, CXCR4, CCR2), cell proliferation (p16/CDKN2A, MKI67, p14/ARF), extracellular matrix remodeling (MMP9, ITGA2), lymphangiogenesis (XLKD1/LYVE), oxidative stress (CYP2E1), and cytoskeleton microtubule organization (STMN2/SCG10). |
| 3306 | 15661146 | Other genes dysregulated in F1-CH-C, albeit less markedly than IFN-alpha/beta- and IFN-gamma-inducible genes, were mainly involved in the activation of lymphocytes infiltrating the liver (IFNG, TNF, CXCL6, IL6, CCL8, CXCR3, CXCR4, CCR2), cell proliferation (p16/CDKN2A, MKI67, p14/ARF), extracellular matrix remodeling (MMP9, ITGA2), lymphangiogenesis (XLKD1/LYVE), oxidative stress (CYP2E1), and cytoskeleton microtubule organization (STMN2/SCG10). |
| 3307 | 15661146 | Other genes dysregulated in F1-CH-C, albeit less markedly than IFN-alpha/beta- and IFN-gamma-inducible genes, were mainly involved in the activation of lymphocytes infiltrating the liver (IFNG, TNF, CXCL6, IL6, CCL8, CXCR3, CXCR4, CCR2), cell proliferation (p16/CDKN2A, MKI67, p14/ARF), extracellular matrix remodeling (MMP9, ITGA2), lymphangiogenesis (XLKD1/LYVE), oxidative stress (CYP2E1), and cytoskeleton microtubule organization (STMN2/SCG10). |
| 3308 | 15507306 | Peripheral blood mononuclear cells (PBMC) isolated from these pigs responded to PRRSV exposure with a limited increase in their expression of the Th1 immune markers, IFNG, tumor necrosis factor-alpha and interleukin-15 (IL15), and a reduction in the quantity of mRNAs encoding the innate and inflammatory proteins, IL1B, IL8 and IFNA. |
| 3309 | 15507306 | Peripheral blood mononuclear cells (PBMC) isolated from these pigs responded to PRRSV exposure with a limited increase in their expression of the Th1 immune markers, IFNG, tumor necrosis factor-alpha and interleukin-15 (IL15), and a reduction in the quantity of mRNAs encoding the innate and inflammatory proteins, IL1B, IL8 and IFNA. |
| 3310 | 15507306 | Peripheral blood mononuclear cells (PBMC) isolated from these pigs responded to PRRSV exposure with a limited increase in their expression of the Th1 immune markers, IFNG, tumor necrosis factor-alpha and interleukin-15 (IL15), and a reduction in the quantity of mRNAs encoding the innate and inflammatory proteins, IL1B, IL8 and IFNA. |
| 3311 | 15507306 | Efforts to enhance Th1 immunity, by utilizing an expression plasmid encoding porcine IFNA (pINA) as an adjuvant, resulted in a temporary increase in the frequency of PRRSV-specific IFNG SC but only minor changes overall in the expression of Th1 associated cytokine or innate immune marker mRNA by virus-stimulated PBMC. |
| 3312 | 15507306 | Efforts to enhance Th1 immunity, by utilizing an expression plasmid encoding porcine IFNA (pINA) as an adjuvant, resulted in a temporary increase in the frequency of PRRSV-specific IFNG SC but only minor changes overall in the expression of Th1 associated cytokine or innate immune marker mRNA by virus-stimulated PBMC. |
| 3313 | 15507306 | Efforts to enhance Th1 immunity, by utilizing an expression plasmid encoding porcine IFNA (pINA) as an adjuvant, resulted in a temporary increase in the frequency of PRRSV-specific IFNG SC but only minor changes overall in the expression of Th1 associated cytokine or innate immune marker mRNA by virus-stimulated PBMC. |
| 3314 | 15507306 | Administration of pINA, however, did correlate with decreased IL1B secretion by cultured, unstimulated PBMC but had no effect on their ability to release IFNG. |
| 3315 | 15507306 | Administration of pINA, however, did correlate with decreased IL1B secretion by cultured, unstimulated PBMC but had no effect on their ability to release IFNG. |
| 3316 | 15507306 | Administration of pINA, however, did correlate with decreased IL1B secretion by cultured, unstimulated PBMC but had no effect on their ability to release IFNG. |
| 3317 | 15498860 | In examining the relationship between genotype and cytolytic T-lymphocyte (CTL) function, transforming growth factor beta (TGF-beta) inhibited restimulation of CTLs in PBLs with adenosine at IFNG base + 874, but not in PBLs homozygous for thymidine. |
| 3318 | 15498860 | Importantly, neutralization of TGF-beta in hu PBL-SCID mice injected with A/A genotype PBLs resulted in reduced LPD development and expanded human CD8(+) cells. |
| 3319 | 15490153 | MHC class I chain-related gene A (MICA), a putative independent susceptibility gene in autoimmune diseases, encodes a surface protein present in epithelial cells that binds to NKG2D, an activating receptor of NK, alphabeta and gammadelta T cells, and could function as a stress-inducible activator of the innate immune response. |
| 3320 | 15490153 | MHC class I chain-related gene A (MICA), a putative independent susceptibility gene in autoimmune diseases, encodes a surface protein present in epithelial cells that binds to NKG2D, an activating receptor of NK, alphabeta and gammadelta T cells, and could function as a stress-inducible activator of the innate immune response. |
| 3321 | 15490153 | Total RNA was purified and MICA, IFNG and NKG2D mRNA were quantified by fluorescent real-time RT-PCR. |
| 3322 | 15490153 | Total RNA was purified and MICA, IFNG and NKG2D mRNA were quantified by fluorescent real-time RT-PCR. |
| 3323 | 15490153 | MICA expression was detected in both patients and controls, but incubation with gliadin induced a strong increase in samples from the treated CD group compared with the non-CD controls (P=0.028), while no differences were observed for IFNG or NKG2D mRNA levels. |
| 3324 | 15490153 | MICA expression was detected in both patients and controls, but incubation with gliadin induced a strong increase in samples from the treated CD group compared with the non-CD controls (P=0.028), while no differences were observed for IFNG or NKG2D mRNA levels. |
| 3325 | 15350745 | Assessment of anti-bovine IL4 and IFN gamma antibodies to label IL4 and IFN gamma in lymphocytes of the koala and brushtail possum. |
| 3326 | 15350745 | Assessment of anti-bovine IL4 and IFN gamma antibodies to label IL4 and IFN gamma in lymphocytes of the koala and brushtail possum. |
| 3327 | 15350745 | We assess anti-bovine IL4 and IFN gamma (IFNg) antibodies for their ability to label IL4 and IFNg in koala (Phascolarctos cinereus), common brushtail possum (Trichosurus vulpecula) and mountain brushtail possum (Trichosurus caninus) lymphocytes using flow cytometry and immunohistochemistry to determine their applicability to studies of host response to intracellular pathogens. |
| 3328 | 15350745 | We assess anti-bovine IL4 and IFN gamma (IFNg) antibodies for their ability to label IL4 and IFNg in koala (Phascolarctos cinereus), common brushtail possum (Trichosurus vulpecula) and mountain brushtail possum (Trichosurus caninus) lymphocytes using flow cytometry and immunohistochemistry to determine their applicability to studies of host response to intracellular pathogens. |
| 3329 | 15304658 | When linked to the murine Ifng gene (-3.4 to +5.6 kb) and transiently transfected into EL-4 cells, these elements clearly enhanced IFN-gamma expression in response to ionomycin and phorbol 12-myristate 13-acetate and weakly enhanced expression in response to T-bet. |
| 3330 | 15304658 | When linked to the murine Ifng gene (-3.4 to +5.6 kb) and transiently transfected into EL-4 cells, these elements clearly enhanced IFN-gamma expression in response to ionomycin and phorbol 12-myristate 13-acetate and weakly enhanced expression in response to T-bet. |
| 3331 | 15304658 | When linked to the murine Ifng gene (-3.4 to +5.6 kb) and transiently transfected into EL-4 cells, these elements clearly enhanced IFN-gamma expression in response to ionomycin and phorbol 12-myristate 13-acetate and weakly enhanced expression in response to T-bet. |
| 3332 | 15304658 | When linked to the murine Ifng gene (-3.4 to +5.6 kb) and transiently transfected into EL-4 cells, these elements clearly enhanced IFN-gamma expression in response to ionomycin and phorbol 12-myristate 13-acetate and weakly enhanced expression in response to T-bet. |
| 3333 | 15304658 | A DNase I hypersensitive site and extragenic transcripts at IFNgCNS2 correlated positively with the capacity of primary T cell subsets to produce IFN-gamma. |
| 3334 | 15304658 | A DNase I hypersensitive site and extragenic transcripts at IFNgCNS2 correlated positively with the capacity of primary T cell subsets to produce IFN-gamma. |
| 3335 | 15304658 | A DNase I hypersensitive site and extragenic transcripts at IFNgCNS2 correlated positively with the capacity of primary T cell subsets to produce IFN-gamma. |
| 3336 | 15304658 | A DNase I hypersensitive site and extragenic transcripts at IFNgCNS2 correlated positively with the capacity of primary T cell subsets to produce IFN-gamma. |
| 3337 | 15304658 | Transcriptionally favorable histone modifications in the Ifng promoter, intronic regions, IFNgCNS2, and, although less pronounced, IFNgCNS1 increased as naïve T cells differentiated into IFN-gamma-producing effector CD8+ and T helper (TH) 1 T cells, but not into TH2 T cells. |
| 3338 | 15304658 | Transcriptionally favorable histone modifications in the Ifng promoter, intronic regions, IFNgCNS2, and, although less pronounced, IFNgCNS1 increased as naïve T cells differentiated into IFN-gamma-producing effector CD8+ and T helper (TH) 1 T cells, but not into TH2 T cells. |
| 3339 | 15304658 | Transcriptionally favorable histone modifications in the Ifng promoter, intronic regions, IFNgCNS2, and, although less pronounced, IFNgCNS1 increased as naïve T cells differentiated into IFN-gamma-producing effector CD8+ and T helper (TH) 1 T cells, but not into TH2 T cells. |
| 3340 | 15304658 | Transcriptionally favorable histone modifications in the Ifng promoter, intronic regions, IFNgCNS2, and, although less pronounced, IFNgCNS1 increased as naïve T cells differentiated into IFN-gamma-producing effector CD8+ and T helper (TH) 1 T cells, but not into TH2 T cells. |
| 3341 | 15304658 | Like IFN-gamma expression, these histone modifications were T-bet-dependent in CD4+ cells, but not CD8+ T cells. |
| 3342 | 15304658 | Like IFN-gamma expression, these histone modifications were T-bet-dependent in CD4+ cells, but not CD8+ T cells. |
| 3343 | 15304658 | Like IFN-gamma expression, these histone modifications were T-bet-dependent in CD4+ cells, but not CD8+ T cells. |
| 3344 | 15304658 | Like IFN-gamma expression, these histone modifications were T-bet-dependent in CD4+ cells, but not CD8+ T cells. |
| 3345 | 15280353 | To better understand the control of T helper (TH) 1-expressed genes, we compared and contrasted acetylation and expression for three key genes, IFNG, TBET, and IL18RAP and found them to be distinctly regulated. |
| 3346 | 15280353 | To better understand the control of T helper (TH) 1-expressed genes, we compared and contrasted acetylation and expression for three key genes, IFNG, TBET, and IL18RAP and found them to be distinctly regulated. |
| 3347 | 15280353 | To better understand the control of T helper (TH) 1-expressed genes, we compared and contrasted acetylation and expression for three key genes, IFNG, TBET, and IL18RAP and found them to be distinctly regulated. |
| 3348 | 15280353 | To better understand the control of T helper (TH) 1-expressed genes, we compared and contrasted acetylation and expression for three key genes, IFNG, TBET, and IL18RAP and found them to be distinctly regulated. |
| 3349 | 15280353 | To better understand the control of T helper (TH) 1-expressed genes, we compared and contrasted acetylation and expression for three key genes, IFNG, TBET, and IL18RAP and found them to be distinctly regulated. |
| 3350 | 15280353 | The TBET and the IFNG genes, but not the IL18RAP gene, showed preferential acetylation of histones H3 and H4 during TH1 differentiation. |
| 3351 | 15280353 | The TBET and the IFNG genes, but not the IL18RAP gene, showed preferential acetylation of histones H3 and H4 during TH1 differentiation. |
| 3352 | 15280353 | The TBET and the IFNG genes, but not the IL18RAP gene, showed preferential acetylation of histones H3 and H4 during TH1 differentiation. |
| 3353 | 15280353 | The TBET and the IFNG genes, but not the IL18RAP gene, showed preferential acetylation of histones H3 and H4 during TH1 differentiation. |
| 3354 | 15280353 | The TBET and the IFNG genes, but not the IL18RAP gene, showed preferential acetylation of histones H3 and H4 during TH1 differentiation. |
| 3355 | 15280353 | Histone H3 acetylation of IFNG and TBET genes occurred with different kinetics, however, and was distinctively regulated by cytokines. |
| 3356 | 15280353 | Histone H3 acetylation of IFNG and TBET genes occurred with different kinetics, however, and was distinctively regulated by cytokines. |
| 3357 | 15280353 | Histone H3 acetylation of IFNG and TBET genes occurred with different kinetics, however, and was distinctively regulated by cytokines. |
| 3358 | 15280353 | Histone H3 acetylation of IFNG and TBET genes occurred with different kinetics, however, and was distinctively regulated by cytokines. |
| 3359 | 15280353 | Histone H3 acetylation of IFNG and TBET genes occurred with different kinetics, however, and was distinctively regulated by cytokines. |
| 3360 | 15280353 | Interleukin (IL)-12 and IL-18 enhanced the histone acetylation of the IFNG gene. |
| 3361 | 15280353 | Interleukin (IL)-12 and IL-18 enhanced the histone acetylation of the IFNG gene. |
| 3362 | 15280353 | Interleukin (IL)-12 and IL-18 enhanced the histone acetylation of the IFNG gene. |
| 3363 | 15280353 | Interleukin (IL)-12 and IL-18 enhanced the histone acetylation of the IFNG gene. |
| 3364 | 15280353 | Interleukin (IL)-12 and IL-18 enhanced the histone acetylation of the IFNG gene. |
| 3365 | 15280353 | By contrast, histone acetylation of the TBET gene was markedly suppressed by IL-4, whereas IL-12 and IL-18 had only modest effects suggesting that histone acetylation during TH1 differentiation is a process that is regulated by various factors at multiple levels. |
| 3366 | 15280353 | By contrast, histone acetylation of the TBET gene was markedly suppressed by IL-4, whereas IL-12 and IL-18 had only modest effects suggesting that histone acetylation during TH1 differentiation is a process that is regulated by various factors at multiple levels. |
| 3367 | 15280353 | By contrast, histone acetylation of the TBET gene was markedly suppressed by IL-4, whereas IL-12 and IL-18 had only modest effects suggesting that histone acetylation during TH1 differentiation is a process that is regulated by various factors at multiple levels. |
| 3368 | 15280353 | By contrast, histone acetylation of the TBET gene was markedly suppressed by IL-4, whereas IL-12 and IL-18 had only modest effects suggesting that histone acetylation during TH1 differentiation is a process that is regulated by various factors at multiple levels. |
| 3369 | 15280353 | By contrast, histone acetylation of the TBET gene was markedly suppressed by IL-4, whereas IL-12 and IL-18 had only modest effects suggesting that histone acetylation during TH1 differentiation is a process that is regulated by various factors at multiple levels. |
| 3370 | 15280353 | By treating Th2 cells with a histone deacetylase inhibitor, we restored histone acetylation of the IFNG and TBET genes, but it did not fully restore their expression in TH2 cells, again suggesting that histone acetylation explains one but not all the aspects of TH1-specific gene expression. |
| 3371 | 15280353 | By treating Th2 cells with a histone deacetylase inhibitor, we restored histone acetylation of the IFNG and TBET genes, but it did not fully restore their expression in TH2 cells, again suggesting that histone acetylation explains one but not all the aspects of TH1-specific gene expression. |
| 3372 | 15280353 | By treating Th2 cells with a histone deacetylase inhibitor, we restored histone acetylation of the IFNG and TBET genes, but it did not fully restore their expression in TH2 cells, again suggesting that histone acetylation explains one but not all the aspects of TH1-specific gene expression. |
| 3373 | 15280353 | By treating Th2 cells with a histone deacetylase inhibitor, we restored histone acetylation of the IFNG and TBET genes, but it did not fully restore their expression in TH2 cells, again suggesting that histone acetylation explains one but not all the aspects of TH1-specific gene expression. |
| 3374 | 15280353 | By treating Th2 cells with a histone deacetylase inhibitor, we restored histone acetylation of the IFNG and TBET genes, but it did not fully restore their expression in TH2 cells, again suggesting that histone acetylation explains one but not all the aspects of TH1-specific gene expression. |
| 3375 | 15271977 | A distal region in the interferon-gamma gene is a site of epigenetic remodeling and transcriptional regulation by interleukin-2. |
| 3376 | 15271977 | A distal region in the interferon-gamma gene is a site of epigenetic remodeling and transcriptional regulation by interleukin-2. |
| 3377 | 15271977 | A distal region in the interferon-gamma gene is a site of epigenetic remodeling and transcriptional regulation by interleukin-2. |
| 3378 | 15271977 | A distal region in the interferon-gamma gene is a site of epigenetic remodeling and transcriptional regulation by interleukin-2. |
| 3379 | 15271977 | A distal region in the interferon-gamma gene is a site of epigenetic remodeling and transcriptional regulation by interleukin-2. |
| 3380 | 15271977 | A distal region in the interferon-gamma gene is a site of epigenetic remodeling and transcriptional regulation by interleukin-2. |
| 3381 | 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. |
| 3382 | 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. |
| 3383 | 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. |
| 3384 | 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. |
| 3385 | 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. |
| 3386 | 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. |
| 3387 | 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. |
| 3388 | 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. |
| 3389 | 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. |
| 3390 | 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. |
| 3391 | 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. |
| 3392 | 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. |
| 3393 | 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. |
| 3394 | 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. |
| 3395 | 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. |
| 3396 | 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. |
| 3397 | 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. |
| 3398 | 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. |
| 3399 | 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. |
| 3400 | 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. |
| 3401 | 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. |
| 3402 | 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. |
| 3403 | 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. |
| 3404 | 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. |
| 3405 | 15271977 | The effect of IL-2 was lost when the Stat5 motif was disrupted. |
| 3406 | 15271977 | The effect of IL-2 was lost when the Stat5 motif was disrupted. |
| 3407 | 15271977 | The effect of IL-2 was lost when the Stat5 motif was disrupted. |
| 3408 | 15271977 | The effect of IL-2 was lost when the Stat5 motif was disrupted. |
| 3409 | 15271977 | The effect of IL-2 was lost when the Stat5 motif was disrupted. |
| 3410 | 15271977 | The effect of IL-2 was lost when the Stat5 motif was disrupted. |
| 3411 | 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. |
| 3412 | 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. |
| 3413 | 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. |
| 3414 | 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. |
| 3415 | 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. |
| 3416 | 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. |
| 3417 | 15241679 | Therefore, we focused on the Th1-specific T-box transcription factor gene (T-bet), which contributes to the induction of the hallmark Th1 cytokine, IFN-gamma. |
| 3418 | 15241679 | Therefore, we focused on the Th1-specific T-box transcription factor gene (T-bet), which contributes to the induction of the hallmark Th1 cytokine, IFN-gamma. |
| 3419 | 15241679 | Therefore, we focused on the Th1-specific T-box transcription factor gene (T-bet), which contributes to the induction of the hallmark Th1 cytokine, IFN-gamma. |
| 3420 | 15241679 | Furthermore, Gln33 T-bet showed a significantly higher transcriptional activity of the IFNG gene via a dual luciferase reporter assay. |
| 3421 | 15241679 | Furthermore, Gln33 T-bet showed a significantly higher transcriptional activity of the IFNG gene via a dual luciferase reporter assay. |
| 3422 | 15241679 | Furthermore, Gln33 T-bet showed a significantly higher transcriptional activity of the IFNG gene via a dual luciferase reporter assay. |
| 3423 | 15241679 | Our study suggests the first evidence of an association between type 1 diabetes and polymorphisms in the T-bet gene, and that variation in T-bet transcriptional activity may play a role in the development of type 1 diabetes, possibly through the effect on IFN-gamma production in Th1 cells. |
| 3424 | 15241679 | Our study suggests the first evidence of an association between type 1 diabetes and polymorphisms in the T-bet gene, and that variation in T-bet transcriptional activity may play a role in the development of type 1 diabetes, possibly through the effect on IFN-gamma production in Th1 cells. |
| 3425 | 15241679 | Our study suggests the first evidence of an association between type 1 diabetes and polymorphisms in the T-bet gene, and that variation in T-bet transcriptional activity may play a role in the development of type 1 diabetes, possibly through the effect on IFN-gamma production in Th1 cells. |
| 3426 | 15194744 | PAR2 activation alters colonic paracellular permeability in mice via IFN-gamma-dependent and -independent pathways. |
| 3427 | 15194744 | PAR2 activation alters colonic paracellular permeability in mice via IFN-gamma-dependent and -independent pathways. |
| 3428 | 15194744 | PAR2 activation alters colonic paracellular permeability in mice via IFN-gamma-dependent and -independent pathways. |
| 3429 | 15194744 | We further investigated the possible involvement of interferon gamma (IFN-gamma) and calmodulin-dependent activation of myosin light chain kinase (MLCK), and alterations of zonula occludens-1 (ZO-1) localization in PAR(2)-induced responses. |
| 3430 | 15194744 | We further investigated the possible involvement of interferon gamma (IFN-gamma) and calmodulin-dependent activation of myosin light chain kinase (MLCK), and alterations of zonula occludens-1 (ZO-1) localization in PAR(2)-induced responses. |
| 3431 | 15194744 | We further investigated the possible involvement of interferon gamma (IFN-gamma) and calmodulin-dependent activation of myosin light chain kinase (MLCK), and alterations of zonula occludens-1 (ZO-1) localization in PAR(2)-induced responses. |
| 3432 | 15194744 | Western blotting showed phosphorylation of mucosal myosin light chain (MLC) expression after both doses of SLIGRL. |
| 3433 | 15194744 | Western blotting showed phosphorylation of mucosal myosin light chain (MLC) expression after both doses of SLIGRL. |
| 3434 | 15194744 | Western blotting showed phosphorylation of mucosal myosin light chain (MLC) expression after both doses of SLIGRL. |
| 3435 | 15194744 | Finally, we have shown that direct activation of PAR(2) on enterocytes is responsible for increased permeability and ZO-1 disruption. |
| 3436 | 15194744 | Finally, we have shown that direct activation of PAR(2) on enterocytes is responsible for increased permeability and ZO-1 disruption. |
| 3437 | 15194744 | Finally, we have shown that direct activation of PAR(2) on enterocytes is responsible for increased permeability and ZO-1 disruption. |
| 3438 | 15194744 | The resulting tight junction opening does not depend upon IFN-gamma secretion, while the increased permeability in response to the high dose of PAR(2) agonist involves IFN-gamma secretion. |
| 3439 | 15194744 | The resulting tight junction opening does not depend upon IFN-gamma secretion, while the increased permeability in response to the high dose of PAR(2) agonist involves IFN-gamma secretion. |
| 3440 | 15194744 | The resulting tight junction opening does not depend upon IFN-gamma secretion, while the increased permeability in response to the high dose of PAR(2) agonist involves IFN-gamma secretion. |
| 3441 | 15187113 | We hypothesized that IL-12 pretreatments would result in endogenous IFN-gamma production, and that this, in turn, would up-regulate levels of Janus kinase-STAT signaling intermediates and lead to increased expression of genes regulated by IFN-alpha. |
| 3442 | 15187113 | We hypothesized that IL-12 pretreatments would result in endogenous IFN-gamma production, and that this, in turn, would up-regulate levels of Janus kinase-STAT signaling intermediates and lead to increased expression of genes regulated by IFN-alpha. |
| 3443 | 15187113 | We hypothesized that IL-12 pretreatments would result in endogenous IFN-gamma production, and that this, in turn, would up-regulate levels of Janus kinase-STAT signaling intermediates and lead to increased expression of genes regulated by IFN-alpha. |
| 3444 | 15187113 | We hypothesized that IL-12 pretreatments would result in endogenous IFN-gamma production, and that this, in turn, would up-regulate levels of Janus kinase-STAT signaling intermediates and lead to increased expression of genes regulated by IFN-alpha. |
| 3445 | 15187113 | We hypothesized that IL-12 pretreatments would result in endogenous IFN-gamma production, and that this, in turn, would up-regulate levels of Janus kinase-STAT signaling intermediates and lead to increased expression of genes regulated by IFN-alpha. |
| 3446 | 15187113 | We hypothesized that IL-12 pretreatments would result in endogenous IFN-gamma production, and that this, in turn, would up-regulate levels of Janus kinase-STAT signaling intermediates and lead to increased expression of genes regulated by IFN-alpha. |
| 3447 | 15187113 | Pretreatment of PBMCs and tumor cells with IFN-gamma-containing supernatants from IL-12-stimulated PBMCs led to up-regulation of STAT1, STAT2, and IFN regulatory factor 9 (IRF9) and potentiated IFN-alpha-induced STAT signaling within PBMCs and tumor cells. |
| 3448 | 15187113 | Pretreatment of PBMCs and tumor cells with IFN-gamma-containing supernatants from IL-12-stimulated PBMCs led to up-regulation of STAT1, STAT2, and IFN regulatory factor 9 (IRF9) and potentiated IFN-alpha-induced STAT signaling within PBMCs and tumor cells. |
| 3449 | 15187113 | Pretreatment of PBMCs and tumor cells with IFN-gamma-containing supernatants from IL-12-stimulated PBMCs led to up-regulation of STAT1, STAT2, and IFN regulatory factor 9 (IRF9) and potentiated IFN-alpha-induced STAT signaling within PBMCs and tumor cells. |
| 3450 | 15187113 | Pretreatment of PBMCs and tumor cells with IFN-gamma-containing supernatants from IL-12-stimulated PBMCs led to up-regulation of STAT1, STAT2, and IFN regulatory factor 9 (IRF9) and potentiated IFN-alpha-induced STAT signaling within PBMCs and tumor cells. |
| 3451 | 15187113 | Pretreatment of PBMCs and tumor cells with IFN-gamma-containing supernatants from IL-12-stimulated PBMCs led to up-regulation of STAT1, STAT2, and IFN regulatory factor 9 (IRF9) and potentiated IFN-alpha-induced STAT signaling within PBMCs and tumor cells. |
| 3452 | 15187113 | Pretreatment of PBMCs and tumor cells with IFN-gamma-containing supernatants from IL-12-stimulated PBMCs led to up-regulation of STAT1, STAT2, and IFN regulatory factor 9 (IRF9) and potentiated IFN-alpha-induced STAT signaling within PBMCs and tumor cells. |
| 3453 | 15187113 | Pretreatment of HT144 melanoma cells and PBMCs with IFN-gamma or IFN-gamma-containing supernatants enhanced the actions of IFN-alpha at the transcriptional level, as measured by real-time RT PCR analysis of the IFN-stimulated gene 15. |
| 3454 | 15187113 | Pretreatment of HT144 melanoma cells and PBMCs with IFN-gamma or IFN-gamma-containing supernatants enhanced the actions of IFN-alpha at the transcriptional level, as measured by real-time RT PCR analysis of the IFN-stimulated gene 15. |
| 3455 | 15187113 | Pretreatment of HT144 melanoma cells and PBMCs with IFN-gamma or IFN-gamma-containing supernatants enhanced the actions of IFN-alpha at the transcriptional level, as measured by real-time RT PCR analysis of the IFN-stimulated gene 15. |
| 3456 | 15187113 | Pretreatment of HT144 melanoma cells and PBMCs with IFN-gamma or IFN-gamma-containing supernatants enhanced the actions of IFN-alpha at the transcriptional level, as measured by real-time RT PCR analysis of the IFN-stimulated gene 15. |
| 3457 | 15187113 | Pretreatment of HT144 melanoma cells and PBMCs with IFN-gamma or IFN-gamma-containing supernatants enhanced the actions of IFN-alpha at the transcriptional level, as measured by real-time RT PCR analysis of the IFN-stimulated gene 15. |
| 3458 | 15187113 | Pretreatment of HT144 melanoma cells and PBMCs with IFN-gamma or IFN-gamma-containing supernatants enhanced the actions of IFN-alpha at the transcriptional level, as measured by real-time RT PCR analysis of the IFN-stimulated gene 15. |
| 3459 | 15187113 | Experiments in wild-type C57BL/6 and IFN-gamma receptor knockout (B6.129S7-Ifngr(tm1Agt)) mice demonstrated that a regimen of IL-12 pretreatment, followed by IFN-alpha, could cure mice of i.p. |
| 3460 | 15187113 | Experiments in wild-type C57BL/6 and IFN-gamma receptor knockout (B6.129S7-Ifngr(tm1Agt)) mice demonstrated that a regimen of IL-12 pretreatment, followed by IFN-alpha, could cure mice of i.p. |
| 3461 | 15187113 | Experiments in wild-type C57BL/6 and IFN-gamma receptor knockout (B6.129S7-Ifngr(tm1Agt)) mice demonstrated that a regimen of IL-12 pretreatment, followed by IFN-alpha, could cure mice of i.p. |
| 3462 | 15187113 | Experiments in wild-type C57BL/6 and IFN-gamma receptor knockout (B6.129S7-Ifngr(tm1Agt)) mice demonstrated that a regimen of IL-12 pretreatment, followed by IFN-alpha, could cure mice of i.p. |
| 3463 | 15187113 | Experiments in wild-type C57BL/6 and IFN-gamma receptor knockout (B6.129S7-Ifngr(tm1Agt)) mice demonstrated that a regimen of IL-12 pretreatment, followed by IFN-alpha, could cure mice of i.p. |
| 3464 | 15187113 | Experiments in wild-type C57BL/6 and IFN-gamma receptor knockout (B6.129S7-Ifngr(tm1Agt)) mice demonstrated that a regimen of IL-12 pretreatment, followed by IFN-alpha, could cure mice of i.p. |
| 3465 | 15187113 | However, this treatment regimen did not significantly prolong the survival of IFN-gamma-deficient (B6.129S7-Ifng(tm1Ts)) mice compared with mice treated with IFN-alpha alone. |
| 3466 | 15187113 | However, this treatment regimen did not significantly prolong the survival of IFN-gamma-deficient (B6.129S7-Ifng(tm1Ts)) mice compared with mice treated with IFN-alpha alone. |
| 3467 | 15187113 | However, this treatment regimen did not significantly prolong the survival of IFN-gamma-deficient (B6.129S7-Ifng(tm1Ts)) mice compared with mice treated with IFN-alpha alone. |
| 3468 | 15187113 | However, this treatment regimen did not significantly prolong the survival of IFN-gamma-deficient (B6.129S7-Ifng(tm1Ts)) mice compared with mice treated with IFN-alpha alone. |
| 3469 | 15187113 | However, this treatment regimen did not significantly prolong the survival of IFN-gamma-deficient (B6.129S7-Ifng(tm1Ts)) mice compared with mice treated with IFN-alpha alone. |
| 3470 | 15187113 | However, this treatment regimen did not significantly prolong the survival of IFN-gamma-deficient (B6.129S7-Ifng(tm1Ts)) mice compared with mice treated with IFN-alpha alone. |
| 3471 | 15187113 | These results suggest that the response to IFN-alpha immunotherapy can be significantly enhanced by IL-12 pretreatment, and this effect is dependent upon endogenous IFN-gamma production and its actions on melanoma cells. |
| 3472 | 15187113 | These results suggest that the response to IFN-alpha immunotherapy can be significantly enhanced by IL-12 pretreatment, and this effect is dependent upon endogenous IFN-gamma production and its actions on melanoma cells. |
| 3473 | 15187113 | These results suggest that the response to IFN-alpha immunotherapy can be significantly enhanced by IL-12 pretreatment, and this effect is dependent upon endogenous IFN-gamma production and its actions on melanoma cells. |
| 3474 | 15187113 | These results suggest that the response to IFN-alpha immunotherapy can be significantly enhanced by IL-12 pretreatment, and this effect is dependent upon endogenous IFN-gamma production and its actions on melanoma cells. |
| 3475 | 15187113 | These results suggest that the response to IFN-alpha immunotherapy can be significantly enhanced by IL-12 pretreatment, and this effect is dependent upon endogenous IFN-gamma production and its actions on melanoma cells. |
| 3476 | 15187113 | These results suggest that the response to IFN-alpha immunotherapy can be significantly enhanced by IL-12 pretreatment, and this effect is dependent upon endogenous IFN-gamma production and its actions on melanoma cells. |
| 3477 | 15183000 | This publication describes the cloning of full or partial length sequences for pig TBX21 (T-bet), MYD88, ICSBP1, CD8A (CD8alpha), CD8B (CD8beta), and CD28 cDNAs. |
| 3478 | 15183000 | This publication describes the cloning of full or partial length sequences for pig TBX21 (T-bet), MYD88, ICSBP1, CD8A (CD8alpha), CD8B (CD8beta), and CD28 cDNAs. |
| 3479 | 15183000 | Real-time PCR assays have been developed for the relative quantitation of these products as well as previously characterized transcripts that encode exon A-containing CD45, HLX1, IRF1, STAT1 and RPL32. |
| 3480 | 15183000 | Real-time PCR assays have been developed for the relative quantitation of these products as well as previously characterized transcripts that encode exon A-containing CD45, HLX1, IRF1, STAT1 and RPL32. |
| 3481 | 15183000 | When used for examining temporal immune gene expression in the liver of Toxoplasma gondii infected pigs, the positive regulators of Th1 responses, IRF1, MYD88, and STAT1, were found to be expressed prior to the simultaneous upregulation of interferon gamma (IFNG), HLX1 and TBX21 gene expression. |
| 3482 | 15183000 | When used for examining temporal immune gene expression in the liver of Toxoplasma gondii infected pigs, the positive regulators of Th1 responses, IRF1, MYD88, and STAT1, were found to be expressed prior to the simultaneous upregulation of interferon gamma (IFNG), HLX1 and TBX21 gene expression. |
| 3483 | 15183000 | In contrast, in the mesenteric lymph node (MLN), only expression of IRF1 and IFNG was significantly upregulated. |
| 3484 | 15183000 | In contrast, in the mesenteric lymph node (MLN), only expression of IRF1 and IFNG was significantly upregulated. |
| 3485 | 15182327 | The role of IFN-gamma receptor 1 (IFNGR1) and IFN-gamma receptor 2 (IFNGR2) gene polymorphisms has not been studied in MS, and, for the IFNG gene polymorphism there is only one previous study, which incorporates clinical, but not imaging, data. |
| 3486 | 15182327 | The role of IFN-gamma receptor 1 (IFNGR1) and IFN-gamma receptor 2 (IFNGR2) gene polymorphisms has not been studied in MS, and, for the IFNG gene polymorphism there is only one previous study, which incorporates clinical, but not imaging, data. |
| 3487 | 15182327 | The role of IFN-gamma receptor 1 (IFNGR1) and IFN-gamma receptor 2 (IFNGR2) gene polymorphisms has not been studied in MS, and, for the IFNG gene polymorphism there is only one previous study, which incorporates clinical, but not imaging, data. |
| 3488 | 15182327 | The role of IFN-gamma receptor 1 (IFNGR1) and IFN-gamma receptor 2 (IFNGR2) gene polymorphisms has not been studied in MS, and, for the IFNG gene polymorphism there is only one previous study, which incorporates clinical, but not imaging, data. |
| 3489 | 15182327 | The aim of this study was to investigate whether polymorphisms in the IFNG and IFNGR1 and IFNGR2 genes are associated with susceptibility to MS, or disease characteristics, as defined by clinical and imaging criteria. |
| 3490 | 15182327 | The aim of this study was to investigate whether polymorphisms in the IFNG and IFNGR1 and IFNGR2 genes are associated with susceptibility to MS, or disease characteristics, as defined by clinical and imaging criteria. |
| 3491 | 15182327 | The aim of this study was to investigate whether polymorphisms in the IFNG and IFNGR1 and IFNGR2 genes are associated with susceptibility to MS, or disease characteristics, as defined by clinical and imaging criteria. |
| 3492 | 15182327 | The aim of this study was to investigate whether polymorphisms in the IFNG and IFNGR1 and IFNGR2 genes are associated with susceptibility to MS, or disease characteristics, as defined by clinical and imaging criteria. |
| 3493 | 15182327 | Genotypes for IFNG, IFNGR1 and IFNGR2 were determined in 509 patients with MS and in 193 healthy controls. |
| 3494 | 15182327 | Genotypes for IFNG, IFNGR1 and IFNGR2 were determined in 509 patients with MS and in 193 healthy controls. |
| 3495 | 15182327 | Genotypes for IFNG, IFNGR1 and IFNGR2 were determined in 509 patients with MS and in 193 healthy controls. |
| 3496 | 15182327 | Genotypes for IFNG, IFNGR1 and IFNGR2 were determined in 509 patients with MS and in 193 healthy controls. |
| 3497 | 15182327 | No significant differences in the distribution of IFNG, IFNGR1 and IFNGR2 genotype and allele frequencies were found between patients and controls. |
| 3498 | 15182327 | No significant differences in the distribution of IFNG, IFNGR1 and IFNGR2 genotype and allele frequencies were found between patients and controls. |
| 3499 | 15182327 | No significant differences in the distribution of IFNG, IFNGR1 and IFNGR2 genotype and allele frequencies were found between patients and controls. |
| 3500 | 15182327 | No significant differences in the distribution of IFNG, IFNGR1 and IFNGR2 genotype and allele frequencies were found between patients and controls. |
| 3501 | 15182327 | The IFNGR1 and IFNGR2 gene polymorphisms studied do not exert an important influence on MS susceptibility, but allele IFNGR2*Arg64 may be associated with a progressive disease onset. |
| 3502 | 15182327 | The IFNGR1 and IFNGR2 gene polymorphisms studied do not exert an important influence on MS susceptibility, but allele IFNGR2*Arg64 may be associated with a progressive disease onset. |
| 3503 | 15182327 | The IFNGR1 and IFNGR2 gene polymorphisms studied do not exert an important influence on MS susceptibility, but allele IFNGR2*Arg64 may be associated with a progressive disease onset. |
| 3504 | 15182327 | The IFNGR1 and IFNGR2 gene polymorphisms studied do not exert an important influence on MS susceptibility, but allele IFNGR2*Arg64 may be associated with a progressive disease onset. |
| 3505 | 15166131 | Interferon-gamma gene dinucleotide (CA) repeat and interleukin-4 promoter region (-590C/T) polymorphisms in Japanese patients with endometriosis. |
| 3506 | 15115612 | LIGHT sensitizes IFN-gamma-mediated apoptosis of HT-29 human carcinoma cells through both death receptor and mitochondria pathways. |
| 3507 | 15115612 | LIGHT sensitizes IFN-gamma-mediated apoptosis of HT-29 human carcinoma cells through both death receptor and mitochondria pathways. |
| 3508 | 15115612 | LIGHT sensitizes IFN-gamma-mediated apoptosis of HT-29 human carcinoma cells through both death receptor and mitochondria pathways. |
| 3509 | 15115612 | LIGHT sensitizes IFN-gamma-mediated apoptosis of HT-29 human carcinoma cells through both death receptor and mitochondria pathways. |
| 3510 | 15115612 | LIGHT sensitizes IFN-gamma-mediated apoptosis of HT-29 human carcinoma cells through both death receptor and mitochondria pathways. |
| 3511 | 15115612 | LIGHT [homologous to lymphotoxins, shows inducible expression, and competes with herpes simplex virus glycoprotein D for herpes virus entry mediator (HVEM/TR2)] is a new member of TNF superfamily. |
| 3512 | 15115612 | LIGHT [homologous to lymphotoxins, shows inducible expression, and competes with herpes simplex virus glycoprotein D for herpes virus entry mediator (HVEM/TR2)] is a new member of TNF superfamily. |
| 3513 | 15115612 | LIGHT [homologous to lymphotoxins, shows inducible expression, and competes with herpes simplex virus glycoprotein D for herpes virus entry mediator (HVEM/TR2)] is a new member of TNF superfamily. |
| 3514 | 15115612 | LIGHT [homologous to lymphotoxins, shows inducible expression, and competes with herpes simplex virus glycoprotein D for herpes virus entry mediator (HVEM/TR2)] is a new member of TNF superfamily. |
| 3515 | 15115612 | LIGHT [homologous to lymphotoxins, shows inducible expression, and competes with herpes simplex virus glycoprotein D for herpes virus entry mediator (HVEM/TR2)] is a new member of TNF superfamily. |
| 3516 | 15115612 | The HT-29 colon cancer cell line is the most sensitive to LIGHT-induced, IFNg-mediated apoptosis among the cell lines we have examined so far. |
| 3517 | 15115612 | The HT-29 colon cancer cell line is the most sensitive to LIGHT-induced, IFNg-mediated apoptosis among the cell lines we have examined so far. |
| 3518 | 15115612 | The HT-29 colon cancer cell line is the most sensitive to LIGHT-induced, IFNg-mediated apoptosis among the cell lines we have examined so far. |
| 3519 | 15115612 | The HT-29 colon cancer cell line is the most sensitive to LIGHT-induced, IFNg-mediated apoptosis among the cell lines we have examined so far. |
| 3520 | 15115612 | The HT-29 colon cancer cell line is the most sensitive to LIGHT-induced, IFNg-mediated apoptosis among the cell lines we have examined so far. |
| 3521 | 15115612 | Besides downregulation of Bcl-XL, upregulation of Bak, and activation of both PARP [poly (ADP-ribose) polymerase] and DFF45 (DNA fragmentation factor), LIGHT-induced, IFNg-mediated apoptosis of HT-29 cells involves extensive caspase activation. |
| 3522 | 15115612 | Besides downregulation of Bcl-XL, upregulation of Bak, and activation of both PARP [poly (ADP-ribose) polymerase] and DFF45 (DNA fragmentation factor), LIGHT-induced, IFNg-mediated apoptosis of HT-29 cells involves extensive caspase activation. |
| 3523 | 15115612 | Besides downregulation of Bcl-XL, upregulation of Bak, and activation of both PARP [poly (ADP-ribose) polymerase] and DFF45 (DNA fragmentation factor), LIGHT-induced, IFNg-mediated apoptosis of HT-29 cells involves extensive caspase activation. |
| 3524 | 15115612 | Besides downregulation of Bcl-XL, upregulation of Bak, and activation of both PARP [poly (ADP-ribose) polymerase] and DFF45 (DNA fragmentation factor), LIGHT-induced, IFNg-mediated apoptosis of HT-29 cells involves extensive caspase activation. |
| 3525 | 15115612 | Besides downregulation of Bcl-XL, upregulation of Bak, and activation of both PARP [poly (ADP-ribose) polymerase] and DFF45 (DNA fragmentation factor), LIGHT-induced, IFNg-mediated apoptosis of HT-29 cells involves extensive caspase activation. |
| 3526 | 15115612 | Caspase-8 and caspase-9 activation, as shown by their cleavages appeared as early as 24 h after treatment, whereas caspase-3 and caspase-7 activation, as shown by their cleavages occurred after 72 h of LIGHT treatment. |
| 3527 | 15115612 | Caspase-8 and caspase-9 activation, as shown by their cleavages appeared as early as 24 h after treatment, whereas caspase-3 and caspase-7 activation, as shown by their cleavages occurred after 72 h of LIGHT treatment. |
| 3528 | 15115612 | Caspase-8 and caspase-9 activation, as shown by their cleavages appeared as early as 24 h after treatment, whereas caspase-3 and caspase-7 activation, as shown by their cleavages occurred after 72 h of LIGHT treatment. |
| 3529 | 15115612 | Caspase-8 and caspase-9 activation, as shown by their cleavages appeared as early as 24 h after treatment, whereas caspase-3 and caspase-7 activation, as shown by their cleavages occurred after 72 h of LIGHT treatment. |
| 3530 | 15115612 | Caspase-8 and caspase-9 activation, as shown by their cleavages appeared as early as 24 h after treatment, whereas caspase-3 and caspase-7 activation, as shown by their cleavages occurred after 72 h of LIGHT treatment. |
| 3531 | 15115612 | Caspase-3 inhibitor Z-DEVD-FMK (benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone) and a broad range caspase inhibitor Z-VAD-FMK (benzyloxycarbonyl-Val-Ala-Asp fluoromethylketone) were able to block LIGHT-induced, IFNg-mediated apoptosis of HT-29 cells. |
| 3532 | 15115612 | Caspase-3 inhibitor Z-DEVD-FMK (benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone) and a broad range caspase inhibitor Z-VAD-FMK (benzyloxycarbonyl-Val-Ala-Asp fluoromethylketone) were able to block LIGHT-induced, IFNg-mediated apoptosis of HT-29 cells. |
| 3533 | 15115612 | Caspase-3 inhibitor Z-DEVD-FMK (benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone) and a broad range caspase inhibitor Z-VAD-FMK (benzyloxycarbonyl-Val-Ala-Asp fluoromethylketone) were able to block LIGHT-induced, IFNg-mediated apoptosis of HT-29 cells. |
| 3534 | 15115612 | Caspase-3 inhibitor Z-DEVD-FMK (benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone) and a broad range caspase inhibitor Z-VAD-FMK (benzyloxycarbonyl-Val-Ala-Asp fluoromethylketone) were able to block LIGHT-induced, IFNg-mediated apoptosis of HT-29 cells. |
| 3535 | 15115612 | Caspase-3 inhibitor Z-DEVD-FMK (benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone) and a broad range caspase inhibitor Z-VAD-FMK (benzyloxycarbonyl-Val-Ala-Asp fluoromethylketone) were able to block LIGHT-induced, IFNg-mediated apoptosis of HT-29 cells. |
| 3536 | 15115612 | These results suggest that LIGHT-induced, IFNg-mediated apoptosis of HT-29 cells is caspase-dependent, and LIGHT signaling is mediated through both death receptor and mitochondria pathways. |
| 3537 | 15115612 | These results suggest that LIGHT-induced, IFNg-mediated apoptosis of HT-29 cells is caspase-dependent, and LIGHT signaling is mediated through both death receptor and mitochondria pathways. |
| 3538 | 15115612 | These results suggest that LIGHT-induced, IFNg-mediated apoptosis of HT-29 cells is caspase-dependent, and LIGHT signaling is mediated through both death receptor and mitochondria pathways. |
| 3539 | 15115612 | These results suggest that LIGHT-induced, IFNg-mediated apoptosis of HT-29 cells is caspase-dependent, and LIGHT signaling is mediated through both death receptor and mitochondria pathways. |
| 3540 | 15115612 | These results suggest that LIGHT-induced, IFNg-mediated apoptosis of HT-29 cells is caspase-dependent, and LIGHT signaling is mediated through both death receptor and mitochondria pathways. |
| 3541 | 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. |
| 3542 | 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. |
| 3543 | 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. |
| 3544 | 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. |
| 3545 | 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. |
| 3546 | 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. |
| 3547 | 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. |
| 3548 | 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. |
| 3549 | 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. |
| 3550 | 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. |
| 3551 | 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. |
| 3552 | 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. |
| 3553 | 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. |
| 3554 | 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. |
| 3555 | 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. |
| 3556 | 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. |
| 3557 | 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. |
| 3558 | 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. |
| 3559 | 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. |
| 3560 | 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. |
| 3561 | 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. |
| 3562 | 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. |
| 3563 | 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. |
| 3564 | 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. |
| 3565 | 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. |
| 3566 | 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. |
| 3567 | 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. |
| 3568 | 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. |
| 3569 | 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. |
| 3570 | 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. |
| 3571 | 15073568 | CRH, 10(-7) M, significantly reversed the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of IFNg production. |
| 3572 | 15073568 | CRH, 10(-7) M, significantly reversed the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of IFNg production. |
| 3573 | 15073568 | CRH, 10(-7) M, significantly reversed the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of IFNg production. |
| 3574 | 15073568 | CRH, 10(-7) M, significantly reversed the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of IFNg production. |
| 3575 | 15073568 | CRH, 10(-7) M, significantly reversed the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of IFNg production. |
| 3576 | 15073568 | CRH, 10(-7) M, significantly reversed the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of IFNg production. |
| 3577 | 15073568 | CRH at all concentrations significantly blocked the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of TNFalpha production. |
| 3578 | 15073568 | CRH at all concentrations significantly blocked the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of TNFalpha production. |
| 3579 | 15073568 | CRH at all concentrations significantly blocked the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of TNFalpha production. |
| 3580 | 15073568 | CRH at all concentrations significantly blocked the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of TNFalpha production. |
| 3581 | 15073568 | CRH at all concentrations significantly blocked the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of TNFalpha production. |
| 3582 | 15073568 | CRH at all concentrations significantly blocked the 5-HT (1.5 microg/mL and 15 microg/mL)-induced suppression of TNFalpha production. |
| 3583 | 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. |
| 3584 | 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. |
| 3585 | 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. |
| 3586 | 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. |
| 3587 | 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. |
| 3588 | 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. |
| 3589 | 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. |
| 3590 | 15021309 | No SNPs at IFNG, IL2, IL12B, TNF, or CCL2 (MCP1) showed any association with HIV-related outcomes. |
| 3591 | 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. |
| 3592 | 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. |
| 3593 | 15004750 | To identify a key genetic factor in the pathogenesis of sarcoidosis, we investigated single nucleotide polymorphisms within 10 candidate genes involved in type 1 immune process ( IFNA17, IFNB, IFNG, IFNGR1, IFNGR2, IL12B, IL12RB1, IL12RB2, ETA-1, and NRAMP1) in an association-based study of 102 Japanese patients with sarcoidosis, 114 with tuberculosis, and 110 control subjects. |
| 3594 | 15004750 | We further typed another IFNA polymorphism ( IFNA10 60T-->A) and confirmed two major haplotypes of the IFNA gene, viz., allele 1: IFNA10 [60T]- IFNA17 [551T] and allele 2: IFNA10 [60A]- IFNA17 [551G], in the Japanese population. |
| 3595 | 14767694 | Chromosome 12 genes that showed association with the disease in at least one report include: the signal transducer and activator of transcription 6 gene ( STAT6), the nitrogen oxide synthetase 1 gene ( NOS1), the interferon gamma gene ( IFNG), and the activation-induced cytidine deaminase gene ( AICDA). |
| 3596 | 14767694 | Chromosome 12 genes that showed association with the disease in at least one report include: the signal transducer and activator of transcription 6 gene ( STAT6), the nitrogen oxide synthetase 1 gene ( NOS1), the interferon gamma gene ( IFNG), and the activation-induced cytidine deaminase gene ( AICDA). |
| 3597 | 14767694 | Chromosome 12 genes that showed association with the disease in at least one report include: the signal transducer and activator of transcription 6 gene ( STAT6), the nitrogen oxide synthetase 1 gene ( NOS1), the interferon gamma gene ( IFNG), and the activation-induced cytidine deaminase gene ( AICDA). |
| 3598 | 14767694 | To investigate association between chromosome 12 candidate genes and asthma, distributions of alleles and genotypes of repeat polymorphisms of STAT6, NOS1, and IFNG were compared between controls and patients. |
| 3599 | 14767694 | To investigate association between chromosome 12 candidate genes and asthma, distributions of alleles and genotypes of repeat polymorphisms of STAT6, NOS1, and IFNG were compared between controls and patients. |
| 3600 | 14767694 | To investigate association between chromosome 12 candidate genes and asthma, distributions of alleles and genotypes of repeat polymorphisms of STAT6, NOS1, and IFNG were compared between controls and patients. |
| 3601 | 14767694 | The NOS1 intron 2 GT repeat and STAT6 exon 1 GT repeat were associated with asthma. |
| 3602 | 14767694 | The NOS1 intron 2 GT repeat and STAT6 exon 1 GT repeat were associated with asthma. |
| 3603 | 14767694 | The NOS1 intron 2 GT repeat and STAT6 exon 1 GT repeat were associated with asthma. |
| 3604 | 14767694 | Neither the IFNG intron 1 CA repeat nor 465C/T of AICDA showed any association with asthma. |
| 3605 | 14767694 | Neither the IFNG intron 1 CA repeat nor 465C/T of AICDA showed any association with asthma. |
| 3606 | 14767694 | Neither the IFNG intron 1 CA repeat nor 465C/T of AICDA showed any association with asthma. |
| 3607 | 14767694 | Our results suggest that NOS1 and STAT6 are asthma-susceptibility genes and that chromosome region 12q24.23-q24.33 contains other susceptibility gene(s). |
| 3608 | 14767694 | Our results suggest that NOS1 and STAT6 are asthma-susceptibility genes and that chromosome region 12q24.23-q24.33 contains other susceptibility gene(s). |
| 3609 | 14767694 | Our results suggest that NOS1 and STAT6 are asthma-susceptibility genes and that chromosome region 12q24.23-q24.33 contains other susceptibility gene(s). |
| 3610 | 14691261 | Here, we analyze chromatin conformation of the 24-kb region of the Ifng gene during CD4(+) T helper (Th) cell differentiation. |
| 3611 | 14675398 | Polymorphisms of the interferon gamma and interleukin 10 genes in human brucellosis. |
| 3612 | 14675398 | Polymorphisms of the interferon gamma and interleukin 10 genes in human brucellosis. |
| 3613 | 14675398 | We genotyped 83 patients with brucellosis and 101 controls to determine the influence of polymorphisms of the interferon gamma (IFNG) and interleukin 10 (IL10) genes on protection against, or susceptibility to, human brucellosis and its complications. |
| 3614 | 14675398 | We genotyped 83 patients with brucellosis and 101 controls to determine the influence of polymorphisms of the interferon gamma (IFNG) and interleukin 10 (IL10) genes on protection against, or susceptibility to, human brucellosis and its complications. |
| 3615 | 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). |
| 3616 | 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). |
| 3617 | 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. |
| 3618 | 12947554 | [Expression of Fas, FasL and IFN-gamma in gastric cancer]. |
| 3619 | 12931271 | IGFs, basic FGF, and glucose modulate proliferation and apoptosis induced by IFNgamma but not by IL-1beta in rat INS-1E beta-cells. |
| 3620 | 12931271 | IGFs, basic FGF, and glucose modulate proliferation and apoptosis induced by IFNgamma but not by IL-1beta in rat INS-1E beta-cells. |
| 3621 | 12931271 | IGFs, basic FGF, and glucose modulate proliferation and apoptosis induced by IFNgamma but not by IL-1beta in rat INS-1E beta-cells. |
| 3622 | 12931271 | IGFs, basic FGF, and glucose modulate proliferation and apoptosis induced by IFNgamma but not by IL-1beta in rat INS-1E beta-cells. |
| 3623 | 12931271 | We investigated the effects of glucose and beta-cell growth factors (IGF-I, IGF-II, bFGF) on growth and apoptosis in the presence and absence of apoptosis inducing cytokines (IFNgamma, Il-1beta, TNFalpha). |
| 3624 | 12931271 | We investigated the effects of glucose and beta-cell growth factors (IGF-I, IGF-II, bFGF) on growth and apoptosis in the presence and absence of apoptosis inducing cytokines (IFNgamma, Il-1beta, TNFalpha). |
| 3625 | 12931271 | We investigated the effects of glucose and beta-cell growth factors (IGF-I, IGF-II, bFGF) on growth and apoptosis in the presence and absence of apoptosis inducing cytokines (IFNgamma, Il-1beta, TNFalpha). |
| 3626 | 12931271 | We investigated the effects of glucose and beta-cell growth factors (IGF-I, IGF-II, bFGF) on growth and apoptosis in the presence and absence of apoptosis inducing cytokines (IFNgamma, Il-1beta, TNFalpha). |
| 3627 | 12931271 | The cytokines IFNg and IL-1beta, but not TNFalpha strongly induced INS-1E beta-cell apoptosis. |
| 3628 | 12931271 | The cytokines IFNg and IL-1beta, but not TNFalpha strongly induced INS-1E beta-cell apoptosis. |
| 3629 | 12931271 | The cytokines IFNg and IL-1beta, but not TNFalpha strongly induced INS-1E beta-cell apoptosis. |
| 3630 | 12931271 | The cytokines IFNg and IL-1beta, but not TNFalpha strongly induced INS-1E beta-cell apoptosis. |
| 3631 | 12931271 | Most importantly, IGF-II and bFGF inhibited apoptosis induced by IFNg, but not by IL-1beta. |
| 3632 | 12931271 | Most importantly, IGF-II and bFGF inhibited apoptosis induced by IFNg, but not by IL-1beta. |
| 3633 | 12931271 | Most importantly, IGF-II and bFGF inhibited apoptosis induced by IFNg, but not by IL-1beta. |
| 3634 | 12931271 | Most importantly, IGF-II and bFGF inhibited apoptosis induced by IFNg, but not by IL-1beta. |
| 3635 | 12931271 | Cytokines IFNg and IL-1beta differentially interfere with intracellular signaling cascades stimulated by IGFs and bFGF or glucose, respectively. |
| 3636 | 12931271 | Cytokines IFNg and IL-1beta differentially interfere with intracellular signaling cascades stimulated by IGFs and bFGF or glucose, respectively. |
| 3637 | 12931271 | Cytokines IFNg and IL-1beta differentially interfere with intracellular signaling cascades stimulated by IGFs and bFGF or glucose, respectively. |
| 3638 | 12931271 | Cytokines IFNg and IL-1beta differentially interfere with intracellular signaling cascades stimulated by IGFs and bFGF or glucose, respectively. |
| 3639 | 12854077 | A tumor necrosis factor-alpha-inducible promoter variant of interferon-gamma accelerates CD4+ T cell depletion in human immunodeficiency virus-1-infected individuals. |
| 3640 | 12854077 | A tumor necrosis factor-alpha-inducible promoter variant of interferon-gamma accelerates CD4+ T cell depletion in human immunodeficiency virus-1-infected individuals. |
| 3641 | 12854077 | A tumor necrosis factor-alpha-inducible promoter variant of interferon-gamma accelerates CD4+ T cell depletion in human immunodeficiency virus-1-infected individuals. |
| 3642 | 12854077 | A tumor necrosis factor-alpha-inducible promoter variant of interferon-gamma accelerates CD4+ T cell depletion in human immunodeficiency virus-1-infected individuals. |
| 3643 | 12854077 | A polymorphism, -179G/T, in the promoter of the interferon (IFN)-gamma gene (IFNG) confers differential tumor necrosis factor-alpha (TNF-alpha) inducibility to the IFNG promoter. |
| 3644 | 12854077 | A polymorphism, -179G/T, in the promoter of the interferon (IFN)-gamma gene (IFNG) confers differential tumor necrosis factor-alpha (TNF-alpha) inducibility to the IFNG promoter. |
| 3645 | 12854077 | A polymorphism, -179G/T, in the promoter of the interferon (IFN)-gamma gene (IFNG) confers differential tumor necrosis factor-alpha (TNF-alpha) inducibility to the IFNG promoter. |
| 3646 | 12854077 | A polymorphism, -179G/T, in the promoter of the interferon (IFN)-gamma gene (IFNG) confers differential tumor necrosis factor-alpha (TNF-alpha) inducibility to the IFNG promoter. |
| 3647 | 12854077 | In 298 African American human immunodeficiency virus (HIV)-1 seroconverters, the IFNG -179G/T genotype was associated with accelerated progression to CD4 <200 and AIDS-1993, a finding suggesting that IFNG -179T is a risk factor for AIDS progression, as measured by CD4 cell count. |
| 3648 | 12854077 | In 298 African American human immunodeficiency virus (HIV)-1 seroconverters, the IFNG -179G/T genotype was associated with accelerated progression to CD4 <200 and AIDS-1993, a finding suggesting that IFNG -179T is a risk factor for AIDS progression, as measured by CD4 cell count. |
| 3649 | 12854077 | In 298 African American human immunodeficiency virus (HIV)-1 seroconverters, the IFNG -179G/T genotype was associated with accelerated progression to CD4 <200 and AIDS-1993, a finding suggesting that IFNG -179T is a risk factor for AIDS progression, as measured by CD4 cell count. |
| 3650 | 12854077 | In 298 African American human immunodeficiency virus (HIV)-1 seroconverters, the IFNG -179G/T genotype was associated with accelerated progression to CD4 <200 and AIDS-1993, a finding suggesting that IFNG -179T is a risk factor for AIDS progression, as measured by CD4 cell count. |
| 3651 | 12854077 | It is possible that increased IFN-gamma production induced by TNF-alpha when -179T is present causes CD4 cell depletion by apoptosis. |
| 3652 | 12854077 | It is possible that increased IFN-gamma production induced by TNF-alpha when -179T is present causes CD4 cell depletion by apoptosis. |
| 3653 | 12854077 | It is possible that increased IFN-gamma production induced by TNF-alpha when -179T is present causes CD4 cell depletion by apoptosis. |
| 3654 | 12854077 | It is possible that increased IFN-gamma production induced by TNF-alpha when -179T is present causes CD4 cell depletion by apoptosis. |
| 3655 | 12751959 | In addition, ginsan induced the endogenous production of cytokines such as Il1, Il6, Ifng and Il12, which are required for hematopoietic recovery, and was able to enhance Th1 function while interfering with the Th2 response in irradiated mice. |
| 3656 | 12719555 | Interestingly, Tmevpg1 is down regulated after in vitro stimulation of murine CD4(+) or CD8(+) splenocytes, whereas Ifng is up regulated. |
| 3657 | 12719555 | Interestingly, Tmevpg1 is down regulated after in vitro stimulation of murine CD4(+) or CD8(+) splenocytes, whereas Ifng is up regulated. |
| 3658 | 12719555 | Similar patterns of expression of TMEVPG1 and IFNG were observed in human NK cells and CD4(+) and CD8(+) T lymphocytes. |
| 3659 | 12719555 | Similar patterns of expression of TMEVPG1 and IFNG were observed in human NK cells and CD4(+) and CD8(+) T lymphocytes. |
| 3660 | 12643791 | The NO levels in the cultured salivary gland epithelial cells were increased by treatment with a combination of interferon gamma (Ifng), interleukin 1-beta (Il1b), and tumor necrosis factor alpha (Tnfa). |
| 3661 | 12552499 | Impact of interferon-gamma and interleukin-4 gene polymorphisms on development and progression of IgA nephropathy in Japanese patients. |
| 3662 | 12486605 | Among these the most striking ones are the genes coding for the cytokines interleukin-22 (IL-22) and interleukin-26 (IL-26) that constitute together with IFNG a cytokine cluster on chromosome 12q14. |
| 3663 | 12447360 | We found that in these conditions human naive T cells acquired stable histone hyperacetylation at either the Ifng or Il4 promoter. |
| 3664 | 12447360 | We found that in these conditions human naive T cells acquired stable histone hyperacetylation at either the Ifng or Il4 promoter. |
| 3665 | 12447360 | Such cytokine flexibility was absent in a subset of T(H)2 cells that failed to up-regulate T-bet and to express interferon-gamma when stimulated under T(H)1 conditions. |
| 3666 | 12447360 | Such cytokine flexibility was absent in a subset of T(H)2 cells that failed to up-regulate T-bet and to express interferon-gamma when stimulated under T(H)1 conditions. |
| 3667 | 12435110 | Accurate microsatellite typing and inter-study comparison: pitfalls and solutions using interferon-gamma (IFNG) and natural resistance-associated macrophage protein 2 (NRAMP2) genes as examples. |
| 3668 | 12435110 | Accurate microsatellite typing and inter-study comparison: pitfalls and solutions using interferon-gamma (IFNG) and natural resistance-associated macrophage protein 2 (NRAMP2) genes as examples. |
| 3669 | 12435110 | We report on the typing of natural resistance-associated macrophage protein (NRAMP2) and interferon-y (IFNG) gene microsatellites as examples, the latter of which is crucial to many pathogenic processes. |
| 3670 | 12435110 | We report on the typing of natural resistance-associated macrophage protein (NRAMP2) and interferon-y (IFNG) gene microsatellites as examples, the latter of which is crucial to many pathogenic processes. |
| 3671 | 12427367 | Other cytokines such as transforming growth factor-beta, interferon-gamma (IFNg), and interleukin-18 are also likely to be important in SpA. |
| 3672 | 12417450 | Oral terbutaline differentially affects cytokine (IL-10, IL-12, TNF, IFNg) release in multiple sclerosis patients and controls. |
| 3673 | 12417450 | Oral terbutaline differentially affects cytokine (IL-10, IL-12, TNF, IFNg) release in multiple sclerosis patients and controls. |
| 3674 | 12417450 | In this study, we investigated the effects of terbutaline (5 mg) on IL-10, IL-12, IFN-gamma and TNF-alpha production in whole blood stimulation cultures. |
| 3675 | 12417450 | In this study, we investigated the effects of terbutaline (5 mg) on IL-10, IL-12, IFN-gamma and TNF-alpha production in whole blood stimulation cultures. |
| 3676 | 12417450 | IL-10 and IL-12 production were significantly enhanced in controls but not in MS patients (p=0.03 and p=0.001). |
| 3677 | 12417450 | IL-10 and IL-12 production were significantly enhanced in controls but not in MS patients (p=0.03 and p=0.001). |
| 3678 | 12417450 | We conclude that administration of terbutaline induces anti-inflammatory (IL-10) as well as IL-12 protein production in healthy controls but not in MS patients. |
| 3679 | 12417450 | We conclude that administration of terbutaline induces anti-inflammatory (IL-10) as well as IL-12 protein production in healthy controls but not in MS patients. |
| 3680 | 12165204 | These lately discovered genes, relevant to immune disorders of mononuclear phagocytes and neutrophils, include defects in the interferon gamma (IFNg)/interleukin 12 (IL-12) pathway, such as IFNg receptor (IFNgR) defects, IL-12 defect, IL-12 receptor (IL-12R) defect, and signal transducer and activator of transcription 1 (STAT-1) defect. |
| 3681 | 12047360 | Allele frequencies of polymorphisms of TNFA, IL-6, IL-10 and IFNG in an Italian Caucasian population. |
| 3682 | 12047360 | Allele frequencies of polymorphisms of TNFA, IL-6, IL-10 and IFNG in an Italian Caucasian population. |
| 3683 | 12047360 | Allele frequencies of polymorphisms of TNFA, IL-6, IL-10 and IFNG in an Italian Caucasian population. |
| 3684 | 12047360 | The polymorphisms analysed were those of tumour necrosis factor alpha (TNFA), interleukin 6 (IL-6), interleukin 10 (IL-10) and interferon gamma (IFNG). |
| 3685 | 12047360 | The polymorphisms analysed were those of tumour necrosis factor alpha (TNFA), interleukin 6 (IL-6), interleukin 10 (IL-10) and interferon gamma (IFNG). |
| 3686 | 12047360 | The polymorphisms analysed were those of tumour necrosis factor alpha (TNFA), interleukin 6 (IL-6), interleukin 10 (IL-10) and interferon gamma (IFNG). |
| 3687 | 12047360 | The frequencies of IL-6 alleles - 174C and -174G were 29.0 and 71.0%, respectively; for IFNG polymorphisms at position -874, in the population under evaluation, the alleles -874T and -874A were present in 44.7 and 55.3% of the subjects, respectively. |
| 3688 | 12047360 | The frequencies of IL-6 alleles - 174C and -174G were 29.0 and 71.0%, respectively; for IFNG polymorphisms at position -874, in the population under evaluation, the alleles -874T and -874A were present in 44.7 and 55.3% of the subjects, respectively. |
| 3689 | 12047360 | The frequencies of IL-6 alleles - 174C and -174G were 29.0 and 71.0%, respectively; for IFNG polymorphisms at position -874, in the population under evaluation, the alleles -874T and -874A were present in 44.7 and 55.3% of the subjects, respectively. |
| 3690 | 11821159 | Polymorphisms of interferon-gamma gene CA-repeat and interleukin-10 promoter region (-592A/C) in Japanese type I diabetes. |
| 3691 | 11821159 | Polymorphisms of interferon-gamma gene CA-repeat and interleukin-10 promoter region (-592A/C) in Japanese type I diabetes. |
| 3692 | 11821159 | Polymorphisms of interferon-gamma gene CA-repeat and interleukin-10 promoter region (-592A/C) in Japanese type I diabetes. |
| 3693 | 11821159 | Polymorphisms of interferon-gamma gene CA-repeat and interleukin-10 promoter region (-592A/C) in Japanese type I diabetes. |
| 3694 | 11821159 | We investigated the association of the polymorphisms of interferon-gamma gene (IFNG) CA-repeat and IL-10-592A/C with clinical heterogeneity of type I diabetes as well as susceptibility to type I diabetes. |
| 3695 | 11821159 | We investigated the association of the polymorphisms of interferon-gamma gene (IFNG) CA-repeat and IL-10-592A/C with clinical heterogeneity of type I diabetes as well as susceptibility to type I diabetes. |
| 3696 | 11821159 | We investigated the association of the polymorphisms of interferon-gamma gene (IFNG) CA-repeat and IL-10-592A/C with clinical heterogeneity of type I diabetes as well as susceptibility to type I diabetes. |
| 3697 | 11821159 | We investigated the association of the polymorphisms of interferon-gamma gene (IFNG) CA-repeat and IL-10-592A/C with clinical heterogeneity of type I diabetes as well as susceptibility to type I diabetes. |
| 3698 | 11821159 | These results suggest that the IFNG CA-repeat and the IL-10-592A/C polymorphisms are not strong determinants of susceptibility to the development of type I diabetes in Japanese individuals. |
| 3699 | 11821159 | These results suggest that the IFNG CA-repeat and the IL-10-592A/C polymorphisms are not strong determinants of susceptibility to the development of type I diabetes in Japanese individuals. |
| 3700 | 11821159 | These results suggest that the IFNG CA-repeat and the IL-10-592A/C polymorphisms are not strong determinants of susceptibility to the development of type I diabetes in Japanese individuals. |
| 3701 | 11821159 | These results suggest that the IFNG CA-repeat and the IL-10-592A/C polymorphisms are not strong determinants of susceptibility to the development of type I diabetes in Japanese individuals. |
| 3702 | 11821159 | However, both the IFNG CA-repeat and the IL-10-592A/C polymorphisms are associated with clinical heterogeneity in type I diabetes. |
| 3703 | 11821159 | However, both the IFNG CA-repeat and the IL-10-592A/C polymorphisms are associated with clinical heterogeneity in type I diabetes. |
| 3704 | 11821159 | However, both the IFNG CA-repeat and the IL-10-592A/C polymorphisms are associated with clinical heterogeneity in type I diabetes. |
| 3705 | 11821159 | However, both the IFNG CA-repeat and the IL-10-592A/C polymorphisms are associated with clinical heterogeneity in type I diabetes. |
| 3706 | 11592486 | Chromosomal localization of the genes encoding SCNN1A, BTG1, IFNG and MAOA on chicken chromosome 1 by fluorescence in-situ hybridization. |
| 3707 | 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. |
| 3708 | 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. |
| 3709 | 11316066 | In a previous study, we demonstrated a significant association between high IL-10 secretion in mixed lymphocyte culture (MLC), together with HLA mismatching for at least 4-6 antigens, with the occurrence of acute rejection following renal transplantation. |
| 3710 | 11316066 | In a previous study, we demonstrated a significant association between high IL-10 secretion in mixed lymphocyte culture (MLC), together with HLA mismatching for at least 4-6 antigens, with the occurrence of acute rejection following renal transplantation. |
| 3711 | 11316066 | Cytokine protein secretion in MLC for IL-4, IL-6, IL-10 and IFN-gamma was measured by ELISA in 49 patient-donor pairs. |
| 3712 | 11316066 | Cytokine protein secretion in MLC for IL-4, IL-6, IL-10 and IFN-gamma was measured by ELISA in 49 patient-donor pairs. |
| 3713 | 11316066 | In both patient and control groups, single nucleotide polymorphism analysis for IL-4 G(-590)T, IL-6 G(-174)C, IL-10 G(-1082)A, IL-10 C(-819)T, IL-10 C(-592)A, TNF-alpha G(-308)A and microsatellite analysis for IFNG (CA repeat) was performed. |
| 3714 | 11316066 | In both patient and control groups, single nucleotide polymorphism analysis for IL-4 G(-590)T, IL-6 G(-174)C, IL-10 G(-1082)A, IL-10 C(-819)T, IL-10 C(-592)A, TNF-alpha G(-308)A and microsatellite analysis for IFNG (CA repeat) was performed. |
| 3715 | 11217546 | This phase corresponds to early release of so-called inflammatory cytokines (IL1, IL6, IL8). |
| 3716 | 11217546 | The second phase consists of recognition of bacterial antigens by helper CD4 lymphocytes, which mainly release IL2 and IFNg (Th1 response). |
| 3717 | 11121210 | Radiation of the esophagus of C3H/HeNsd mice with 35 or 37 Gy of 6 MV X rays induces significantly increased RNA transcription for interleukin 1 (Il1), tumor necrosis factor alpha (Tnf), interferon gamma inducing factor (Ifngr), and interferon gamma (Ifng). |
| 3718 | 11121210 | An equivalent therapeutic plasmid weight of 10 microgram ALP plasmid in the same 500 microliter of liposomes, correlated to around 52-60% of alkaline phosphatase-positive cells in the squamous layer of the esophagus at 24 h. |
| 3719 | 11121210 | Mice with orthotopic thoracic tumors composed of 32D-v-abl cells that received intraesophageal SOD2-PL treatment showed transgenic mRNA in the esophagus at 24 h, but no detectable human SOD2 transgene mRNA in explanted tumors by nested RT-PCR. |
| 3720 | 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. |
| 3721 | 11057100 | [Secretion of interleukin-2 (IL-2) and interferon (IFN gamma)in whole blood cell culture stimulated with mitogens in patients with lung neoplasms]. |
| 3722 | 10828606 | Chromosomal localization of the genes encoding ALDH, BMP-2, R-FABP, IFN-gamma, RXR-gamma, and VIM in chicken by fluorescence in situ hybridization. |
| 3723 | 10828606 | Chromosomal localization of the genes encoding ALDH, BMP-2, R-FABP, IFN-gamma, RXR-gamma, and VIM in chicken by fluorescence in situ hybridization. |
| 3724 | 10828606 | Six structural genes encoding ALDH, BMP-2, R-FABP, IFN-gamma, RXR-gamma and VIM were mapped in the chicken by fluorescence in situ hybridization (FISH) using genomic and cDNA clones as probes. |
| 3725 | 10828606 | Six structural genes encoding ALDH, BMP-2, R-FABP, IFN-gamma, RXR-gamma and VIM were mapped in the chicken by fluorescence in situ hybridization (FISH) using genomic and cDNA clones as probes. |
| 3726 | 10793767 | This was achieved by dosing serum levels of IFNg, produced by Th1 lymphocytes and IL-4, produced by Th2 lymphocytes. |
| 3727 | 10714554 | The aim of this study was to investigate the frequency of a CA dinucleotide repeat polymorphism in the interferon-gamma (IFN-gamma) gene (IFNG) and a C(-590)T polymorphism of the interleukin-4 (IL-4) gene in 236 Caucasoid patients with type 1 diabetes. |
| 3728 | 10588826 | PDX-1 and Msx-2 expression in the regenerating and developing pancreas. |
| 3729 | 10588826 | PDX-1 and Msx-2 expression in the regenerating and developing pancreas. |
| 3730 | 10588826 | PDX-1 and Msx-2 expression in the regenerating and developing pancreas. |
| 3731 | 10588826 | PDX-1 and Msx-2 expression in the regenerating and developing pancreas. |
| 3732 | 10588826 | Importantly, we have found that PDX-1, a transcription factor required for insulin gene transcription as well as for pancreatic development during embryogenesis, is expressed in the duct cells of IFNg mice. |
| 3733 | 10588826 | Importantly, we have found that PDX-1, a transcription factor required for insulin gene transcription as well as for pancreatic development during embryogenesis, is expressed in the duct cells of IFNg mice. |
| 3734 | 10588826 | Importantly, we have found that PDX-1, a transcription factor required for insulin gene transcription as well as for pancreatic development during embryogenesis, is expressed in the duct cells of IFNg mice. |
| 3735 | 10588826 | Importantly, we have found that PDX-1, a transcription factor required for insulin gene transcription as well as for pancreatic development during embryogenesis, is expressed in the duct cells of IFNg mice. |
| 3736 | 10588826 | This striking observation suggests an important role for PDX-1 in the marked regeneration observed in IFNg mice, paralleling its critical function during ontogeny. |
| 3737 | 10588826 | This striking observation suggests an important role for PDX-1 in the marked regeneration observed in IFNg mice, paralleling its critical function during ontogeny. |
| 3738 | 10588826 | This striking observation suggests an important role for PDX-1 in the marked regeneration observed in IFNg mice, paralleling its critical function during ontogeny. |
| 3739 | 10588826 | This striking observation suggests an important role for PDX-1 in the marked regeneration observed in IFNg mice, paralleling its critical function during ontogeny. |
| 3740 | 10588826 | Also demonstrated was elevated expression of the homeobox-containing protein Msx-2 in the pancreata of fetal mice as well as in adult IFNg mice, identifying this molecule as a novel marker associated with pancreatic development and regeneration as well. |
| 3741 | 10588826 | Also demonstrated was elevated expression of the homeobox-containing protein Msx-2 in the pancreata of fetal mice as well as in adult IFNg mice, identifying this molecule as a novel marker associated with pancreatic development and regeneration as well. |
| 3742 | 10588826 | Also demonstrated was elevated expression of the homeobox-containing protein Msx-2 in the pancreata of fetal mice as well as in adult IFNg mice, identifying this molecule as a novel marker associated with pancreatic development and regeneration as well. |
| 3743 | 10588826 | Also demonstrated was elevated expression of the homeobox-containing protein Msx-2 in the pancreata of fetal mice as well as in adult IFNg mice, identifying this molecule as a novel marker associated with pancreatic development and regeneration as well. |
| 3744 | 10588826 | The identification of PDX-1 and Msx in the ducts of the IFNg transgenic pancreas but not in the ducts of the non-transgenic pancreas suggests that these molecules are associated with endocrine precursor cells in the ducts of the IFNg transgenic mouse. |
| 3745 | 10588826 | The identification of PDX-1 and Msx in the ducts of the IFNg transgenic pancreas but not in the ducts of the non-transgenic pancreas suggests that these molecules are associated with endocrine precursor cells in the ducts of the IFNg transgenic mouse. |
| 3746 | 10588826 | The identification of PDX-1 and Msx in the ducts of the IFNg transgenic pancreas but not in the ducts of the non-transgenic pancreas suggests that these molecules are associated with endocrine precursor cells in the ducts of the IFNg transgenic mouse. |
| 3747 | 10588826 | The identification of PDX-1 and Msx in the ducts of the IFNg transgenic pancreas but not in the ducts of the non-transgenic pancreas suggests that these molecules are associated with endocrine precursor cells in the ducts of the IFNg transgenic mouse. |
| 3748 | 10521926 | We investigated whether IFNB or IFNG, at various concentrations (2- 300 IU/ml) and for a range of durations of exposure (from 48 h before to 8 h after irradiation), were able to modify the radiation response of HeLa, C4-1, Me-180, C33-A and SiHa cells. |
| 3749 | 10521926 | We investigated whether IFNB or IFNG, at various concentrations (2- 300 IU/ml) and for a range of durations of exposure (from 48 h before to 8 h after irradiation), were able to modify the radiation response of HeLa, C4-1, Me-180, C33-A and SiHa cells. |
| 3750 | 10521926 | A significant change in the initial slope of the dose-response curve was observed more consistently with IFNB than with IFNG. |
| 3751 | 10521926 | A significant change in the initial slope of the dose-response curve was observed more consistently with IFNB than with IFNG. |
| 3752 | 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. |
| 3753 | 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. |
| 3754 | 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. |
| 3755 | 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. |
| 3756 | 10358183 | Also, the ratio of IL-12 to IL-10 mRNA levels was higher in B10.S mice. |
| 3757 | 10358183 | Also, the ratio of IL-12 to IL-10 mRNA levels was higher in B10.S mice. |
| 3758 | 10329377 | In this region, the MDM2 and IFNG genes were noted as known genes that could be involved in human carcinogenesis. |
| 3759 | 10329377 | In this region, the MDM2 and IFNG genes were noted as known genes that could be involved in human carcinogenesis. |
| 3760 | 10329377 | Southern blot analysis of genomic DNA of the tumor revealed the amplification of the MDM2 gene together with the fragment locus, but not the IFNG gene. |
| 3761 | 10329377 | Southern blot analysis of genomic DNA of the tumor revealed the amplification of the MDM2 gene together with the fragment locus, but not the IFNG gene. |
| 3762 | 10233988 | Mouse strains with null mutations in the gamma interferon gene (Ifng) or the gamma interferon receptor gene (Ifngr) have been engineered. |
| 3763 | 10203608 | We explored the relative densitometric measure of a 119 bp fragment of the CDK4 gene versus an 82 bp fragment of the IFNG gene. |
| 3764 | 9772286 | We explored the relative densitometric measure of a 119 bp fragment of the CDK4 gene versus an 82 bp fragment of the IFNG gene. |
| 3765 | 9742402 | Here, we show that lunatic Fringe (IFng), a vertebrate homolog of the Drosophila Fringe gene, is also expressed rhythmically in PSM. |
| 3766 | 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. |
| 3767 | 9656442 | Influence of IL-12 on interferon-gamma production by bovine leucocyte subsets in response to bovine respiratory syncytial virus. |
| 3768 | 9656442 | Influence of IL-12 on interferon-gamma production by bovine leucocyte subsets in response to bovine respiratory syncytial virus. |
| 3769 | 9656442 | Influence of IL-12 on interferon-gamma production by bovine leucocyte subsets in response to bovine respiratory syncytial virus. |
| 3770 | 9656442 | The cytokine IL-12 is a key molecule in the regulation of CD4+ T cell development and specifically potentiates the development of T helper 1 responses in mouse and man. |
| 3771 | 9656442 | The cytokine IL-12 is a key molecule in the regulation of CD4+ T cell development and specifically potentiates the development of T helper 1 responses in mouse and man. |
| 3772 | 9656442 | The cytokine IL-12 is a key molecule in the regulation of CD4+ T cell development and specifically potentiates the development of T helper 1 responses in mouse and man. |
| 3773 | 9656442 | Here the 2A was flanked by sequences encoding the p35 and p40 polypeptides of the heterodimeric cytokine to mediate their cleavage. |
| 3774 | 9656442 | Here the 2A was flanked by sequences encoding the p35 and p40 polypeptides of the heterodimeric cytokine to mediate their cleavage. |
| 3775 | 9656442 | Here the 2A was flanked by sequences encoding the p35 and p40 polypeptides of the heterodimeric cytokine to mediate their cleavage. |
| 3776 | 9656442 | The presence of IL-12 markedly influenced the level of IFNg secreted by these cells, and although IL-12 induced IFNg production in the absence of antigenic stimulation, IFNg production was accelerated and augmented in response to IL-12 and antigen. |
| 3777 | 9656442 | The presence of IL-12 markedly influenced the level of IFNg secreted by these cells, and although IL-12 induced IFNg production in the absence of antigenic stimulation, IFNg production was accelerated and augmented in response to IL-12 and antigen. |
| 3778 | 9656442 | The presence of IL-12 markedly influenced the level of IFNg secreted by these cells, and although IL-12 induced IFNg production in the absence of antigenic stimulation, IFNg production was accelerated and augmented in response to IL-12 and antigen. |
| 3779 | 9656442 | Analysis of the T cell subsets by flow cytometry showed that CD4+ T cells comprised the largest contributors to IFNg production. |
| 3780 | 9656442 | Analysis of the T cell subsets by flow cytometry showed that CD4+ T cells comprised the largest contributors to IFNg production. |
| 3781 | 9656442 | Analysis of the T cell subsets by flow cytometry showed that CD4+ T cells comprised the largest contributors to IFNg production. |
| 3782 | 9512760 | During effective immune responses, the principal cytokine involved appears to be IL-2, with only small, controlled "bursts" of IFN gamma production. |
| 3783 | 9512760 | During effective immune responses, the principal cytokine involved appears to be IL-2, with only small, controlled "bursts" of IFN gamma production. |
| 3784 | 9512760 | However, IL-2 responsiveness is only transient in animals undergoing primary infection, while IFNg production is greatly elevated. |
| 3785 | 9512760 | However, IL-2 responsiveness is only transient in animals undergoing primary infection, while IFNg production is greatly elevated. |
| 3786 | 9058314 | Analysis of an interferon-gamma gene (IFNG) polymorphism in Danish and Finnish insulin-dependent diabetes mellitus (IDDM) patients and control subjects. |
| 3787 | 9058314 | Analysis of an interferon-gamma gene (IFNG) polymorphism in Danish and Finnish insulin-dependent diabetes mellitus (IDDM) patients and control subjects. |
| 3788 | 9058314 | Analysis of an interferon-gamma gene (IFNG) polymorphism in Danish and Finnish insulin-dependent diabetes mellitus (IDDM) patients and control subjects. |
| 3789 | 9058314 | This polymorphism was recently demonstrated to be associated with insulin-dependent diabetes mellitus (IDDM) in Japanese subjects. |
| 3790 | 9058314 | This polymorphism was recently demonstrated to be associated with insulin-dependent diabetes mellitus (IDDM) in Japanese subjects. |
| 3791 | 9058314 | This polymorphism was recently demonstrated to be associated with insulin-dependent diabetes mellitus (IDDM) in Japanese subjects. |
| 3792 | 9058314 | Analysis of data according to HLA-DQB1 susceptibility status did not reveal heterogeneity of risk at the IFN-gamma locus in either of the populations. |
| 3793 | 9058314 | Analysis of data according to HLA-DQB1 susceptibility status did not reveal heterogeneity of risk at the IFN-gamma locus in either of the populations. |
| 3794 | 9058314 | Analysis of data according to HLA-DQB1 susceptibility status did not reveal heterogeneity of risk at the IFN-gamma locus in either of the populations. |
| 3795 | 9058314 | Thus, the modest significance level observed in the Finnish case-control study and the failure to replicate it by the TDT provide little support for the hypothesis that the IFN-gamma gene microsatellite is associated with IDDM. |
| 3796 | 9058314 | Thus, the modest significance level observed in the Finnish case-control study and the failure to replicate it by the TDT provide little support for the hypothesis that the IFN-gamma gene microsatellite is associated with IDDM. |
| 3797 | 9058314 | Thus, the modest significance level observed in the Finnish case-control study and the failure to replicate it by the TDT provide little support for the hypothesis that the IFN-gamma gene microsatellite is associated with IDDM. |
| 3798 | 11173629 | Transcription of mRNA of IFNg and IL-10 were more pronounced in HIV positive and atopic groups than in the healthy control, without lymphocyte phenotype dominance. |
| 3799 | 8912848 | Refined mapping of 12q13-q15 amplicons in human malignant gliomas suggests CDK4/SAS and MDM2 as independent amplification targets. |
| 3800 | 8912848 | The genes most frequently amplified and overexpressed were CDK4 (with coamplification of SAS) and MDM2. |
| 3801 | 8912848 | Because individual malignant gliomas showed CDK4/SAS amplification but no MDM2 amplification and vice versa, the possibility remained of a common amplification target gene located between CDK4 and MDM2. |
| 3802 | 8912848 | All tumors and cell lines were analyzed at eight gene loci and six anonymous loci from 12q13-q15, including seven loci located between CDK4 and MDM2. |
| 3803 | 8912848 | These studies revealed two centers of amplification, one at CDK4/SAS and the other at MDM2. |
| 3804 | 8912848 | A number of loci located close to either MDM2 or CDK4/SAS, including the genes GADD153, GLI, RAP1B, A2MR, and IFNG, were found to be coamplified in some tumors but not overexpressed consistently. |
| 3805 | 8912848 | All amplicons were discontinuous between CDK4/SAS and MDM2. |
| 3806 | 8912848 | Our results thus exclude a common amplification target between CDK4/SAS and MDM2 and provide additional evidence that these genes represent two independent targets of selection. |
| 3807 | 9116875 | In an attempt to understand the mechanism behind these differences we examined age related differences in the phenotype profiles of MNC in parallel with the in vitro production of interleukin IL-6, tumour necrosis factor alpha (TNF alpha) and interferon gamma (IFNg) in neonates, children and adults. |
| 3808 | 9116875 | In an attempt to understand the mechanism behind these differences we examined age related differences in the phenotype profiles of MNC in parallel with the in vitro production of interleukin IL-6, tumour necrosis factor alpha (TNF alpha) and interferon gamma (IFNg) in neonates, children and adults. |
| 3809 | 9116875 | In an attempt to understand the mechanism behind these differences we examined age related differences in the phenotype profiles of MNC in parallel with the in vitro production of interleukin IL-6, tumour necrosis factor alpha (TNF alpha) and interferon gamma (IFNg) in neonates, children and adults. |
| 3810 | 9116875 | In cultures without added polyclonal activators IL-6 and TNF alpha levels in children were 3-6 times higher than those of umbilical cords and adults. |
| 3811 | 9116875 | In cultures without added polyclonal activators IL-6 and TNF alpha levels in children were 3-6 times higher than those of umbilical cords and adults. |
| 3812 | 9116875 | In cultures without added polyclonal activators IL-6 and TNF alpha levels in children were 3-6 times higher than those of umbilical cords and adults. |
| 3813 | 9116875 | Flow cytometry analysis of the phenotypic distribution of MNC revealed age related differences in the expression of CD3, CD4, CD8, CD14, CD19, CD45RA, CD45R0, CD2, LFA-1, ICAM-1 and LFA-3. |
| 3814 | 9116875 | Flow cytometry analysis of the phenotypic distribution of MNC revealed age related differences in the expression of CD3, CD4, CD8, CD14, CD19, CD45RA, CD45R0, CD2, LFA-1, ICAM-1 and LFA-3. |
| 3815 | 9116875 | Flow cytometry analysis of the phenotypic distribution of MNC revealed age related differences in the expression of CD3, CD4, CD8, CD14, CD19, CD45RA, CD45R0, CD2, LFA-1, ICAM-1 and LFA-3. |
| 3816 | 9116875 | The TNF alpha levels in suboptimally stimulated cultures correlated negatively with the expression of LFA-3 and positively with CD45RA, while IFNg correlated positively with CD2, LFA-1, CD45R0 and CD8. |
| 3817 | 9116875 | The TNF alpha levels in suboptimally stimulated cultures correlated negatively with the expression of LFA-3 and positively with CD45RA, while IFNg correlated positively with CD2, LFA-1, CD45R0 and CD8. |
| 3818 | 9116875 | The TNF alpha levels in suboptimally stimulated cultures correlated negatively with the expression of LFA-3 and positively with CD45RA, while IFNg correlated positively with CD2, LFA-1, CD45R0 and CD8. |
| 3819 | 9116875 | In conclusion, the study provides evidence of age related differences in the production of TNF alpha, IL-6 and IFNg among neonates, children and adults. |
| 3820 | 9116875 | In conclusion, the study provides evidence of age related differences in the production of TNF alpha, IL-6 and IFNg among neonates, children and adults. |
| 3821 | 9116875 | In conclusion, the study provides evidence of age related differences in the production of TNF alpha, IL-6 and IFNg among neonates, children and adults. |
| 3822 | 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. |
| 3823 | 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. |
| 3824 | 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. |
| 3825 | 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. |
| 3826 | 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. |
| 3827 | 7587386 | Mapping of the immune interferon gamma gene (IFNG) to chromosome band 12q14 by fluorescence in situ hybridization. |
| 3828 | 7587386 | Mapping of the immune interferon gamma gene (IFNG) to chromosome band 12q14 by fluorescence in situ hybridization. |
| 3829 | 7587386 | The human immune interferon gamma gene (IFNG) was localized to chromosome band 12q14 by fluorescence in situ hybridization. |
| 3830 | 7587386 | The human immune interferon gamma gene (IFNG) was localized to chromosome band 12q14 by fluorescence in situ hybridization. |
| 3831 | 8101856 | Genetic analysis of the gene for porcine submaxillary gland mucin: physical assignment of the MUC and interferon gamma genes to chromosome 5. |
| 3832 | 8101856 | Genetic analysis of the gene for porcine submaxillary gland mucin: physical assignment of the MUC and interferon gamma genes to chromosome 5. |
| 3833 | 8101856 | Genetic analysis of the gene for porcine submaxillary gland mucin: physical assignment of the MUC and interferon gamma genes to chromosome 5. |
| 3834 | 8101856 | The mucin locus was assigned to a previously reported linkage group comprising the markers interferon gamma (IFNG), diacylglycerol kinase (DAGK), and an anonymous microsatellite (S0092). |
| 3835 | 8101856 | The mucin locus was assigned to a previously reported linkage group comprising the markers interferon gamma (IFNG), diacylglycerol kinase (DAGK), and an anonymous microsatellite (S0092). |
| 3836 | 8101856 | The mucin locus was assigned to a previously reported linkage group comprising the markers interferon gamma (IFNG), diacylglycerol kinase (DAGK), and an anonymous microsatellite (S0092). |
| 3837 | 8101856 | Furthermore, the genes for mucin and interferon gamma were physically localized to porcine chromosome 5q2.3 and 5p1.2-q1.1 by fluorescence and radioactive in situ hybridization, respectively, thereby assigning four new markers to chromosome 5. |
| 3838 | 8101856 | Furthermore, the genes for mucin and interferon gamma were physically localized to porcine chromosome 5q2.3 and 5p1.2-q1.1 by fluorescence and radioactive in situ hybridization, respectively, thereby assigning four new markers to chromosome 5. |
| 3839 | 8101856 | Furthermore, the genes for mucin and interferon gamma were physically localized to porcine chromosome 5q2.3 and 5p1.2-q1.1 by fluorescence and radioactive in situ hybridization, respectively, thereby assigning four new markers to chromosome 5. |
| 3840 | 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. |
| 3841 | 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. |
| 3842 | 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. |
| 3843 | 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. |
| 3844 | 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). |
| 3845 | 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). |
| 3846 | 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. |
| 3847 | 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. |
| 3848 | 8389732 | Although the expression of high affinity IL-2 receptors (IL-2R) (p75) was unaffected, exogenously added IL-2 failed to restore proliferation. |
| 3849 | 8389732 | Although the expression of high affinity IL-2 receptors (IL-2R) (p75) was unaffected, exogenously added IL-2 failed to restore proliferation. |
| 3850 | 8244753 | Relative location of the IFNG gene and the class II cytokeratin and HOX3 gene clusters in cattle and humans is discussed. |
| 3851 | 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. |
| 3852 | 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. |
| 3853 | 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'. |
| 3854 | 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'. |
| 3855 | 1357793 | Rapid induction of intercellular adhesion molecule-1 on monocytes and myelomonocytic cell lines after interferon gamma treatment. |
| 3856 | 1357793 | Rapid induction of intercellular adhesion molecule-1 on monocytes and myelomonocytic cell lines after interferon gamma treatment. |
| 3857 | 1357793 | Rapid induction of intercellular adhesion molecule-1 on monocytes and myelomonocytic cell lines after interferon gamma treatment. |
| 3858 | 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). |
| 3859 | 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). |
| 3860 | 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). |
| 3861 | 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. |
| 3862 | 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. |
| 3863 | 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. |
| 3864 | 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. |
| 3865 | 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. |
| 3866 | 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. |
| 3867 | 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. |
| 3868 | 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. |
| 3869 | 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. |
| 3870 | 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. |
| 3871 | 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. |
| 3872 | 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. |
| 3873 | 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. |
| 3874 | 1391316 | Allopregnant (NFR/N [Swiss-derived] H-2q females x 57/Bl H-2b males) and syngeneically pregnant (NFR/N x NFR/N) mice were subjected to daily injections (10(5) U/mouse/day, from Day 5.5 of gestation) of recombinant rat or mouse interferon-gamma (IFNg) in order to investigate its ability to induce extra-embryonic major histocompatibility complex (MHC) expression and antipaternal immune reactions if administered during the first part of the gestation period. |
| 3875 | 1391316 | Allopregnant (NFR/N [Swiss-derived] H-2q females x 57/Bl H-2b males) and syngeneically pregnant (NFR/N x NFR/N) mice were subjected to daily injections (10(5) U/mouse/day, from Day 5.5 of gestation) of recombinant rat or mouse interferon-gamma (IFNg) in order to investigate its ability to induce extra-embryonic major histocompatibility complex (MHC) expression and antipaternal immune reactions if administered during the first part of the gestation period. |
| 3876 | 1391316 | Allopregnant (NFR/N [Swiss-derived] H-2q females x 57/Bl H-2b males) and syngeneically pregnant (NFR/N x NFR/N) mice were subjected to daily injections (10(5) U/mouse/day, from Day 5.5 of gestation) of recombinant rat or mouse interferon-gamma (IFNg) in order to investigate its ability to induce extra-embryonic major histocompatibility complex (MHC) expression and antipaternal immune reactions if administered during the first part of the gestation period. |
| 3877 | 1391316 | Allopregnant (NFR/N [Swiss-derived] H-2q females x 57/Bl H-2b males) and syngeneically pregnant (NFR/N x NFR/N) mice were subjected to daily injections (10(5) U/mouse/day, from Day 5.5 of gestation) of recombinant rat or mouse interferon-gamma (IFNg) in order to investigate its ability to induce extra-embryonic major histocompatibility complex (MHC) expression and antipaternal immune reactions if administered during the first part of the gestation period. |
| 3878 | 1391316 | Allopregnant (NFR/N [Swiss-derived] H-2q females x 57/Bl H-2b males) and syngeneically pregnant (NFR/N x NFR/N) mice were subjected to daily injections (10(5) U/mouse/day, from Day 5.5 of gestation) of recombinant rat or mouse interferon-gamma (IFNg) in order to investigate its ability to induce extra-embryonic major histocompatibility complex (MHC) expression and antipaternal immune reactions if administered during the first part of the gestation period. |
| 3879 | 1391316 | Allopregnant (NFR/N [Swiss-derived] H-2q females x 57/Bl H-2b males) and syngeneically pregnant (NFR/N x NFR/N) mice were subjected to daily injections (10(5) U/mouse/day, from Day 5.5 of gestation) of recombinant rat or mouse interferon-gamma (IFNg) in order to investigate its ability to induce extra-embryonic major histocompatibility complex (MHC) expression and antipaternal immune reactions if administered during the first part of the gestation period. |
| 3880 | 1391316 | Immunohistochemical stainings of cryosectioned tissues at Day 9.5 of pregnancy revealed that IFNg treatment caused a strong induction of MHC class I and class II expression on most cells in the uterus and on several cells in the maternal decidua, while there was a complete absence of detectable MHC class I and class II expression in the extra-embryonic tissues. |
| 3881 | 1391316 | Immunohistochemical stainings of cryosectioned tissues at Day 9.5 of pregnancy revealed that IFNg treatment caused a strong induction of MHC class I and class II expression on most cells in the uterus and on several cells in the maternal decidua, while there was a complete absence of detectable MHC class I and class II expression in the extra-embryonic tissues. |
| 3882 | 1391316 | Immunohistochemical stainings of cryosectioned tissues at Day 9.5 of pregnancy revealed that IFNg treatment caused a strong induction of MHC class I and class II expression on most cells in the uterus and on several cells in the maternal decidua, while there was a complete absence of detectable MHC class I and class II expression in the extra-embryonic tissues. |
| 3883 | 1391316 | Immunohistochemical stainings of cryosectioned tissues at Day 9.5 of pregnancy revealed that IFNg treatment caused a strong induction of MHC class I and class II expression on most cells in the uterus and on several cells in the maternal decidua, while there was a complete absence of detectable MHC class I and class II expression in the extra-embryonic tissues. |
| 3884 | 1391316 | Immunohistochemical stainings of cryosectioned tissues at Day 9.5 of pregnancy revealed that IFNg treatment caused a strong induction of MHC class I and class II expression on most cells in the uterus and on several cells in the maternal decidua, while there was a complete absence of detectable MHC class I and class II expression in the extra-embryonic tissues. |
| 3885 | 1391316 | Immunohistochemical stainings of cryosectioned tissues at Day 9.5 of pregnancy revealed that IFNg treatment caused a strong induction of MHC class I and class II expression on most cells in the uterus and on several cells in the maternal decidua, while there was a complete absence of detectable MHC class I and class II expression in the extra-embryonic tissues. |
| 3886 | 1391316 | Characteristic for a Day 12.5 placenta of an IFNg-treated mouse (including embryo-transferred mice) was a strongly MHC class II-induced maternal decidua and a completely MHC class II-negative fetal placenta. |
| 3887 | 1391316 | Characteristic for a Day 12.5 placenta of an IFNg-treated mouse (including embryo-transferred mice) was a strongly MHC class II-induced maternal decidua and a completely MHC class II-negative fetal placenta. |
| 3888 | 1391316 | Characteristic for a Day 12.5 placenta of an IFNg-treated mouse (including embryo-transferred mice) was a strongly MHC class II-induced maternal decidua and a completely MHC class II-negative fetal placenta. |
| 3889 | 1391316 | Characteristic for a Day 12.5 placenta of an IFNg-treated mouse (including embryo-transferred mice) was a strongly MHC class II-induced maternal decidua and a completely MHC class II-negative fetal placenta. |
| 3890 | 1391316 | Characteristic for a Day 12.5 placenta of an IFNg-treated mouse (including embryo-transferred mice) was a strongly MHC class II-induced maternal decidua and a completely MHC class II-negative fetal placenta. |
| 3891 | 1391316 | Characteristic for a Day 12.5 placenta of an IFNg-treated mouse (including embryo-transferred mice) was a strongly MHC class II-induced maternal decidua and a completely MHC class II-negative fetal placenta. |
| 3892 | 1391316 | The pattern of IFN-induced MHC class I expression was similar to that of class II, with the exception of class I expression on scattered cells within the basal zone. |
| 3893 | 1391316 | The pattern of IFN-induced MHC class I expression was similar to that of class II, with the exception of class I expression on scattered cells within the basal zone. |
| 3894 | 1391316 | The pattern of IFN-induced MHC class I expression was similar to that of class II, with the exception of class I expression on scattered cells within the basal zone. |
| 3895 | 1391316 | The pattern of IFN-induced MHC class I expression was similar to that of class II, with the exception of class I expression on scattered cells within the basal zone. |
| 3896 | 1391316 | The pattern of IFN-induced MHC class I expression was similar to that of class II, with the exception of class I expression on scattered cells within the basal zone. |
| 3897 | 1391316 | The pattern of IFN-induced MHC class I expression was similar to that of class II, with the exception of class I expression on scattered cells within the basal zone. |
| 3898 | 1391316 | Thus, the present study provides immunohistological evidence that IFNg administered in vivo during the first part of gestation is not capable of inducing MHC expression on murine extra-embryonic cells despite an extremely high expression of MHC molecules on decidual cells in intimate contact with extra-embryonic tissues. |
| 3899 | 1391316 | Thus, the present study provides immunohistological evidence that IFNg administered in vivo during the first part of gestation is not capable of inducing MHC expression on murine extra-embryonic cells despite an extremely high expression of MHC molecules on decidual cells in intimate contact with extra-embryonic tissues. |
| 3900 | 1391316 | Thus, the present study provides immunohistological evidence that IFNg administered in vivo during the first part of gestation is not capable of inducing MHC expression on murine extra-embryonic cells despite an extremely high expression of MHC molecules on decidual cells in intimate contact with extra-embryonic tissues. |
| 3901 | 1391316 | Thus, the present study provides immunohistological evidence that IFNg administered in vivo during the first part of gestation is not capable of inducing MHC expression on murine extra-embryonic cells despite an extremely high expression of MHC molecules on decidual cells in intimate contact with extra-embryonic tissues. |
| 3902 | 1391316 | Thus, the present study provides immunohistological evidence that IFNg administered in vivo during the first part of gestation is not capable of inducing MHC expression on murine extra-embryonic cells despite an extremely high expression of MHC molecules on decidual cells in intimate contact with extra-embryonic tissues. |
| 3903 | 1391316 | Thus, the present study provides immunohistological evidence that IFNg administered in vivo during the first part of gestation is not capable of inducing MHC expression on murine extra-embryonic cells despite an extremely high expression of MHC molecules on decidual cells in intimate contact with extra-embryonic tissues. |
| 3904 | 1391316 | It is likely that the resistance to IFNg-mediated induction of MHC expression on extra-embryonic cells is of basic importance for the protection of mammalian semi-allogeneic fetuses. |
| 3905 | 1391316 | It is likely that the resistance to IFNg-mediated induction of MHC expression on extra-embryonic cells is of basic importance for the protection of mammalian semi-allogeneic fetuses. |
| 3906 | 1391316 | It is likely that the resistance to IFNg-mediated induction of MHC expression on extra-embryonic cells is of basic importance for the protection of mammalian semi-allogeneic fetuses. |
| 3907 | 1391316 | It is likely that the resistance to IFNg-mediated induction of MHC expression on extra-embryonic cells is of basic importance for the protection of mammalian semi-allogeneic fetuses. |
| 3908 | 1391316 | It is likely that the resistance to IFNg-mediated induction of MHC expression on extra-embryonic cells is of basic importance for the protection of mammalian semi-allogeneic fetuses. |
| 3909 | 1391316 | It is likely that the resistance to IFNg-mediated induction of MHC expression on extra-embryonic cells is of basic importance for the protection of mammalian semi-allogeneic fetuses. |
| 3910 | 1414596 | TNF, IFNg, and GMCSF, to activate neutrophil function against C. albicans. |
| 3911 | 1414596 | The cytokine-producing LGL differs from the spontaneous tumoricidal LGL by being DR+; otherwise other markers are identical, i.e., CD2(+)-CD16+CD4-CD8-CD15-. |
| 3912 | 1414596 | It is of importance to note that TNF and GMCSF have also been shown to have chemotactic properties on neutrophils (27,28). |
| 3913 | 1414596 | Since TNF is a neutrophil activating factor, this implies that neutrophils may self-regulate function in an autocrine manner or utilize released TNF to recruit neighboring PMN. |
| 3914 | 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). |
| 3915 | 1724447 | The 52 kD myeloid membrane glycoprotein CD14 represents the receptor for complexes of lipopolysaccharide (LPS) and LPS binding protein (LBP); it is involved in LPS induced tumor necrosis factor-alpha production. |
| 3916 | 1724447 | The effect of rIFNg on CD14 in PBL cultures was dose-dependently inhibited by rIL-4 and this inhibition is probably due to an IL-4 mediated blockade of IFNg secretion. |
| 3917 | 1724447 | The results, showing that CD14 antigen expression is upregulated by LPS and downregulated by rIFNg and rIL-4, suggest that the LPS-LBP receptor is involved in the feedback response of IFNg and IL-4 to LPS stimulation. |
| 3918 | 2081597 | Eight loci, including A2M, GLI, HOX3, IFNG, INT1, KRAS2, NKNB, and PAH, were assigned to the previously identified bovine syntenic group U3 represented by GAPD. |
| 3919 | 2081597 | Eight loci, including A2M, GLI, HOX3, IFNG, INT1, KRAS2, NKNB, and PAH, were assigned to the previously identified bovine syntenic group U3 represented by GAPD. |
| 3920 | 2081597 | Additionally, the results predict that ALDH2 is distal to PAH and IFNG on HSA 12, the type II keratin gene complex will reside between q11 and q21 of HSA 12, A2M will map to MMU 6, and LALBA and GLI will map to MMU 15. |
| 3921 | 2081597 | Additionally, the results predict that ALDH2 is distal to PAH and IFNG on HSA 12, the type II keratin gene complex will reside between q11 and q21 of HSA 12, A2M will map to MMU 6, and LALBA and GLI will map to MMU 15. |
| 3922 | 2113589 | When used in combination with interferon gamma (IFNG) or chemotherapeutic drugs targeted at DNA topoisomerase II, synergistic cytotoxicity has been observed. |
| 3923 | 2113589 | When used in combination with interferon gamma (IFNG) or chemotherapeutic drugs targeted at DNA topoisomerase II, synergistic cytotoxicity has been observed. |
| 3924 | 2113589 | When used in combination with interferon gamma (IFNG) or chemotherapeutic drugs targeted at DNA topoisomerase II, synergistic cytotoxicity has been observed. |
| 3925 | 2113589 | When used in combination with interferon gamma (IFNG) or chemotherapeutic drugs targeted at DNA topoisomerase II, synergistic cytotoxicity has been observed. |
| 3926 | 2113589 | The cytotoxicity of TNF and low dose actinomycin-D (AMD) against MBT-2 in vitro was examined alone and following preincubation with IFNG. |
| 3927 | 2113589 | The cytotoxicity of TNF and low dose actinomycin-D (AMD) against MBT-2 in vitro was examined alone and following preincubation with IFNG. |
| 3928 | 2113589 | The cytotoxicity of TNF and low dose actinomycin-D (AMD) against MBT-2 in vitro was examined alone and following preincubation with IFNG. |
| 3929 | 2113589 | The cytotoxicity of TNF and low dose actinomycin-D (AMD) against MBT-2 in vitro was examined alone and following preincubation with IFNG. |
| 3930 | 2113589 | The activity of TNF/AMD in vivo utilizing an intravesical implantation mode (MBT-2) was also evaluated. |
| 3931 | 2113589 | The activity of TNF/AMD in vivo utilizing an intravesical implantation mode (MBT-2) was also evaluated. |
| 3932 | 2113589 | The activity of TNF/AMD in vivo utilizing an intravesical implantation mode (MBT-2) was also evaluated. |
| 3933 | 2113589 | The activity of TNF/AMD in vivo utilizing an intravesical implantation mode (MBT-2) was also evaluated. |
| 3934 | 2113589 | TNF/AMD was cytotoxic for MBT-2 growth in vitro. |
| 3935 | 2113589 | TNF/AMD was cytotoxic for MBT-2 growth in vitro. |
| 3936 | 2113589 | TNF/AMD was cytotoxic for MBT-2 growth in vitro. |
| 3937 | 2113589 | TNF/AMD was cytotoxic for MBT-2 growth in vitro. |
| 3938 | 2113589 | A two hour preincubation with IFNG markedly increased the cytotoxicity of TNF/AMD whereas longer incubations did not enhance cytotoxic activity. |
| 3939 | 2113589 | A two hour preincubation with IFNG markedly increased the cytotoxicity of TNF/AMD whereas longer incubations did not enhance cytotoxic activity. |
| 3940 | 2113589 | A two hour preincubation with IFNG markedly increased the cytotoxicity of TNF/AMD whereas longer incubations did not enhance cytotoxic activity. |
| 3941 | 2113589 | A two hour preincubation with IFNG markedly increased the cytotoxicity of TNF/AMD whereas longer incubations did not enhance cytotoxic activity. |
| 3942 | 2113589 | This study demonstrated that TNF/AMD exhibits cytotoxicity for MBT-2 cells in vitro but is ineffective in reducing implantation of intravesical tumors in vivo. |
| 3943 | 2113589 | This study demonstrated that TNF/AMD exhibits cytotoxicity for MBT-2 cells in vitro but is ineffective in reducing implantation of intravesical tumors in vivo. |
| 3944 | 2113589 | This study demonstrated that TNF/AMD exhibits cytotoxicity for MBT-2 cells in vitro but is ineffective in reducing implantation of intravesical tumors in vivo. |
| 3945 | 2113589 | This study demonstrated that TNF/AMD exhibits cytotoxicity for MBT-2 cells in vitro but is ineffective in reducing implantation of intravesical tumors in vivo. |
| 3946 | 2113589 | The in vitro data suggest brief exposure of MBT-2 cells to IFNG augments the subsequent anti-tumor activity of TNF/AMD. |
| 3947 | 2113589 | The in vitro data suggest brief exposure of MBT-2 cells to IFNG augments the subsequent anti-tumor activity of TNF/AMD. |
| 3948 | 2113589 | The in vitro data suggest brief exposure of MBT-2 cells to IFNG augments the subsequent anti-tumor activity of TNF/AMD. |
| 3949 | 2113589 | The in vitro data suggest brief exposure of MBT-2 cells to IFNG augments the subsequent anti-tumor activity of TNF/AMD. |