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Gene Information
Gene symbol: IL17D
Gene name: interleukin 17D
HGNC ID: 5984
Synonyms: IL-22, IL-27, IL-17D, IL27, FLJ30846
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 15122754 | HCs upregulate surface expression of major histocompatibility complex (MHC) class I molecules and CD1d but not MHC class II molecules Qa-1, CD80, CD86, CD54, or CD95; in addition, they expressed/secreted interleukin (IL)-10 and IL-4 but not IL-1, IL-6, IL-13, interferon (IFN)-gamma, tumor necrosis factor (TNF), IL-4, or IL-27 (i.e., they acquire the HC* phenotype). |
| 2 | 15122754 | HCs* (but not HCs) induced specific activation, proliferation, and IFN-gamma, TNF, and IL-13 release of cocultured naïve CD8(+) T cells. |
| 3 | 15122754 | Only recently activated CD8(+) T blasts (but not recently activated CD4(+) T blasts or activated cells of the innate immune system, including natural killer T [NKT] cells) induced the HC* phenotype that is prominent from day 10 to day 20 postvaccination (i.e., time points at which peak numbers of recently primed CD8(+) T blasts are found in the liver). |
| 4 | 16365602 | They strongly express CD83, CD86, and CCR7 and have potent ability to migrate to CCL21. |
| 5 | 16365602 | In addition, they were able to activate natural killer and T helper 1 (TH1) cells and to induce peptide-antigen-specific cytotoxic T lymphocytes more significantly than monocyte-derived DCs stimulated with a conventional cytokine cocktail of tumor necrosis factor-alpha, interleukin (IL)-1beta, IL-6, and PGE2 (monocyte-conditioned medium [MCM]-mimic DCs). |
| 6 | 16365602 | The profound ability of OPA-DCs to stimulate these effectors is attributable to their higher expression of IL-12p70, IL-23, and IL-27 than MCM-mimic DCs, which was supported by the findings that the neutralization of IL-12p70 and IL-23 reduced the TH1 priming ability of OPA-DCs. |
| 7 | 16642253 | Regulation of innate and adaptive immune responses by the related cytokines IL-12, IL-23, and IL-27. |
| 8 | 16642253 | This point is well illustrated by the IL-12/IL-23/IL-27 family, whose members share ligand and receptor subunits and play somewhat overlapping roles in innate and adaptive immune responses. |
| 9 | 16642253 | Regulation of innate and adaptive immune responses by the related cytokines IL-12, IL-23, and IL-27. |
| 10 | 16642253 | This point is well illustrated by the IL-12/IL-23/IL-27 family, whose members share ligand and receptor subunits and play somewhat overlapping roles in innate and adaptive immune responses. |
| 11 | 16778218 | Interleukin-23 and interleukin-27 exert quite different antitumor and vaccine effects on poorly immunogenic melanoma. |
| 12 | 16778218 | Recent studies revealed that two novel interleukin (IL)-12-related cytokines, IL-23 and IL-27, have potent antitumor activities. |
| 13 | 16778218 | In this study, we investigated the antitumor efficacies of IL-23 and IL-27 on poorly immunogenic B16F10 melanoma and found that the antitumor responses mediated by IL-23 and IL-27 were clearly different. |
| 14 | 16778218 | In contrast, scIL-27-transfected B16F10 (B16/IL-27) tumors exhibited significant retardation of tumor growth from the early stage. |
| 15 | 16778218 | In vivo depletion assay revealed that the antitumor effect of B16/IL-23 was mainly mediated by CD8+ T cells and IFN-gamma whereas that of B16/IL-27 mainly involved natural killer cells and was independent of IFN-gamma. |
| 16 | 16778218 | We also found that antitumor effects of B16/IL-23 and B16/IL-27 were synergistically enhanced by treatment with IL-18 and IL-12, respectively. |
| 17 | 16778218 | Furthermore, B16/IL-23-vaccinated mice developed protective immunity against parental B16F10 tumors but B16/IL-27-vaccinated mice did not. |
| 18 | 16778218 | When combined with prior in vivo depletion of CD25+ T cells, 80% of B16/IL-23-vaccinated mice completely rejected subsequent tumor challenge. |
| 19 | 16778218 | Finally, we showed that the systemic administration of neither IL-23 nor IL-27 induced such intense toxicity as IL-12. |
| 20 | 16778218 | Our data support that IL-23 and IL-27 might play a role in future cytokine-based immunotherapy against poorly immunogenic tumors. |
| 21 | 16778218 | Interleukin-23 and interleukin-27 exert quite different antitumor and vaccine effects on poorly immunogenic melanoma. |
| 22 | 16778218 | Recent studies revealed that two novel interleukin (IL)-12-related cytokines, IL-23 and IL-27, have potent antitumor activities. |
| 23 | 16778218 | In this study, we investigated the antitumor efficacies of IL-23 and IL-27 on poorly immunogenic B16F10 melanoma and found that the antitumor responses mediated by IL-23 and IL-27 were clearly different. |
| 24 | 16778218 | In contrast, scIL-27-transfected B16F10 (B16/IL-27) tumors exhibited significant retardation of tumor growth from the early stage. |
| 25 | 16778218 | In vivo depletion assay revealed that the antitumor effect of B16/IL-23 was mainly mediated by CD8+ T cells and IFN-gamma whereas that of B16/IL-27 mainly involved natural killer cells and was independent of IFN-gamma. |
| 26 | 16778218 | We also found that antitumor effects of B16/IL-23 and B16/IL-27 were synergistically enhanced by treatment with IL-18 and IL-12, respectively. |
| 27 | 16778218 | Furthermore, B16/IL-23-vaccinated mice developed protective immunity against parental B16F10 tumors but B16/IL-27-vaccinated mice did not. |
| 28 | 16778218 | When combined with prior in vivo depletion of CD25+ T cells, 80% of B16/IL-23-vaccinated mice completely rejected subsequent tumor challenge. |
| 29 | 16778218 | Finally, we showed that the systemic administration of neither IL-23 nor IL-27 induced such intense toxicity as IL-12. |
| 30 | 16778218 | Our data support that IL-23 and IL-27 might play a role in future cytokine-based immunotherapy against poorly immunogenic tumors. |
| 31 | 16778218 | Interleukin-23 and interleukin-27 exert quite different antitumor and vaccine effects on poorly immunogenic melanoma. |
| 32 | 16778218 | Recent studies revealed that two novel interleukin (IL)-12-related cytokines, IL-23 and IL-27, have potent antitumor activities. |
| 33 | 16778218 | In this study, we investigated the antitumor efficacies of IL-23 and IL-27 on poorly immunogenic B16F10 melanoma and found that the antitumor responses mediated by IL-23 and IL-27 were clearly different. |
| 34 | 16778218 | In contrast, scIL-27-transfected B16F10 (B16/IL-27) tumors exhibited significant retardation of tumor growth from the early stage. |
| 35 | 16778218 | In vivo depletion assay revealed that the antitumor effect of B16/IL-23 was mainly mediated by CD8+ T cells and IFN-gamma whereas that of B16/IL-27 mainly involved natural killer cells and was independent of IFN-gamma. |
| 36 | 16778218 | We also found that antitumor effects of B16/IL-23 and B16/IL-27 were synergistically enhanced by treatment with IL-18 and IL-12, respectively. |
| 37 | 16778218 | Furthermore, B16/IL-23-vaccinated mice developed protective immunity against parental B16F10 tumors but B16/IL-27-vaccinated mice did not. |
| 38 | 16778218 | When combined with prior in vivo depletion of CD25+ T cells, 80% of B16/IL-23-vaccinated mice completely rejected subsequent tumor challenge. |
| 39 | 16778218 | Finally, we showed that the systemic administration of neither IL-23 nor IL-27 induced such intense toxicity as IL-12. |
| 40 | 16778218 | Our data support that IL-23 and IL-27 might play a role in future cytokine-based immunotherapy against poorly immunogenic tumors. |
| 41 | 16778218 | Interleukin-23 and interleukin-27 exert quite different antitumor and vaccine effects on poorly immunogenic melanoma. |
| 42 | 16778218 | Recent studies revealed that two novel interleukin (IL)-12-related cytokines, IL-23 and IL-27, have potent antitumor activities. |
| 43 | 16778218 | In this study, we investigated the antitumor efficacies of IL-23 and IL-27 on poorly immunogenic B16F10 melanoma and found that the antitumor responses mediated by IL-23 and IL-27 were clearly different. |
| 44 | 16778218 | In contrast, scIL-27-transfected B16F10 (B16/IL-27) tumors exhibited significant retardation of tumor growth from the early stage. |
| 45 | 16778218 | In vivo depletion assay revealed that the antitumor effect of B16/IL-23 was mainly mediated by CD8+ T cells and IFN-gamma whereas that of B16/IL-27 mainly involved natural killer cells and was independent of IFN-gamma. |
| 46 | 16778218 | We also found that antitumor effects of B16/IL-23 and B16/IL-27 were synergistically enhanced by treatment with IL-18 and IL-12, respectively. |
| 47 | 16778218 | Furthermore, B16/IL-23-vaccinated mice developed protective immunity against parental B16F10 tumors but B16/IL-27-vaccinated mice did not. |
| 48 | 16778218 | When combined with prior in vivo depletion of CD25+ T cells, 80% of B16/IL-23-vaccinated mice completely rejected subsequent tumor challenge. |
| 49 | 16778218 | Finally, we showed that the systemic administration of neither IL-23 nor IL-27 induced such intense toxicity as IL-12. |
| 50 | 16778218 | Our data support that IL-23 and IL-27 might play a role in future cytokine-based immunotherapy against poorly immunogenic tumors. |
| 51 | 16778218 | Interleukin-23 and interleukin-27 exert quite different antitumor and vaccine effects on poorly immunogenic melanoma. |
| 52 | 16778218 | Recent studies revealed that two novel interleukin (IL)-12-related cytokines, IL-23 and IL-27, have potent antitumor activities. |
| 53 | 16778218 | In this study, we investigated the antitumor efficacies of IL-23 and IL-27 on poorly immunogenic B16F10 melanoma and found that the antitumor responses mediated by IL-23 and IL-27 were clearly different. |
| 54 | 16778218 | In contrast, scIL-27-transfected B16F10 (B16/IL-27) tumors exhibited significant retardation of tumor growth from the early stage. |
| 55 | 16778218 | In vivo depletion assay revealed that the antitumor effect of B16/IL-23 was mainly mediated by CD8+ T cells and IFN-gamma whereas that of B16/IL-27 mainly involved natural killer cells and was independent of IFN-gamma. |
| 56 | 16778218 | We also found that antitumor effects of B16/IL-23 and B16/IL-27 were synergistically enhanced by treatment with IL-18 and IL-12, respectively. |
| 57 | 16778218 | Furthermore, B16/IL-23-vaccinated mice developed protective immunity against parental B16F10 tumors but B16/IL-27-vaccinated mice did not. |
| 58 | 16778218 | When combined with prior in vivo depletion of CD25+ T cells, 80% of B16/IL-23-vaccinated mice completely rejected subsequent tumor challenge. |
| 59 | 16778218 | Finally, we showed that the systemic administration of neither IL-23 nor IL-27 induced such intense toxicity as IL-12. |
| 60 | 16778218 | Our data support that IL-23 and IL-27 might play a role in future cytokine-based immunotherapy against poorly immunogenic tumors. |
| 61 | 16778218 | Interleukin-23 and interleukin-27 exert quite different antitumor and vaccine effects on poorly immunogenic melanoma. |
| 62 | 16778218 | Recent studies revealed that two novel interleukin (IL)-12-related cytokines, IL-23 and IL-27, have potent antitumor activities. |
| 63 | 16778218 | In this study, we investigated the antitumor efficacies of IL-23 and IL-27 on poorly immunogenic B16F10 melanoma and found that the antitumor responses mediated by IL-23 and IL-27 were clearly different. |
| 64 | 16778218 | In contrast, scIL-27-transfected B16F10 (B16/IL-27) tumors exhibited significant retardation of tumor growth from the early stage. |
| 65 | 16778218 | In vivo depletion assay revealed that the antitumor effect of B16/IL-23 was mainly mediated by CD8+ T cells and IFN-gamma whereas that of B16/IL-27 mainly involved natural killer cells and was independent of IFN-gamma. |
| 66 | 16778218 | We also found that antitumor effects of B16/IL-23 and B16/IL-27 were synergistically enhanced by treatment with IL-18 and IL-12, respectively. |
| 67 | 16778218 | Furthermore, B16/IL-23-vaccinated mice developed protective immunity against parental B16F10 tumors but B16/IL-27-vaccinated mice did not. |
| 68 | 16778218 | When combined with prior in vivo depletion of CD25+ T cells, 80% of B16/IL-23-vaccinated mice completely rejected subsequent tumor challenge. |
| 69 | 16778218 | Finally, we showed that the systemic administration of neither IL-23 nor IL-27 induced such intense toxicity as IL-12. |
| 70 | 16778218 | Our data support that IL-23 and IL-27 might play a role in future cytokine-based immunotherapy against poorly immunogenic tumors. |
| 71 | 16778218 | Interleukin-23 and interleukin-27 exert quite different antitumor and vaccine effects on poorly immunogenic melanoma. |
| 72 | 16778218 | Recent studies revealed that two novel interleukin (IL)-12-related cytokines, IL-23 and IL-27, have potent antitumor activities. |
| 73 | 16778218 | In this study, we investigated the antitumor efficacies of IL-23 and IL-27 on poorly immunogenic B16F10 melanoma and found that the antitumor responses mediated by IL-23 and IL-27 were clearly different. |
| 74 | 16778218 | In contrast, scIL-27-transfected B16F10 (B16/IL-27) tumors exhibited significant retardation of tumor growth from the early stage. |
| 75 | 16778218 | In vivo depletion assay revealed that the antitumor effect of B16/IL-23 was mainly mediated by CD8+ T cells and IFN-gamma whereas that of B16/IL-27 mainly involved natural killer cells and was independent of IFN-gamma. |
| 76 | 16778218 | We also found that antitumor effects of B16/IL-23 and B16/IL-27 were synergistically enhanced by treatment with IL-18 and IL-12, respectively. |
| 77 | 16778218 | Furthermore, B16/IL-23-vaccinated mice developed protective immunity against parental B16F10 tumors but B16/IL-27-vaccinated mice did not. |
| 78 | 16778218 | When combined with prior in vivo depletion of CD25+ T cells, 80% of B16/IL-23-vaccinated mice completely rejected subsequent tumor challenge. |
| 79 | 16778218 | Finally, we showed that the systemic administration of neither IL-23 nor IL-27 induced such intense toxicity as IL-12. |
| 80 | 16778218 | Our data support that IL-23 and IL-27 might play a role in future cytokine-based immunotherapy against poorly immunogenic tumors. |
| 81 | 16926428 | Increased levels of IFN-gamma, interleukin-6 (IL-6), and monocyte chemoattractant protein 1 were detected in the sera of immunocompetent mice in response to infection, and splenic mRNA expression of IFN-gamma, IL-6, IL-12p35, and IL-27 was elevated 24 h postinfection. |
| 82 | 16926428 | The effects of IL-18, IL-27, and IL-12 on stimulation of the rapid IFN-gamma production were investigated in vitro by analyzing IFN-gamma production in the presence of heat-killed B. mallei. |
| 83 | 16926428 | IL-12 was essential for IFN-gamma production in vitro; IL-18 was also involved in induction of IFN-gamma, but IL-27 was not required for IFN-gamma production in response to heat-killed B. mallei. |
| 84 | 16926428 | The main cellular sources of IFN-gamma were identified in vitro as NK cells, CD8+ T cells, and TCRgammadelta T cells. |
| 85 | 16926428 | Increased levels of IFN-gamma, interleukin-6 (IL-6), and monocyte chemoattractant protein 1 were detected in the sera of immunocompetent mice in response to infection, and splenic mRNA expression of IFN-gamma, IL-6, IL-12p35, and IL-27 was elevated 24 h postinfection. |
| 86 | 16926428 | The effects of IL-18, IL-27, and IL-12 on stimulation of the rapid IFN-gamma production were investigated in vitro by analyzing IFN-gamma production in the presence of heat-killed B. mallei. |
| 87 | 16926428 | IL-12 was essential for IFN-gamma production in vitro; IL-18 was also involved in induction of IFN-gamma, but IL-27 was not required for IFN-gamma production in response to heat-killed B. mallei. |
| 88 | 16926428 | The main cellular sources of IFN-gamma were identified in vitro as NK cells, CD8+ T cells, and TCRgammadelta T cells. |
| 89 | 16926428 | Increased levels of IFN-gamma, interleukin-6 (IL-6), and monocyte chemoattractant protein 1 were detected in the sera of immunocompetent mice in response to infection, and splenic mRNA expression of IFN-gamma, IL-6, IL-12p35, and IL-27 was elevated 24 h postinfection. |
| 90 | 16926428 | The effects of IL-18, IL-27, and IL-12 on stimulation of the rapid IFN-gamma production were investigated in vitro by analyzing IFN-gamma production in the presence of heat-killed B. mallei. |
| 91 | 16926428 | IL-12 was essential for IFN-gamma production in vitro; IL-18 was also involved in induction of IFN-gamma, but IL-27 was not required for IFN-gamma production in response to heat-killed B. mallei. |
| 92 | 16926428 | The main cellular sources of IFN-gamma were identified in vitro as NK cells, CD8+ T cells, and TCRgammadelta T cells. |
| 93 | 17068156 | Noninfectious papilloma virus-like particles inhibit HIV-1 replication: implications for immune control of HIV-1 infection by IL-27. |
| 94 | 17068156 | Recent studies demonstrate that VLPs bind to dendritic cells and induce the expression of antiviral cytokines such as interferon-alpha (IFN-alpha), interleukin-10 (IL-10) and IFN-gamma. |
| 95 | 17068156 | Here, we show that VLPs suppress the replication of both X4 and R5 HIV-1 without affecting the expression of CD4, CXCR4, and CCR5. |
| 96 | 17068156 | VLPs induced the genes associated with IFN induction, immune responses, and antiviral responses, among with the recently described cytokine IL-27. |
| 97 | 17068156 | Subsequently, IL-27 was found to be a potent inhibitor of HIV-1 replication in PBMCs, CD4+ T cells, and macrophages. |
| 98 | 17068156 | Taken together, our studies identify a novel role of IL-27 in restricting HIV-1 replication and suggest that further examination of the inhibitory property of IL-27 may pave the way for a novel therapy for HIV-1 infection. |
| 99 | 17068156 | Noninfectious papilloma virus-like particles inhibit HIV-1 replication: implications for immune control of HIV-1 infection by IL-27. |
| 100 | 17068156 | Recent studies demonstrate that VLPs bind to dendritic cells and induce the expression of antiviral cytokines such as interferon-alpha (IFN-alpha), interleukin-10 (IL-10) and IFN-gamma. |
| 101 | 17068156 | Here, we show that VLPs suppress the replication of both X4 and R5 HIV-1 without affecting the expression of CD4, CXCR4, and CCR5. |
| 102 | 17068156 | VLPs induced the genes associated with IFN induction, immune responses, and antiviral responses, among with the recently described cytokine IL-27. |
| 103 | 17068156 | Subsequently, IL-27 was found to be a potent inhibitor of HIV-1 replication in PBMCs, CD4+ T cells, and macrophages. |
| 104 | 17068156 | Taken together, our studies identify a novel role of IL-27 in restricting HIV-1 replication and suggest that further examination of the inhibitory property of IL-27 may pave the way for a novel therapy for HIV-1 infection. |
| 105 | 17068156 | Noninfectious papilloma virus-like particles inhibit HIV-1 replication: implications for immune control of HIV-1 infection by IL-27. |
| 106 | 17068156 | Recent studies demonstrate that VLPs bind to dendritic cells and induce the expression of antiviral cytokines such as interferon-alpha (IFN-alpha), interleukin-10 (IL-10) and IFN-gamma. |
| 107 | 17068156 | Here, we show that VLPs suppress the replication of both X4 and R5 HIV-1 without affecting the expression of CD4, CXCR4, and CCR5. |
| 108 | 17068156 | VLPs induced the genes associated with IFN induction, immune responses, and antiviral responses, among with the recently described cytokine IL-27. |
| 109 | 17068156 | Subsequently, IL-27 was found to be a potent inhibitor of HIV-1 replication in PBMCs, CD4+ T cells, and macrophages. |
| 110 | 17068156 | Taken together, our studies identify a novel role of IL-27 in restricting HIV-1 replication and suggest that further examination of the inhibitory property of IL-27 may pave the way for a novel therapy for HIV-1 infection. |
| 111 | 17068156 | Noninfectious papilloma virus-like particles inhibit HIV-1 replication: implications for immune control of HIV-1 infection by IL-27. |
| 112 | 17068156 | Recent studies demonstrate that VLPs bind to dendritic cells and induce the expression of antiviral cytokines such as interferon-alpha (IFN-alpha), interleukin-10 (IL-10) and IFN-gamma. |
| 113 | 17068156 | Here, we show that VLPs suppress the replication of both X4 and R5 HIV-1 without affecting the expression of CD4, CXCR4, and CCR5. |
| 114 | 17068156 | VLPs induced the genes associated with IFN induction, immune responses, and antiviral responses, among with the recently described cytokine IL-27. |
| 115 | 17068156 | Subsequently, IL-27 was found to be a potent inhibitor of HIV-1 replication in PBMCs, CD4+ T cells, and macrophages. |
| 116 | 17068156 | Taken together, our studies identify a novel role of IL-27 in restricting HIV-1 replication and suggest that further examination of the inhibitory property of IL-27 may pave the way for a novel therapy for HIV-1 infection. |
| 117 | 17699845 | By promoting IFN-gamma production, proliferation, and cytolytic activity of natural killer and T cells, IL-12 induces cellular immunity. |
| 118 | 17699845 | In addition, IL-12 induces an antiangiogenic program mediated by IFN-gamma-inducible genes and by lymphocyte-endothelial cell cross-talk. |
| 119 | 17699845 | More effective application of this cytokine, and of newly identified IL-12 family members (IL-23 and IL-27), should be evaluated as therapeutic agents with considerable potential in cancer patients. |
| 120 | 18209095 | Distinct, specific IL-17- and IL-22-producing CD4+ T cell subsets contribute to the human anti-mycobacterial immune response. |
| 121 | 18209095 | We investigated whether the proinflammatory T cell cytokines IL-17 and IL-22 are induced by human mycobacterial infection. |
| 122 | 18209095 | Remarkably, >20% of specific cytokine-producing CD4(+) T cells in peripheral blood of healthy, mycobacteria-exposed adults expressed IL-17 or IL-22. |
| 123 | 18209095 | Specific IL-17- and IL-22-producing CD4(+) T cells were distinct from each other and from Th1 cytokine-producing cells. |
| 124 | 18209095 | IL-17 was not detected in this fluid, which may be due to suppression by Th1 cytokines, as PBMC IL-17 production was inhibited by IFN-gamma in vitro. |
| 125 | 18209095 | IL-17- and IL-22-producing CD4(+) T cells may play important roles in the human immune response to mycobacteria. |
| 126 | 18209095 | Distinct, specific IL-17- and IL-22-producing CD4+ T cell subsets contribute to the human anti-mycobacterial immune response. |
| 127 | 18209095 | We investigated whether the proinflammatory T cell cytokines IL-17 and IL-22 are induced by human mycobacterial infection. |
| 128 | 18209095 | Remarkably, >20% of specific cytokine-producing CD4(+) T cells in peripheral blood of healthy, mycobacteria-exposed adults expressed IL-17 or IL-22. |
| 129 | 18209095 | Specific IL-17- and IL-22-producing CD4(+) T cells were distinct from each other and from Th1 cytokine-producing cells. |
| 130 | 18209095 | IL-17 was not detected in this fluid, which may be due to suppression by Th1 cytokines, as PBMC IL-17 production was inhibited by IFN-gamma in vitro. |
| 131 | 18209095 | IL-17- and IL-22-producing CD4(+) T cells may play important roles in the human immune response to mycobacteria. |
| 132 | 18209095 | Distinct, specific IL-17- and IL-22-producing CD4+ T cell subsets contribute to the human anti-mycobacterial immune response. |
| 133 | 18209095 | We investigated whether the proinflammatory T cell cytokines IL-17 and IL-22 are induced by human mycobacterial infection. |
| 134 | 18209095 | Remarkably, >20% of specific cytokine-producing CD4(+) T cells in peripheral blood of healthy, mycobacteria-exposed adults expressed IL-17 or IL-22. |
| 135 | 18209095 | Specific IL-17- and IL-22-producing CD4(+) T cells were distinct from each other and from Th1 cytokine-producing cells. |
| 136 | 18209095 | IL-17 was not detected in this fluid, which may be due to suppression by Th1 cytokines, as PBMC IL-17 production was inhibited by IFN-gamma in vitro. |
| 137 | 18209095 | IL-17- and IL-22-producing CD4(+) T cells may play important roles in the human immune response to mycobacteria. |
| 138 | 18209095 | Distinct, specific IL-17- and IL-22-producing CD4+ T cell subsets contribute to the human anti-mycobacterial immune response. |
| 139 | 18209095 | We investigated whether the proinflammatory T cell cytokines IL-17 and IL-22 are induced by human mycobacterial infection. |
| 140 | 18209095 | Remarkably, >20% of specific cytokine-producing CD4(+) T cells in peripheral blood of healthy, mycobacteria-exposed adults expressed IL-17 or IL-22. |
| 141 | 18209095 | Specific IL-17- and IL-22-producing CD4(+) T cells were distinct from each other and from Th1 cytokine-producing cells. |
| 142 | 18209095 | IL-17 was not detected in this fluid, which may be due to suppression by Th1 cytokines, as PBMC IL-17 production was inhibited by IFN-gamma in vitro. |
| 143 | 18209095 | IL-17- and IL-22-producing CD4(+) T cells may play important roles in the human immune response to mycobacteria. |
| 144 | 18209095 | Distinct, specific IL-17- and IL-22-producing CD4+ T cell subsets contribute to the human anti-mycobacterial immune response. |
| 145 | 18209095 | We investigated whether the proinflammatory T cell cytokines IL-17 and IL-22 are induced by human mycobacterial infection. |
| 146 | 18209095 | Remarkably, >20% of specific cytokine-producing CD4(+) T cells in peripheral blood of healthy, mycobacteria-exposed adults expressed IL-17 or IL-22. |
| 147 | 18209095 | Specific IL-17- and IL-22-producing CD4(+) T cells were distinct from each other and from Th1 cytokine-producing cells. |
| 148 | 18209095 | IL-17 was not detected in this fluid, which may be due to suppression by Th1 cytokines, as PBMC IL-17 production was inhibited by IFN-gamma in vitro. |
| 149 | 18209095 | IL-17- and IL-22-producing CD4(+) T cells may play important roles in the human immune response to mycobacteria. |
| 150 | 19038785 | Specifically, 12 immune biomolecules (including gamma interferon [IFN-gamma], interleukin-21 [IL-21], IL-27, IL-17f, CXCL9, CXCL10, and CXCL11) were differentially regulated, relative to the levels for naïve controls, in the lungs of vaccinated mice at this time point. |
| 151 | 19038785 | Although the vaccine-related immune responses evoked in mice immunized with the DNA vaccine were relatively limited at 10 days postinfection, upregulation of IFN-gamma RNA synthesis as well as increased expression levels of CXCL9, CXCL10, and CXCL11 chemokines were detected. |
| 152 | 19430645 | By examining this organism, researchers have identified many of the requirements for resistance to intracellular pathogens and characterized numerous regulatory factors, including interleukin-10 (IL-10) and IL-27, which control inflammatory processes. |
| 153 | 19458207 | Among the consistently upregulated cytokines detected in the immune cocultures are gamma interferon, growth differentiation factor 15, interleukin-21 (IL-21), IL-27, and tumor necrosis factor alpha. |
| 154 | 20112107 | T helper type 17 (Th17) cells are a distinct lineage of T cells that produce the effector molecules IL-17, IL-17F, IL-21, and IL-22. |
| 155 | 20182729 | T helper type 17 (Th17) cells are a distinct lineage of T cells that produce the effector molecules IL-17, IL-17F, IL-21, and IL-22. |
| 156 | 20454646 | A pivotal role for interleukin-27 in CD8+ T cell functions and generation of cytotoxic T lymphocytes. |
| 157 | 20454646 | Interleukin (IL)-27, a member of the IL-6/IL-12 heterodimeric cytokine family, acts on naive CD4+ T cells and plays pivotal roles as a proinflammatory cytokine to promote the early initiation of type-1 helper differentiation and also as an antiinflammatory cytokine to limit the T cell hyperactivity and production of pro-inflammatory cytokines. |
| 158 | 20454646 | Recent studies revealed that IL-27 plays an important role in CD8+ T cells as well. |
| 159 | 20454646 | Therefore, this article reviews current understanding of the role of IL-27 in CD8+ T cell functions and generation of CTLs. |
| 160 | 20454646 | A pivotal role for interleukin-27 in CD8+ T cell functions and generation of cytotoxic T lymphocytes. |
| 161 | 20454646 | Interleukin (IL)-27, a member of the IL-6/IL-12 heterodimeric cytokine family, acts on naive CD4+ T cells and plays pivotal roles as a proinflammatory cytokine to promote the early initiation of type-1 helper differentiation and also as an antiinflammatory cytokine to limit the T cell hyperactivity and production of pro-inflammatory cytokines. |
| 162 | 20454646 | Recent studies revealed that IL-27 plays an important role in CD8+ T cells as well. |
| 163 | 20454646 | Therefore, this article reviews current understanding of the role of IL-27 in CD8+ T cell functions and generation of CTLs. |
| 164 | 20483237 | In fish, prior to pufferfish (Fugu rubripes and Tetraodon nigroviridis) and zebrafish (Danio rerio) genome sequencing, only a handful of cytokines like IL-1beta, TNF-alpha, TGFbeta, some CXC (including IL-8) and CC chemokine genes were identified. |
| 165 | 20483237 | Pro-inflammatory cytokines like TNF's, IL-6 and IL-17 family have been cloned. |
| 166 | 20483237 | Among the T(H)1 type interleukins, IL-2, IL-15, IL-12alpha, IL-12beta, IL-18 have been cloned. |
| 167 | 20483237 | Among IL-10 and its family members, IL-10, IL-19/20, IL-22 and IL-26 have been discovered. |
| 168 | 20483237 | However, T(H)2 cytokines (IL-4, IL-5 and IL-13), IL-3, IL-7 and IL-9 are yet to be discovered from fish. |
| 169 | 20488794 | Furthermore, this diet resulted in low mRNA expression levels of IL-17, IFN regulatory factor 4, IL-21, IL-22, and IL-23 without alteration of other genes, such as RORgammat, TGF-beta, IL-6, IL-25, and IL-27 in the small intestine ileum. |
| 170 | 20488794 | Interestingly, the VAD diet elicited high levels of mucin MUC2 by goblet cell hyperplasia and subsequently reduced gut microbiome, including segmented filamentous bacteria. |
| 171 | 20488794 | Much like wild-type mice, the VAD diet-fed MyD88-/-TRIF-/- mice had significantly fewer IL-17-secreting CD4+ T cells than the control diet-fed MyD88-/-TRIF-/- mice. |
| 172 | 20504940 | Interleukin-22 (IL-22) production by pulmonary Natural Killer cells and the potential role of IL-22 during primary influenza virus infection. |
| 173 | 20504940 | We set out to test the hypothesis that interleukin-22 (IL-22), a cytokine crucial for epithelial cell homeostasis and recovery from tissue injury, would be protective during influenza virus infection. |
| 174 | 20504940 | Recent studies have identified phenotypically and functionally unique intestinal NK cells capable of producing the cytokine IL-22. |
| 175 | 20504940 | Unlike gut NK cells that produce IL-22, the surface phenotypes of lung NK cells were similar to those of spleen NK cells and were characteristically mature. |
| 176 | 20504940 | With mitogen stimulation, both single and double IL-22- and gamma interferon (IFN-gamma)-producing lung NK cells were detected. |
| 177 | 20504940 | However, only the IL-22(+) IFN-gamma(-) lung NK subset was observed after stimulation with IL-23. |
| 178 | 20504940 | IL-23 receptor (IL-23R) blocking dramatically inhibited IL-22 production, but not IFN-gamma production. |
| 179 | 20504940 | Furthermore, we found that NK1.1(+) or CD27(-) lung NK cells were the primary sources of IL-22. |
| 180 | 20504940 | After influenza virus infection, lung NK cells were quickly activated to produce both IFN-gamma and IL-22 and had increased cytotoxic potential. |
| 181 | 20504940 | The level of IL-22 in the lung tissue declined shortly after infection, gradually returning to the baseline after virus clearance, although the IL-22 gene expression was maintained. |
| 182 | 20504940 | Furthermore, depletion of NK cells with or without influenza virus infection reduced the protein level of IL-22 in the lung. |
| 183 | 20504940 | Our data suggest that during primary respiratory viral infection, IL-22 seems to a play a marginal role for protection, indicating a differential requirement of this cytokine for bacterial and viral infections. |
| 184 | 20504940 | Interleukin-22 (IL-22) production by pulmonary Natural Killer cells and the potential role of IL-22 during primary influenza virus infection. |
| 185 | 20504940 | We set out to test the hypothesis that interleukin-22 (IL-22), a cytokine crucial for epithelial cell homeostasis and recovery from tissue injury, would be protective during influenza virus infection. |
| 186 | 20504940 | Recent studies have identified phenotypically and functionally unique intestinal NK cells capable of producing the cytokine IL-22. |
| 187 | 20504940 | Unlike gut NK cells that produce IL-22, the surface phenotypes of lung NK cells were similar to those of spleen NK cells and were characteristically mature. |
| 188 | 20504940 | With mitogen stimulation, both single and double IL-22- and gamma interferon (IFN-gamma)-producing lung NK cells were detected. |
| 189 | 20504940 | However, only the IL-22(+) IFN-gamma(-) lung NK subset was observed after stimulation with IL-23. |
| 190 | 20504940 | IL-23 receptor (IL-23R) blocking dramatically inhibited IL-22 production, but not IFN-gamma production. |
| 191 | 20504940 | Furthermore, we found that NK1.1(+) or CD27(-) lung NK cells were the primary sources of IL-22. |
| 192 | 20504940 | After influenza virus infection, lung NK cells were quickly activated to produce both IFN-gamma and IL-22 and had increased cytotoxic potential. |
| 193 | 20504940 | The level of IL-22 in the lung tissue declined shortly after infection, gradually returning to the baseline after virus clearance, although the IL-22 gene expression was maintained. |
| 194 | 20504940 | Furthermore, depletion of NK cells with or without influenza virus infection reduced the protein level of IL-22 in the lung. |
| 195 | 20504940 | Our data suggest that during primary respiratory viral infection, IL-22 seems to a play a marginal role for protection, indicating a differential requirement of this cytokine for bacterial and viral infections. |
| 196 | 20504940 | Interleukin-22 (IL-22) production by pulmonary Natural Killer cells and the potential role of IL-22 during primary influenza virus infection. |
| 197 | 20504940 | We set out to test the hypothesis that interleukin-22 (IL-22), a cytokine crucial for epithelial cell homeostasis and recovery from tissue injury, would be protective during influenza virus infection. |
| 198 | 20504940 | Recent studies have identified phenotypically and functionally unique intestinal NK cells capable of producing the cytokine IL-22. |
| 199 | 20504940 | Unlike gut NK cells that produce IL-22, the surface phenotypes of lung NK cells were similar to those of spleen NK cells and were characteristically mature. |
| 200 | 20504940 | With mitogen stimulation, both single and double IL-22- and gamma interferon (IFN-gamma)-producing lung NK cells were detected. |
| 201 | 20504940 | However, only the IL-22(+) IFN-gamma(-) lung NK subset was observed after stimulation with IL-23. |
| 202 | 20504940 | IL-23 receptor (IL-23R) blocking dramatically inhibited IL-22 production, but not IFN-gamma production. |
| 203 | 20504940 | Furthermore, we found that NK1.1(+) or CD27(-) lung NK cells were the primary sources of IL-22. |
| 204 | 20504940 | After influenza virus infection, lung NK cells were quickly activated to produce both IFN-gamma and IL-22 and had increased cytotoxic potential. |
| 205 | 20504940 | The level of IL-22 in the lung tissue declined shortly after infection, gradually returning to the baseline after virus clearance, although the IL-22 gene expression was maintained. |
| 206 | 20504940 | Furthermore, depletion of NK cells with or without influenza virus infection reduced the protein level of IL-22 in the lung. |
| 207 | 20504940 | Our data suggest that during primary respiratory viral infection, IL-22 seems to a play a marginal role for protection, indicating a differential requirement of this cytokine for bacterial and viral infections. |
| 208 | 20504940 | Interleukin-22 (IL-22) production by pulmonary Natural Killer cells and the potential role of IL-22 during primary influenza virus infection. |
| 209 | 20504940 | We set out to test the hypothesis that interleukin-22 (IL-22), a cytokine crucial for epithelial cell homeostasis and recovery from tissue injury, would be protective during influenza virus infection. |
| 210 | 20504940 | Recent studies have identified phenotypically and functionally unique intestinal NK cells capable of producing the cytokine IL-22. |
| 211 | 20504940 | Unlike gut NK cells that produce IL-22, the surface phenotypes of lung NK cells were similar to those of spleen NK cells and were characteristically mature. |
| 212 | 20504940 | With mitogen stimulation, both single and double IL-22- and gamma interferon (IFN-gamma)-producing lung NK cells were detected. |
| 213 | 20504940 | However, only the IL-22(+) IFN-gamma(-) lung NK subset was observed after stimulation with IL-23. |
| 214 | 20504940 | IL-23 receptor (IL-23R) blocking dramatically inhibited IL-22 production, but not IFN-gamma production. |
| 215 | 20504940 | Furthermore, we found that NK1.1(+) or CD27(-) lung NK cells were the primary sources of IL-22. |
| 216 | 20504940 | After influenza virus infection, lung NK cells were quickly activated to produce both IFN-gamma and IL-22 and had increased cytotoxic potential. |
| 217 | 20504940 | The level of IL-22 in the lung tissue declined shortly after infection, gradually returning to the baseline after virus clearance, although the IL-22 gene expression was maintained. |
| 218 | 20504940 | Furthermore, depletion of NK cells with or without influenza virus infection reduced the protein level of IL-22 in the lung. |
| 219 | 20504940 | Our data suggest that during primary respiratory viral infection, IL-22 seems to a play a marginal role for protection, indicating a differential requirement of this cytokine for bacterial and viral infections. |
| 220 | 20504940 | Interleukin-22 (IL-22) production by pulmonary Natural Killer cells and the potential role of IL-22 during primary influenza virus infection. |
| 221 | 20504940 | We set out to test the hypothesis that interleukin-22 (IL-22), a cytokine crucial for epithelial cell homeostasis and recovery from tissue injury, would be protective during influenza virus infection. |
| 222 | 20504940 | Recent studies have identified phenotypically and functionally unique intestinal NK cells capable of producing the cytokine IL-22. |
| 223 | 20504940 | Unlike gut NK cells that produce IL-22, the surface phenotypes of lung NK cells were similar to those of spleen NK cells and were characteristically mature. |
| 224 | 20504940 | With mitogen stimulation, both single and double IL-22- and gamma interferon (IFN-gamma)-producing lung NK cells were detected. |
| 225 | 20504940 | However, only the IL-22(+) IFN-gamma(-) lung NK subset was observed after stimulation with IL-23. |
| 226 | 20504940 | IL-23 receptor (IL-23R) blocking dramatically inhibited IL-22 production, but not IFN-gamma production. |
| 227 | 20504940 | Furthermore, we found that NK1.1(+) or CD27(-) lung NK cells were the primary sources of IL-22. |
| 228 | 20504940 | After influenza virus infection, lung NK cells were quickly activated to produce both IFN-gamma and IL-22 and had increased cytotoxic potential. |
| 229 | 20504940 | The level of IL-22 in the lung tissue declined shortly after infection, gradually returning to the baseline after virus clearance, although the IL-22 gene expression was maintained. |
| 230 | 20504940 | Furthermore, depletion of NK cells with or without influenza virus infection reduced the protein level of IL-22 in the lung. |
| 231 | 20504940 | Our data suggest that during primary respiratory viral infection, IL-22 seems to a play a marginal role for protection, indicating a differential requirement of this cytokine for bacterial and viral infections. |
| 232 | 20504940 | Interleukin-22 (IL-22) production by pulmonary Natural Killer cells and the potential role of IL-22 during primary influenza virus infection. |
| 233 | 20504940 | We set out to test the hypothesis that interleukin-22 (IL-22), a cytokine crucial for epithelial cell homeostasis and recovery from tissue injury, would be protective during influenza virus infection. |
| 234 | 20504940 | Recent studies have identified phenotypically and functionally unique intestinal NK cells capable of producing the cytokine IL-22. |
| 235 | 20504940 | Unlike gut NK cells that produce IL-22, the surface phenotypes of lung NK cells were similar to those of spleen NK cells and were characteristically mature. |
| 236 | 20504940 | With mitogen stimulation, both single and double IL-22- and gamma interferon (IFN-gamma)-producing lung NK cells were detected. |
| 237 | 20504940 | However, only the IL-22(+) IFN-gamma(-) lung NK subset was observed after stimulation with IL-23. |
| 238 | 20504940 | IL-23 receptor (IL-23R) blocking dramatically inhibited IL-22 production, but not IFN-gamma production. |
| 239 | 20504940 | Furthermore, we found that NK1.1(+) or CD27(-) lung NK cells were the primary sources of IL-22. |
| 240 | 20504940 | After influenza virus infection, lung NK cells were quickly activated to produce both IFN-gamma and IL-22 and had increased cytotoxic potential. |
| 241 | 20504940 | The level of IL-22 in the lung tissue declined shortly after infection, gradually returning to the baseline after virus clearance, although the IL-22 gene expression was maintained. |
| 242 | 20504940 | Furthermore, depletion of NK cells with or without influenza virus infection reduced the protein level of IL-22 in the lung. |
| 243 | 20504940 | Our data suggest that during primary respiratory viral infection, IL-22 seems to a play a marginal role for protection, indicating a differential requirement of this cytokine for bacterial and viral infections. |
| 244 | 20504940 | Interleukin-22 (IL-22) production by pulmonary Natural Killer cells and the potential role of IL-22 during primary influenza virus infection. |
| 245 | 20504940 | We set out to test the hypothesis that interleukin-22 (IL-22), a cytokine crucial for epithelial cell homeostasis and recovery from tissue injury, would be protective during influenza virus infection. |
| 246 | 20504940 | Recent studies have identified phenotypically and functionally unique intestinal NK cells capable of producing the cytokine IL-22. |
| 247 | 20504940 | Unlike gut NK cells that produce IL-22, the surface phenotypes of lung NK cells were similar to those of spleen NK cells and were characteristically mature. |
| 248 | 20504940 | With mitogen stimulation, both single and double IL-22- and gamma interferon (IFN-gamma)-producing lung NK cells were detected. |
| 249 | 20504940 | However, only the IL-22(+) IFN-gamma(-) lung NK subset was observed after stimulation with IL-23. |
| 250 | 20504940 | IL-23 receptor (IL-23R) blocking dramatically inhibited IL-22 production, but not IFN-gamma production. |
| 251 | 20504940 | Furthermore, we found that NK1.1(+) or CD27(-) lung NK cells were the primary sources of IL-22. |
| 252 | 20504940 | After influenza virus infection, lung NK cells were quickly activated to produce both IFN-gamma and IL-22 and had increased cytotoxic potential. |
| 253 | 20504940 | The level of IL-22 in the lung tissue declined shortly after infection, gradually returning to the baseline after virus clearance, although the IL-22 gene expression was maintained. |
| 254 | 20504940 | Furthermore, depletion of NK cells with or without influenza virus infection reduced the protein level of IL-22 in the lung. |
| 255 | 20504940 | Our data suggest that during primary respiratory viral infection, IL-22 seems to a play a marginal role for protection, indicating a differential requirement of this cytokine for bacterial and viral infections. |
| 256 | 20504940 | Interleukin-22 (IL-22) production by pulmonary Natural Killer cells and the potential role of IL-22 during primary influenza virus infection. |
| 257 | 20504940 | We set out to test the hypothesis that interleukin-22 (IL-22), a cytokine crucial for epithelial cell homeostasis and recovery from tissue injury, would be protective during influenza virus infection. |
| 258 | 20504940 | Recent studies have identified phenotypically and functionally unique intestinal NK cells capable of producing the cytokine IL-22. |
| 259 | 20504940 | Unlike gut NK cells that produce IL-22, the surface phenotypes of lung NK cells were similar to those of spleen NK cells and were characteristically mature. |
| 260 | 20504940 | With mitogen stimulation, both single and double IL-22- and gamma interferon (IFN-gamma)-producing lung NK cells were detected. |
| 261 | 20504940 | However, only the IL-22(+) IFN-gamma(-) lung NK subset was observed after stimulation with IL-23. |
| 262 | 20504940 | IL-23 receptor (IL-23R) blocking dramatically inhibited IL-22 production, but not IFN-gamma production. |
| 263 | 20504940 | Furthermore, we found that NK1.1(+) or CD27(-) lung NK cells were the primary sources of IL-22. |
| 264 | 20504940 | After influenza virus infection, lung NK cells were quickly activated to produce both IFN-gamma and IL-22 and had increased cytotoxic potential. |
| 265 | 20504940 | The level of IL-22 in the lung tissue declined shortly after infection, gradually returning to the baseline after virus clearance, although the IL-22 gene expression was maintained. |
| 266 | 20504940 | Furthermore, depletion of NK cells with or without influenza virus infection reduced the protein level of IL-22 in the lung. |
| 267 | 20504940 | Our data suggest that during primary respiratory viral infection, IL-22 seems to a play a marginal role for protection, indicating a differential requirement of this cytokine for bacterial and viral infections. |
| 268 | 20504940 | Interleukin-22 (IL-22) production by pulmonary Natural Killer cells and the potential role of IL-22 during primary influenza virus infection. |
| 269 | 20504940 | We set out to test the hypothesis that interleukin-22 (IL-22), a cytokine crucial for epithelial cell homeostasis and recovery from tissue injury, would be protective during influenza virus infection. |
| 270 | 20504940 | Recent studies have identified phenotypically and functionally unique intestinal NK cells capable of producing the cytokine IL-22. |
| 271 | 20504940 | Unlike gut NK cells that produce IL-22, the surface phenotypes of lung NK cells were similar to those of spleen NK cells and were characteristically mature. |
| 272 | 20504940 | With mitogen stimulation, both single and double IL-22- and gamma interferon (IFN-gamma)-producing lung NK cells were detected. |
| 273 | 20504940 | However, only the IL-22(+) IFN-gamma(-) lung NK subset was observed after stimulation with IL-23. |
| 274 | 20504940 | IL-23 receptor (IL-23R) blocking dramatically inhibited IL-22 production, but not IFN-gamma production. |
| 275 | 20504940 | Furthermore, we found that NK1.1(+) or CD27(-) lung NK cells were the primary sources of IL-22. |
| 276 | 20504940 | After influenza virus infection, lung NK cells were quickly activated to produce both IFN-gamma and IL-22 and had increased cytotoxic potential. |
| 277 | 20504940 | The level of IL-22 in the lung tissue declined shortly after infection, gradually returning to the baseline after virus clearance, although the IL-22 gene expression was maintained. |
| 278 | 20504940 | Furthermore, depletion of NK cells with or without influenza virus infection reduced the protein level of IL-22 in the lung. |
| 279 | 20504940 | Our data suggest that during primary respiratory viral infection, IL-22 seems to a play a marginal role for protection, indicating a differential requirement of this cytokine for bacterial and viral infections. |
| 280 | 20504940 | Interleukin-22 (IL-22) production by pulmonary Natural Killer cells and the potential role of IL-22 during primary influenza virus infection. |
| 281 | 20504940 | We set out to test the hypothesis that interleukin-22 (IL-22), a cytokine crucial for epithelial cell homeostasis and recovery from tissue injury, would be protective during influenza virus infection. |
| 282 | 20504940 | Recent studies have identified phenotypically and functionally unique intestinal NK cells capable of producing the cytokine IL-22. |
| 283 | 20504940 | Unlike gut NK cells that produce IL-22, the surface phenotypes of lung NK cells were similar to those of spleen NK cells and were characteristically mature. |
| 284 | 20504940 | With mitogen stimulation, both single and double IL-22- and gamma interferon (IFN-gamma)-producing lung NK cells were detected. |
| 285 | 20504940 | However, only the IL-22(+) IFN-gamma(-) lung NK subset was observed after stimulation with IL-23. |
| 286 | 20504940 | IL-23 receptor (IL-23R) blocking dramatically inhibited IL-22 production, but not IFN-gamma production. |
| 287 | 20504940 | Furthermore, we found that NK1.1(+) or CD27(-) lung NK cells were the primary sources of IL-22. |
| 288 | 20504940 | After influenza virus infection, lung NK cells were quickly activated to produce both IFN-gamma and IL-22 and had increased cytotoxic potential. |
| 289 | 20504940 | The level of IL-22 in the lung tissue declined shortly after infection, gradually returning to the baseline after virus clearance, although the IL-22 gene expression was maintained. |
| 290 | 20504940 | Furthermore, depletion of NK cells with or without influenza virus infection reduced the protein level of IL-22 in the lung. |
| 291 | 20504940 | Our data suggest that during primary respiratory viral infection, IL-22 seems to a play a marginal role for protection, indicating a differential requirement of this cytokine for bacterial and viral infections. |
| 292 | 20504940 | Interleukin-22 (IL-22) production by pulmonary Natural Killer cells and the potential role of IL-22 during primary influenza virus infection. |
| 293 | 20504940 | We set out to test the hypothesis that interleukin-22 (IL-22), a cytokine crucial for epithelial cell homeostasis and recovery from tissue injury, would be protective during influenza virus infection. |
| 294 | 20504940 | Recent studies have identified phenotypically and functionally unique intestinal NK cells capable of producing the cytokine IL-22. |
| 295 | 20504940 | Unlike gut NK cells that produce IL-22, the surface phenotypes of lung NK cells were similar to those of spleen NK cells and were characteristically mature. |
| 296 | 20504940 | With mitogen stimulation, both single and double IL-22- and gamma interferon (IFN-gamma)-producing lung NK cells were detected. |
| 297 | 20504940 | However, only the IL-22(+) IFN-gamma(-) lung NK subset was observed after stimulation with IL-23. |
| 298 | 20504940 | IL-23 receptor (IL-23R) blocking dramatically inhibited IL-22 production, but not IFN-gamma production. |
| 299 | 20504940 | Furthermore, we found that NK1.1(+) or CD27(-) lung NK cells were the primary sources of IL-22. |
| 300 | 20504940 | After influenza virus infection, lung NK cells were quickly activated to produce both IFN-gamma and IL-22 and had increased cytotoxic potential. |
| 301 | 20504940 | The level of IL-22 in the lung tissue declined shortly after infection, gradually returning to the baseline after virus clearance, although the IL-22 gene expression was maintained. |
| 302 | 20504940 | Furthermore, depletion of NK cells with or without influenza virus infection reduced the protein level of IL-22 in the lung. |
| 303 | 20504940 | Our data suggest that during primary respiratory viral infection, IL-22 seems to a play a marginal role for protection, indicating a differential requirement of this cytokine for bacterial and viral infections. |
| 304 | 20504940 | Interleukin-22 (IL-22) production by pulmonary Natural Killer cells and the potential role of IL-22 during primary influenza virus infection. |
| 305 | 20504940 | We set out to test the hypothesis that interleukin-22 (IL-22), a cytokine crucial for epithelial cell homeostasis and recovery from tissue injury, would be protective during influenza virus infection. |
| 306 | 20504940 | Recent studies have identified phenotypically and functionally unique intestinal NK cells capable of producing the cytokine IL-22. |
| 307 | 20504940 | Unlike gut NK cells that produce IL-22, the surface phenotypes of lung NK cells were similar to those of spleen NK cells and were characteristically mature. |
| 308 | 20504940 | With mitogen stimulation, both single and double IL-22- and gamma interferon (IFN-gamma)-producing lung NK cells were detected. |
| 309 | 20504940 | However, only the IL-22(+) IFN-gamma(-) lung NK subset was observed after stimulation with IL-23. |
| 310 | 20504940 | IL-23 receptor (IL-23R) blocking dramatically inhibited IL-22 production, but not IFN-gamma production. |
| 311 | 20504940 | Furthermore, we found that NK1.1(+) or CD27(-) lung NK cells were the primary sources of IL-22. |
| 312 | 20504940 | After influenza virus infection, lung NK cells were quickly activated to produce both IFN-gamma and IL-22 and had increased cytotoxic potential. |
| 313 | 20504940 | The level of IL-22 in the lung tissue declined shortly after infection, gradually returning to the baseline after virus clearance, although the IL-22 gene expression was maintained. |
| 314 | 20504940 | Furthermore, depletion of NK cells with or without influenza virus infection reduced the protein level of IL-22 in the lung. |
| 315 | 20504940 | Our data suggest that during primary respiratory viral infection, IL-22 seems to a play a marginal role for protection, indicating a differential requirement of this cytokine for bacterial and viral infections. |
| 316 | 20626289 | To determine whether cytokines and T-cell subsets other than Th1 cells contribute to secondary immune responses against Francisella species, we investigated production of Th17-associated cytokines IL-17 and IL-22 in a recall response to Francisella tularensis. |
| 317 | 20626289 | Gene expression analysis by real-time PCR showed that IL-17 and IL-22 transcripts were induced in immune PBMCs at a significantly higher level than in cells from nonvaccinated volunteers stimulated with LVS or B38 antigens at 24 h. |
| 318 | 20626289 | In addition, we detected both cell-associated and secreted IL-22 at 24 h after stimulation and IL-17 at 72 h post-stimulation. |
| 319 | 20626289 | Intracellular IL-22 and IL-17 were observed in memory CD4+ cells and less in memory CD8+ cells. |
| 320 | 20626289 | To determine whether cytokines and T-cell subsets other than Th1 cells contribute to secondary immune responses against Francisella species, we investigated production of Th17-associated cytokines IL-17 and IL-22 in a recall response to Francisella tularensis. |
| 321 | 20626289 | Gene expression analysis by real-time PCR showed that IL-17 and IL-22 transcripts were induced in immune PBMCs at a significantly higher level than in cells from nonvaccinated volunteers stimulated with LVS or B38 antigens at 24 h. |
| 322 | 20626289 | In addition, we detected both cell-associated and secreted IL-22 at 24 h after stimulation and IL-17 at 72 h post-stimulation. |
| 323 | 20626289 | Intracellular IL-22 and IL-17 were observed in memory CD4+ cells and less in memory CD8+ cells. |
| 324 | 20626289 | To determine whether cytokines and T-cell subsets other than Th1 cells contribute to secondary immune responses against Francisella species, we investigated production of Th17-associated cytokines IL-17 and IL-22 in a recall response to Francisella tularensis. |
| 325 | 20626289 | Gene expression analysis by real-time PCR showed that IL-17 and IL-22 transcripts were induced in immune PBMCs at a significantly higher level than in cells from nonvaccinated volunteers stimulated with LVS or B38 antigens at 24 h. |
| 326 | 20626289 | In addition, we detected both cell-associated and secreted IL-22 at 24 h after stimulation and IL-17 at 72 h post-stimulation. |
| 327 | 20626289 | Intracellular IL-22 and IL-17 were observed in memory CD4+ cells and less in memory CD8+ cells. |
| 328 | 20626289 | To determine whether cytokines and T-cell subsets other than Th1 cells contribute to secondary immune responses against Francisella species, we investigated production of Th17-associated cytokines IL-17 and IL-22 in a recall response to Francisella tularensis. |
| 329 | 20626289 | Gene expression analysis by real-time PCR showed that IL-17 and IL-22 transcripts were induced in immune PBMCs at a significantly higher level than in cells from nonvaccinated volunteers stimulated with LVS or B38 antigens at 24 h. |
| 330 | 20626289 | In addition, we detected both cell-associated and secreted IL-22 at 24 h after stimulation and IL-17 at 72 h post-stimulation. |
| 331 | 20626289 | Intracellular IL-22 and IL-17 were observed in memory CD4+ cells and less in memory CD8+ cells. |
| 332 | 21334341 | P1.HTR, an immunogenic variant of the P815 mastocytoma cell line, was used to generate stably transfected cell clones with expression vectors encoding the human CD134L transmembrane protein fused with either mouse IL-22BP or IL-9. |
| 333 | 21334341 | Following repeated injections of living tumor cells expressing the mIL-22BP construct, mice developed autoantibodies that bind to mIL-22BP and inhibit its interaction with IL-22 in vitro. |
| 334 | 21412284 | We have found that coinfection of HSV-IL-2-infected mice with recombinant viruses expressing IL-12p35, IL-12p40 or IL-12p35+IL-12p40 did not block the CNS demyelination, and that coinfection with a recombinant virus expressing interferon (IFN)-γ exacerbated it. |
| 335 | 21412284 | In contrast, coinfection with a recombinant virus expressing IL-4 reduced demyelination, whereas coinfection of HSV-IL-2-infected mice with a recombinant HSV-1 expressing the IL-12 heterodimer (HSV-IL-12p70) blocked the CNS demyelination in a dose-dependent manner. |
| 336 | 21412284 | Injection of mice with IL-12p35 DNA, IL-12p40 DNA, IL-12p35+IL-12p40 DNA or IL-23 DNA did not have any effect on HSV-IL-2-induced demyelination, whereas injection of IL-27 DNA increased the severity of the CNS demyelination in the HSV-IL-2-infected mice. |
| 337 | 21412284 | This study demonstrates for the first time that IL-12p70 can block HSV-IL-2-induced CNS demyelination and that IL-35 can also reduce this demyelination, whereas IFN-γ and IL-27 exacerbated the demyelination in the CNS of the HSV-IL-2-infected mice. |
| 338 | 21412284 | We have found that coinfection of HSV-IL-2-infected mice with recombinant viruses expressing IL-12p35, IL-12p40 or IL-12p35+IL-12p40 did not block the CNS demyelination, and that coinfection with a recombinant virus expressing interferon (IFN)-γ exacerbated it. |
| 339 | 21412284 | In contrast, coinfection with a recombinant virus expressing IL-4 reduced demyelination, whereas coinfection of HSV-IL-2-infected mice with a recombinant HSV-1 expressing the IL-12 heterodimer (HSV-IL-12p70) blocked the CNS demyelination in a dose-dependent manner. |
| 340 | 21412284 | Injection of mice with IL-12p35 DNA, IL-12p40 DNA, IL-12p35+IL-12p40 DNA or IL-23 DNA did not have any effect on HSV-IL-2-induced demyelination, whereas injection of IL-27 DNA increased the severity of the CNS demyelination in the HSV-IL-2-infected mice. |
| 341 | 21412284 | This study demonstrates for the first time that IL-12p70 can block HSV-IL-2-induced CNS demyelination and that IL-35 can also reduce this demyelination, whereas IFN-γ and IL-27 exacerbated the demyelination in the CNS of the HSV-IL-2-infected mice. |
| 342 | 21565243 | Quantitative RT-PCR revealed genes encoding IFN-γ, IL-17, IL-22, T-bet, RORC, and granulysin were up-regulated in PBMC stimulated with live Map three months post infection compared to the response of PBMC pre-infection. |
| 343 | 21768283 | Although IFN-γ, interleukin 17 (IL-17), and IL-22 were stimulated by these live vaccines, only RB51-mediated protection was codependent upon IL-17 in BALB/c mice. |
| 344 | 21921206 | Using a total of 28 baboons, different vaccination strategies were used including recombinant Sm-p80 protein formulated in Toll-like receptor 7 and Toll-like receptor 9 agonists, and DNA priming followed by boosting with protein plus adjuvants. |
| 345 | 21921206 | Production and expression of several cytokines (interleukin 2 [IL-2], interferon γ, IL-12α, IL-1β, IL-6, and IL-22) were up-regulated in vaccinated animals. |
| 346 | 22301139 | Interleukin-27 (IL-27) and IL-23 regulate Th1, Th17, and/or Th2 cellular immune responses. |
| 347 | 22301139 | These results suggested that Th1-, Th2-, and Th17-like memory responses and, in particular, excessive Th2- and Th17-like memory responses were closely associated with VED; IL-27 may inhibit VED following respiratory syncytial virus infection by regulating cellular memory responses. |
| 348 | 22301139 | Interleukin-27 (IL-27) and IL-23 regulate Th1, Th17, and/or Th2 cellular immune responses. |
| 349 | 22301139 | These results suggested that Th1-, Th2-, and Th17-like memory responses and, in particular, excessive Th2- and Th17-like memory responses were closely associated with VED; IL-27 may inhibit VED following respiratory syncytial virus infection by regulating cellular memory responses. |
| 350 | 22327491 | Adoptive transfer of in vitro isolated lymphocyte subsets revealed that reconstituting mice with IsdB specific CD3+ or CD4+ T-cells conferred antigen specific protection while CD8(+) T-cells, CD19(+) B-cells and plasma cells (CD138(high)B220(int)CD19(lo)) alone were not protective. |
| 351 | 22327491 | A combination of CD3(+) T-cells plus CD19(+) B-cells conferred protection in CB-17 SCID mice, whereas bovine serum albumin (BSA) immune lymphocytes did not confer protection. |
| 352 | 22327491 | In vitro assays indicated that isolated IsdB specific splenocytes from immunized mice produced abundant IL-17A, much less IFN-γ and no detectable IL-4. |
| 353 | 22327491 | IL-23 deficient mice were not protected from a lethal challenge by IsdB vaccination, pointing to a critical role for CD4(+) Th17 in IsdB-mediated vaccination. |
| 354 | 22327491 | Neutralizing IL-17A, but not IL-22 in vivo significantly increased mortality in IsdB immunized mice; whereas, neutralizing IFN-γ did not alter IsdB-mediated protection. |
| 355 | 22384225 | Using flow cytometry we showed that 4 days post infection (DPI), counts of CD4 and B-lymphocytes did not change, CD8 and γδ T-lymphocytes decreased and macrophages and heterophils increased in the spleen. |
| 356 | 22384225 | The expression of interleukin (IL)1β, IL6, IL8, IL18, LITAF, IFNγ and iNOS did not exhibit any clear pattern in the cells sorted from the spleens of vaccinated or non-vaccinated chickens. |
| 357 | 22384225 | Only IL17 and IL22 showed a differential expression in the CD4 T-lymphocytes of the vaccinated and non-vaccinated chickens at 4 DPI, both being expressed at a higher level in the non-vaccinated chickens. |
| 358 | 22384225 | Due to a similar IFNγ expression in the CD4 T-lymphocytes in both the vaccinated and non-vaccinated chickens, and a variable IL17 expression oscillating around IFNγ expression levels, the IL17∶IFNγ ratio in CD4 T-lymphocytes was found to be central for the outcome of the immune response. |
| 359 | 22504663 | IL-22 and IFN-γ responses were also detected, but these cytokines originated from separate CD4+ T cell subsets. |
| 360 | 22711885 | We also found that human NK cells produce IL-22, which inhibits intracellular growth of M. tuberculosis, and that NK cells lyse M. tuberculosis-expanded CD4(+)CD25(+)FOXP3(+) T regulatory cells (Tregs). |
| 361 | 22711885 | Depletion of NK1.1(+) cells at the time of BCG vaccination increased the number of immunosuppressive Tregs (CD4(+)CD25(hi), 95% Foxp3(+)) after challenge with M. tuberculosis H37Rv, and NK1.1(+) cells lysed expanded but not natural Tregs in BCG-vaccinated mice. |
| 362 | 22711885 | IL-22 at the time of vaccination reversed these effects and enhanced Ag-specific CD4(+) cell responses in BCG-vaccinated mice after challenge with M. tuberculosis H37Rv. |
| 363 | 22711885 | We also found that human NK cells produce IL-22, which inhibits intracellular growth of M. tuberculosis, and that NK cells lyse M. tuberculosis-expanded CD4(+)CD25(+)FOXP3(+) T regulatory cells (Tregs). |
| 364 | 22711885 | Depletion of NK1.1(+) cells at the time of BCG vaccination increased the number of immunosuppressive Tregs (CD4(+)CD25(hi), 95% Foxp3(+)) after challenge with M. tuberculosis H37Rv, and NK1.1(+) cells lysed expanded but not natural Tregs in BCG-vaccinated mice. |
| 365 | 22711885 | IL-22 at the time of vaccination reversed these effects and enhanced Ag-specific CD4(+) cell responses in BCG-vaccinated mice after challenge with M. tuberculosis H37Rv. |
| 366 | 23333555 | We show that CD4+ and CD8+ Teffector/memory (T(EM)) and other subsets produce IL-17A following SEB stimulation. |
| 367 | 23333555 | We also show that IL-17A is co-produced with other pro-inflammatory cytokines (i.e., IL-2, IFN-γ and TNF-α). |
| 368 | 23333555 | Multifunctional IL-17A producing cells possess markers typical of the T(H)17/T(C)17 and T(H)1 subsets, including CCR6, IL-22, and transcription factors retinoic acid receptor-related orphan nuclear receptor (ROR)-γt and T-bet. |
| 369 | 23464355 | Interleukin-27 (IL-27) is a heterodimeric cytokine of the IL-12 family that is produced primarily by antigen-presenting cells and is immunosuppressive toward a variety of immune cell types. |
| 370 | 23464355 | We show that IL-27 gene expression is elevated in cord blood-derived macrophages relative to macrophages originating from healthy adults. |
| 371 | 23464355 | We also evaluated the duration over which elevated IL-27 gene expression may impact immune responses in mice. |
| 372 | 23464355 | Age-dependent analysis of IL-27 gene expression indicated that levels of IL-27 remained significantly elevated throughout infancy and then declined in adult mice. |
| 373 | 23464355 | Neutralization of IL-27 in neonatal macrophages improved the ability of these cells to limit bacterial replication. |
| 374 | 23464355 | Moreover, neutralization of IL-27 during incubation with the Mycobacterium bovis bacillus Calmette-Guérin vaccine augmented the level of interferon-γ elicited from allogeneic CD4+ T lymphocytes. |
| 375 | 23464355 | This suggests that blocking IL-27 during vaccination and infection may improve immune responses in newborn and infant populations. |
| 376 | 23464355 | Interleukin-27 (IL-27) is a heterodimeric cytokine of the IL-12 family that is produced primarily by antigen-presenting cells and is immunosuppressive toward a variety of immune cell types. |
| 377 | 23464355 | We show that IL-27 gene expression is elevated in cord blood-derived macrophages relative to macrophages originating from healthy adults. |
| 378 | 23464355 | We also evaluated the duration over which elevated IL-27 gene expression may impact immune responses in mice. |
| 379 | 23464355 | Age-dependent analysis of IL-27 gene expression indicated that levels of IL-27 remained significantly elevated throughout infancy and then declined in adult mice. |
| 380 | 23464355 | Neutralization of IL-27 in neonatal macrophages improved the ability of these cells to limit bacterial replication. |
| 381 | 23464355 | Moreover, neutralization of IL-27 during incubation with the Mycobacterium bovis bacillus Calmette-Guérin vaccine augmented the level of interferon-γ elicited from allogeneic CD4+ T lymphocytes. |
| 382 | 23464355 | This suggests that blocking IL-27 during vaccination and infection may improve immune responses in newborn and infant populations. |
| 383 | 23464355 | Interleukin-27 (IL-27) is a heterodimeric cytokine of the IL-12 family that is produced primarily by antigen-presenting cells and is immunosuppressive toward a variety of immune cell types. |
| 384 | 23464355 | We show that IL-27 gene expression is elevated in cord blood-derived macrophages relative to macrophages originating from healthy adults. |
| 385 | 23464355 | We also evaluated the duration over which elevated IL-27 gene expression may impact immune responses in mice. |
| 386 | 23464355 | Age-dependent analysis of IL-27 gene expression indicated that levels of IL-27 remained significantly elevated throughout infancy and then declined in adult mice. |
| 387 | 23464355 | Neutralization of IL-27 in neonatal macrophages improved the ability of these cells to limit bacterial replication. |
| 388 | 23464355 | Moreover, neutralization of IL-27 during incubation with the Mycobacterium bovis bacillus Calmette-Guérin vaccine augmented the level of interferon-γ elicited from allogeneic CD4+ T lymphocytes. |
| 389 | 23464355 | This suggests that blocking IL-27 during vaccination and infection may improve immune responses in newborn and infant populations. |
| 390 | 23464355 | Interleukin-27 (IL-27) is a heterodimeric cytokine of the IL-12 family that is produced primarily by antigen-presenting cells and is immunosuppressive toward a variety of immune cell types. |
| 391 | 23464355 | We show that IL-27 gene expression is elevated in cord blood-derived macrophages relative to macrophages originating from healthy adults. |
| 392 | 23464355 | We also evaluated the duration over which elevated IL-27 gene expression may impact immune responses in mice. |
| 393 | 23464355 | Age-dependent analysis of IL-27 gene expression indicated that levels of IL-27 remained significantly elevated throughout infancy and then declined in adult mice. |
| 394 | 23464355 | Neutralization of IL-27 in neonatal macrophages improved the ability of these cells to limit bacterial replication. |
| 395 | 23464355 | Moreover, neutralization of IL-27 during incubation with the Mycobacterium bovis bacillus Calmette-Guérin vaccine augmented the level of interferon-γ elicited from allogeneic CD4+ T lymphocytes. |
| 396 | 23464355 | This suggests that blocking IL-27 during vaccination and infection may improve immune responses in newborn and infant populations. |
| 397 | 23464355 | Interleukin-27 (IL-27) is a heterodimeric cytokine of the IL-12 family that is produced primarily by antigen-presenting cells and is immunosuppressive toward a variety of immune cell types. |
| 398 | 23464355 | We show that IL-27 gene expression is elevated in cord blood-derived macrophages relative to macrophages originating from healthy adults. |
| 399 | 23464355 | We also evaluated the duration over which elevated IL-27 gene expression may impact immune responses in mice. |
| 400 | 23464355 | Age-dependent analysis of IL-27 gene expression indicated that levels of IL-27 remained significantly elevated throughout infancy and then declined in adult mice. |
| 401 | 23464355 | Neutralization of IL-27 in neonatal macrophages improved the ability of these cells to limit bacterial replication. |
| 402 | 23464355 | Moreover, neutralization of IL-27 during incubation with the Mycobacterium bovis bacillus Calmette-Guérin vaccine augmented the level of interferon-γ elicited from allogeneic CD4+ T lymphocytes. |
| 403 | 23464355 | This suggests that blocking IL-27 during vaccination and infection may improve immune responses in newborn and infant populations. |
| 404 | 23464355 | Interleukin-27 (IL-27) is a heterodimeric cytokine of the IL-12 family that is produced primarily by antigen-presenting cells and is immunosuppressive toward a variety of immune cell types. |
| 405 | 23464355 | We show that IL-27 gene expression is elevated in cord blood-derived macrophages relative to macrophages originating from healthy adults. |
| 406 | 23464355 | We also evaluated the duration over which elevated IL-27 gene expression may impact immune responses in mice. |
| 407 | 23464355 | Age-dependent analysis of IL-27 gene expression indicated that levels of IL-27 remained significantly elevated throughout infancy and then declined in adult mice. |
| 408 | 23464355 | Neutralization of IL-27 in neonatal macrophages improved the ability of these cells to limit bacterial replication. |
| 409 | 23464355 | Moreover, neutralization of IL-27 during incubation with the Mycobacterium bovis bacillus Calmette-Guérin vaccine augmented the level of interferon-γ elicited from allogeneic CD4+ T lymphocytes. |
| 410 | 23464355 | This suggests that blocking IL-27 during vaccination and infection may improve immune responses in newborn and infant populations. |
| 411 | 23464355 | Interleukin-27 (IL-27) is a heterodimeric cytokine of the IL-12 family that is produced primarily by antigen-presenting cells and is immunosuppressive toward a variety of immune cell types. |
| 412 | 23464355 | We show that IL-27 gene expression is elevated in cord blood-derived macrophages relative to macrophages originating from healthy adults. |
| 413 | 23464355 | We also evaluated the duration over which elevated IL-27 gene expression may impact immune responses in mice. |
| 414 | 23464355 | Age-dependent analysis of IL-27 gene expression indicated that levels of IL-27 remained significantly elevated throughout infancy and then declined in adult mice. |
| 415 | 23464355 | Neutralization of IL-27 in neonatal macrophages improved the ability of these cells to limit bacterial replication. |
| 416 | 23464355 | Moreover, neutralization of IL-27 during incubation with the Mycobacterium bovis bacillus Calmette-Guérin vaccine augmented the level of interferon-γ elicited from allogeneic CD4+ T lymphocytes. |
| 417 | 23464355 | This suggests that blocking IL-27 during vaccination and infection may improve immune responses in newborn and infant populations. |
| 418 | 23472662 | It contains Epstein-Barr virus-induced gene 3 subunit and IL-27 p35 subunit. |
| 419 | 23472662 | Although its receptor and signaling pathway are not clear, we presumed that its receptor is composed by two chains that might be similar to those receptors of IL-12, IL-23, and IL-27. |
| 420 | 23472662 | It contains Epstein-Barr virus-induced gene 3 subunit and IL-27 p35 subunit. |
| 421 | 23472662 | Although its receptor and signaling pathway are not clear, we presumed that its receptor is composed by two chains that might be similar to those receptors of IL-12, IL-23, and IL-27. |
| 422 | 23486418 | In addition, children with active TB had significantly elevated levels of C-reactive protein, α-2 macroglobulin, and haptoglobin, as well as hemoxygenase 1. |
| 423 | 23486418 | Markers of innate immune activation (lipopolysaccharide [LPS] and lipopolysaccharide-binding protein [LBP]) were significantly lower in ETB than in PTB children. |
| 424 | 23486418 | Although there were no significant differences between the two groups in their levels of cytokines (type 1 [gamma interferon (IFN-γ), tumor necrosis factor α (TNF-α), interleukin 2 (IL-2), and IL-12], type 2 [IL-4, IL-5, IL-13, and IL-33], and most type 17 [IL-17A, IL-22, IL-1β, and IL-6] and type 1 interferons [IFN-α and IFN-β]) or most of the cytokines associated with immune modulation (IL-10 and IL-20), pediatric TB was associated with elevated plasma transforming growth factor β (TGF-β), IL-21, and IL-23 levels. |
| 425 | 23522926 | Interleukin-27 (IL-27), a novel IL-6/IL-12 family cytokine, plays an important role in the early regulation of Th1 responses. |
| 426 | 23522926 | The cytokine IL-27 can exert a variety of immune-regulatory functions including cytotoxic T lymphocyte (CTL), CD4+, CD8+ T lymphocytes activation and interferon-γ (IFN-γ) production. |
| 427 | 23522926 | Lewis lung cancer cell LL/2 transfected with the DOTAP:cholesterol cationic liposome could express the mouse IL-27 (mIL-27) gene at a relative high level. |
| 428 | 23522926 | Both CD4+ and CD8+ T lymphocytes were significantly elevated in these mice vaccinated with LL/2-mIL-27 cell vaccine. |
| 429 | 23522926 | Moreover, after depletion of CD4+, CD8+ T lymphocytes by injection of antibodies against CD4 and CD8, the vaccinated mice inoculated with autologous LL/2 cells were not protected from tumor challenge. |
| 430 | 23522926 | Interleukin-27 (IL-27), a novel IL-6/IL-12 family cytokine, plays an important role in the early regulation of Th1 responses. |
| 431 | 23522926 | The cytokine IL-27 can exert a variety of immune-regulatory functions including cytotoxic T lymphocyte (CTL), CD4+, CD8+ T lymphocytes activation and interferon-γ (IFN-γ) production. |
| 432 | 23522926 | Lewis lung cancer cell LL/2 transfected with the DOTAP:cholesterol cationic liposome could express the mouse IL-27 (mIL-27) gene at a relative high level. |
| 433 | 23522926 | Both CD4+ and CD8+ T lymphocytes were significantly elevated in these mice vaccinated with LL/2-mIL-27 cell vaccine. |
| 434 | 23522926 | Moreover, after depletion of CD4+, CD8+ T lymphocytes by injection of antibodies against CD4 and CD8, the vaccinated mice inoculated with autologous LL/2 cells were not protected from tumor challenge. |
| 435 | 23522926 | Interleukin-27 (IL-27), a novel IL-6/IL-12 family cytokine, plays an important role in the early regulation of Th1 responses. |
| 436 | 23522926 | The cytokine IL-27 can exert a variety of immune-regulatory functions including cytotoxic T lymphocyte (CTL), CD4+, CD8+ T lymphocytes activation and interferon-γ (IFN-γ) production. |
| 437 | 23522926 | Lewis lung cancer cell LL/2 transfected with the DOTAP:cholesterol cationic liposome could express the mouse IL-27 (mIL-27) gene at a relative high level. |
| 438 | 23522926 | Both CD4+ and CD8+ T lymphocytes were significantly elevated in these mice vaccinated with LL/2-mIL-27 cell vaccine. |
| 439 | 23522926 | Moreover, after depletion of CD4+, CD8+ T lymphocytes by injection of antibodies against CD4 and CD8, the vaccinated mice inoculated with autologous LL/2 cells were not protected from tumor challenge. |
| 440 | 23541883 | According to the results of IFN-γ, IL-4, total IgG, IgG1, and IgG2a measurement and the MTT assay, IL-22 obviously caused an increase in IFN-γ production and a decrease in IL-4 production before and after the challenge (p<0.05). |
| 441 | 23684831 | The immune response was characterized by real time PCR quantifying transcripts of interleukins IL1β, IL17, IL22, interferon gamma (IFNγ), inducible NO synthase (iNOS), immunoglobulins IgM, IgA, IgY and Ig light chain, and six genes of acute phase response including avidin, serum amyloid A, extracellular fatty acid-binding protein (Ex-FABP), immune responsive gene 1, chemokine AH221 and trappin-6. |
| 442 | 23716685 | HHLA2 is a member of the B7 family and inhibits human CD4 and CD8 T-cell function. |
| 443 | 23716685 | Here we describe HERV-H LTR-associating protein 2 (HHLA2) as a member of the B7 family that shares 10-18% amino acid identity and 23-33% similarity to other human B7 proteins and phylogenetically forms a subfamily with B7x and B7-H3 within the family. |
| 444 | 23716685 | HHLA2 is expressed in humans but not in mice, which is unique within the B7 and CD28 families. |
| 445 | 23716685 | HHLA2 does not interact with other known members of the CD28 family or the B7 family, but does bind a putative receptor that is constitutively expressed not only on resting and activated CD4 and CD8 T cells but also on antigen-presenting cells. |
| 446 | 23716685 | HHLA2 inhibits proliferation of both CD4 and CD8 T cells in the presence of T-cell receptor signaling. |
| 447 | 23716685 | In addition, HHLA2 significantly reduces cytokine production by T cells including IFN-γ, TNF-α, IL-5, IL-10, IL-13, IL-17A, and IL-22. |
| 448 | 23716685 | Thus, we have identified a unique B7 pathway that is able to inhibit human CD4 and CD8 T-cell proliferation and cytokine production. |
| 449 | 23941891 | Interleukin-22 as a molecular adjuvant facilitates IL-17-producing CD8+ T cell responses against a HBV DNA vaccine in mice. |
| 450 | 23941891 | Interleukin-22 (IL-22) is mainly produced by activated Th1 cells, Th17 cells and NK cells and promotes anti-microbial defense, pro-inflammatory and tissue remodeling responses. |
| 451 | 23941891 | In this study, we tested if a DNA construct expressing IL-22 (pVAX-IL-22) could be used as a molecular adjuvant to enhance host immune responses induced by HBV DNA vaccination (pcD-S2). |
| 452 | 23941891 | However, there was an enhancement of the level of IL-17 expression in antigen specific CD8(+) cytotoxic T lymphocytes (Tc17). |
| 453 | 23941891 | By using CD8 T-cell knockout (KO) and IL-17 KO mice, Tc17 cells were found to be a dominant population driving cytotoxicity. |
| 454 | 23941891 | These results demonstrate that IL-22 might be used as an effective adjuvant to enhance cellular immune responses during HBsAg DNA vaccination since it can induce Tc17 cells to break tolerance in HBsAg transgenic mice. |
| 455 | 23941891 | Interleukin-22 as a molecular adjuvant facilitates IL-17-producing CD8+ T cell responses against a HBV DNA vaccine in mice. |
| 456 | 23941891 | Interleukin-22 (IL-22) is mainly produced by activated Th1 cells, Th17 cells and NK cells and promotes anti-microbial defense, pro-inflammatory and tissue remodeling responses. |
| 457 | 23941891 | In this study, we tested if a DNA construct expressing IL-22 (pVAX-IL-22) could be used as a molecular adjuvant to enhance host immune responses induced by HBV DNA vaccination (pcD-S2). |
| 458 | 23941891 | However, there was an enhancement of the level of IL-17 expression in antigen specific CD8(+) cytotoxic T lymphocytes (Tc17). |
| 459 | 23941891 | By using CD8 T-cell knockout (KO) and IL-17 KO mice, Tc17 cells were found to be a dominant population driving cytotoxicity. |
| 460 | 23941891 | These results demonstrate that IL-22 might be used as an effective adjuvant to enhance cellular immune responses during HBsAg DNA vaccination since it can induce Tc17 cells to break tolerance in HBsAg transgenic mice. |
| 461 | 23941891 | Interleukin-22 as a molecular adjuvant facilitates IL-17-producing CD8+ T cell responses against a HBV DNA vaccine in mice. |
| 462 | 23941891 | Interleukin-22 (IL-22) is mainly produced by activated Th1 cells, Th17 cells and NK cells and promotes anti-microbial defense, pro-inflammatory and tissue remodeling responses. |
| 463 | 23941891 | In this study, we tested if a DNA construct expressing IL-22 (pVAX-IL-22) could be used as a molecular adjuvant to enhance host immune responses induced by HBV DNA vaccination (pcD-S2). |
| 464 | 23941891 | However, there was an enhancement of the level of IL-17 expression in antigen specific CD8(+) cytotoxic T lymphocytes (Tc17). |
| 465 | 23941891 | By using CD8 T-cell knockout (KO) and IL-17 KO mice, Tc17 cells were found to be a dominant population driving cytotoxicity. |
| 466 | 23941891 | These results demonstrate that IL-22 might be used as an effective adjuvant to enhance cellular immune responses during HBsAg DNA vaccination since it can induce Tc17 cells to break tolerance in HBsAg transgenic mice. |
| 467 | 24145856 | Typhi GroEL and IL-22 gene augments immune responses against Salmonella infection. |
| 468 | 24145856 | In this study, the immunomodulatory effect of Interleukin 22 (IL-22) as an adjuvant was studied by DNA vaccination with S. |
| 469 | 24145856 | Further, DNA construct of IL-22 gene fused with GroEL was developed and immunization studies were carried out in mice. |
| 470 | 24145856 | Co-immunization (IL-22+GroEL) further resulted in increase in T-cell proliferative responses, antibody titres (IgG, IgG1, IgG2a) and secretion of IFNγ (Th1), IL-1β and Th2 (IL-4, IL-6) cytokines. |
| 471 | 24145856 | Improved protective efficacy (90%) against lethal challenge by Salmonella was observed with IL-22-GroEL co-expressing DNA vector as compared with plasmid encoding GroEL only (50-60%) or co-immunization group (75-80%). |
| 472 | 24145856 | This study thus shows that co-expression of IL-22 and GroEL genes enhances the immune responses and protective efficacy, circumventing the need of any adjuvant. |
| 473 | 24145856 | Typhi GroEL and IL-22 gene augments immune responses against Salmonella infection. |
| 474 | 24145856 | In this study, the immunomodulatory effect of Interleukin 22 (IL-22) as an adjuvant was studied by DNA vaccination with S. |
| 475 | 24145856 | Further, DNA construct of IL-22 gene fused with GroEL was developed and immunization studies were carried out in mice. |
| 476 | 24145856 | Co-immunization (IL-22+GroEL) further resulted in increase in T-cell proliferative responses, antibody titres (IgG, IgG1, IgG2a) and secretion of IFNγ (Th1), IL-1β and Th2 (IL-4, IL-6) cytokines. |
| 477 | 24145856 | Improved protective efficacy (90%) against lethal challenge by Salmonella was observed with IL-22-GroEL co-expressing DNA vector as compared with plasmid encoding GroEL only (50-60%) or co-immunization group (75-80%). |
| 478 | 24145856 | This study thus shows that co-expression of IL-22 and GroEL genes enhances the immune responses and protective efficacy, circumventing the need of any adjuvant. |
| 479 | 24145856 | Typhi GroEL and IL-22 gene augments immune responses against Salmonella infection. |
| 480 | 24145856 | In this study, the immunomodulatory effect of Interleukin 22 (IL-22) as an adjuvant was studied by DNA vaccination with S. |
| 481 | 24145856 | Further, DNA construct of IL-22 gene fused with GroEL was developed and immunization studies were carried out in mice. |
| 482 | 24145856 | Co-immunization (IL-22+GroEL) further resulted in increase in T-cell proliferative responses, antibody titres (IgG, IgG1, IgG2a) and secretion of IFNγ (Th1), IL-1β and Th2 (IL-4, IL-6) cytokines. |
| 483 | 24145856 | Improved protective efficacy (90%) against lethal challenge by Salmonella was observed with IL-22-GroEL co-expressing DNA vector as compared with plasmid encoding GroEL only (50-60%) or co-immunization group (75-80%). |
| 484 | 24145856 | This study thus shows that co-expression of IL-22 and GroEL genes enhances the immune responses and protective efficacy, circumventing the need of any adjuvant. |
| 485 | 24145856 | Typhi GroEL and IL-22 gene augments immune responses against Salmonella infection. |
| 486 | 24145856 | In this study, the immunomodulatory effect of Interleukin 22 (IL-22) as an adjuvant was studied by DNA vaccination with S. |
| 487 | 24145856 | Further, DNA construct of IL-22 gene fused with GroEL was developed and immunization studies were carried out in mice. |
| 488 | 24145856 | Co-immunization (IL-22+GroEL) further resulted in increase in T-cell proliferative responses, antibody titres (IgG, IgG1, IgG2a) and secretion of IFNγ (Th1), IL-1β and Th2 (IL-4, IL-6) cytokines. |
| 489 | 24145856 | Improved protective efficacy (90%) against lethal challenge by Salmonella was observed with IL-22-GroEL co-expressing DNA vector as compared with plasmid encoding GroEL only (50-60%) or co-immunization group (75-80%). |
| 490 | 24145856 | This study thus shows that co-expression of IL-22 and GroEL genes enhances the immune responses and protective efficacy, circumventing the need of any adjuvant. |
| 491 | 24145856 | Typhi GroEL and IL-22 gene augments immune responses against Salmonella infection. |
| 492 | 24145856 | In this study, the immunomodulatory effect of Interleukin 22 (IL-22) as an adjuvant was studied by DNA vaccination with S. |
| 493 | 24145856 | Further, DNA construct of IL-22 gene fused with GroEL was developed and immunization studies were carried out in mice. |
| 494 | 24145856 | Co-immunization (IL-22+GroEL) further resulted in increase in T-cell proliferative responses, antibody titres (IgG, IgG1, IgG2a) and secretion of IFNγ (Th1), IL-1β and Th2 (IL-4, IL-6) cytokines. |
| 495 | 24145856 | Improved protective efficacy (90%) against lethal challenge by Salmonella was observed with IL-22-GroEL co-expressing DNA vector as compared with plasmid encoding GroEL only (50-60%) or co-immunization group (75-80%). |
| 496 | 24145856 | This study thus shows that co-expression of IL-22 and GroEL genes enhances the immune responses and protective efficacy, circumventing the need of any adjuvant. |
| 497 | 24145856 | Typhi GroEL and IL-22 gene augments immune responses against Salmonella infection. |
| 498 | 24145856 | In this study, the immunomodulatory effect of Interleukin 22 (IL-22) as an adjuvant was studied by DNA vaccination with S. |
| 499 | 24145856 | Further, DNA construct of IL-22 gene fused with GroEL was developed and immunization studies were carried out in mice. |
| 500 | 24145856 | Co-immunization (IL-22+GroEL) further resulted in increase in T-cell proliferative responses, antibody titres (IgG, IgG1, IgG2a) and secretion of IFNγ (Th1), IL-1β and Th2 (IL-4, IL-6) cytokines. |
| 501 | 24145856 | Improved protective efficacy (90%) against lethal challenge by Salmonella was observed with IL-22-GroEL co-expressing DNA vector as compared with plasmid encoding GroEL only (50-60%) or co-immunization group (75-80%). |
| 502 | 24145856 | This study thus shows that co-expression of IL-22 and GroEL genes enhances the immune responses and protective efficacy, circumventing the need of any adjuvant. |
| 503 | 24182427 | The role of CC chemokines, interleukin-17 (IL-17), IL-22 and invariant natural killer T cells in mediating the exacerbation of disease in immune-competent mice is highlighted. |
| 504 | 24238108 | IL-23 induces IL-22 and IL-17 production in response to Chlamydia muridarum genital tract infection, but the absence of these cytokines does not influence disease pathogenesis. |
| 505 | 24477852 | Diarrheal stools from patients with CDI (CDI-positive diarrheal stools) showed higher relative amounts of the following inflammatory markers than the diarrheal stools from CDI-negative patients (CDI-negative diarrheal stools): C5a, CD40L, granulocyte colony-stimulating factor, I-309, interleukin-13 (IL-13), IL-16, IL-27, monocyte chemoattractant protein 1, tumor necrosis factor alpha, and IL-8. |
| 506 | 24477852 | IL-8 and IL-23 were present in a larger number of CDI-positive diarrheal stools than CDI-negative diarrheal stools. |
| 507 | 24492530 | IL-22 appears to promote keratinocyte dedifferentiation and increased antimicrobial peptide synthesis while TNF-α and IL-17 induce leukocyte localization within the psoriatic plaque. |
| 508 | 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. |
| 509 | 24577508 | Type 3 innate lymphoid cells (ILC3) are key players in antimicrobial defense in intestinal mucosa, through interleukin 17 and interleukin 22 (IL-22) production. |
| 510 | 24577508 | We first observed that lung mucosa harbors a discrete population of ILC3 expressing CD127, CD90, CCR6, and the transcriptional factor RORγt. |
| 511 | 24577508 | In addition, lung ILC3 were identified as a major source of IL-22 in response to interleukin 23 stimulation. |
| 512 | 24577508 | During Streptococcus pneumoniae infection, ILC3 rapidly accumulated in the lung tissue to produce IL-22. |
| 513 | 24577508 | In response to S. pneumoniae, dendritic cells and MyD88, an important adaptor of innate immunity, play critical functions in IL-22 production by ILC3. |
| 514 | 24577508 | Finally, administration of the Toll-like receptor 5 agonist flagellin during S. pneumoniae challenge exacerbated IL-22 production by ILC3, a process that protects against lethal infection. |
| 515 | 24577508 | Type 3 innate lymphoid cells (ILC3) are key players in antimicrobial defense in intestinal mucosa, through interleukin 17 and interleukin 22 (IL-22) production. |
| 516 | 24577508 | We first observed that lung mucosa harbors a discrete population of ILC3 expressing CD127, CD90, CCR6, and the transcriptional factor RORγt. |
| 517 | 24577508 | In addition, lung ILC3 were identified as a major source of IL-22 in response to interleukin 23 stimulation. |
| 518 | 24577508 | During Streptococcus pneumoniae infection, ILC3 rapidly accumulated in the lung tissue to produce IL-22. |
| 519 | 24577508 | In response to S. pneumoniae, dendritic cells and MyD88, an important adaptor of innate immunity, play critical functions in IL-22 production by ILC3. |
| 520 | 24577508 | Finally, administration of the Toll-like receptor 5 agonist flagellin during S. pneumoniae challenge exacerbated IL-22 production by ILC3, a process that protects against lethal infection. |
| 521 | 24577508 | Type 3 innate lymphoid cells (ILC3) are key players in antimicrobial defense in intestinal mucosa, through interleukin 17 and interleukin 22 (IL-22) production. |
| 522 | 24577508 | We first observed that lung mucosa harbors a discrete population of ILC3 expressing CD127, CD90, CCR6, and the transcriptional factor RORγt. |
| 523 | 24577508 | In addition, lung ILC3 were identified as a major source of IL-22 in response to interleukin 23 stimulation. |
| 524 | 24577508 | During Streptococcus pneumoniae infection, ILC3 rapidly accumulated in the lung tissue to produce IL-22. |
| 525 | 24577508 | In response to S. pneumoniae, dendritic cells and MyD88, an important adaptor of innate immunity, play critical functions in IL-22 production by ILC3. |
| 526 | 24577508 | Finally, administration of the Toll-like receptor 5 agonist flagellin during S. pneumoniae challenge exacerbated IL-22 production by ILC3, a process that protects against lethal infection. |
| 527 | 24577508 | Type 3 innate lymphoid cells (ILC3) are key players in antimicrobial defense in intestinal mucosa, through interleukin 17 and interleukin 22 (IL-22) production. |
| 528 | 24577508 | We first observed that lung mucosa harbors a discrete population of ILC3 expressing CD127, CD90, CCR6, and the transcriptional factor RORγt. |
| 529 | 24577508 | In addition, lung ILC3 were identified as a major source of IL-22 in response to interleukin 23 stimulation. |
| 530 | 24577508 | During Streptococcus pneumoniae infection, ILC3 rapidly accumulated in the lung tissue to produce IL-22. |
| 531 | 24577508 | In response to S. pneumoniae, dendritic cells and MyD88, an important adaptor of innate immunity, play critical functions in IL-22 production by ILC3. |
| 532 | 24577508 | Finally, administration of the Toll-like receptor 5 agonist flagellin during S. pneumoniae challenge exacerbated IL-22 production by ILC3, a process that protects against lethal infection. |
| 533 | 24577508 | Type 3 innate lymphoid cells (ILC3) are key players in antimicrobial defense in intestinal mucosa, through interleukin 17 and interleukin 22 (IL-22) production. |
| 534 | 24577508 | We first observed that lung mucosa harbors a discrete population of ILC3 expressing CD127, CD90, CCR6, and the transcriptional factor RORγt. |
| 535 | 24577508 | In addition, lung ILC3 were identified as a major source of IL-22 in response to interleukin 23 stimulation. |
| 536 | 24577508 | During Streptococcus pneumoniae infection, ILC3 rapidly accumulated in the lung tissue to produce IL-22. |
| 537 | 24577508 | In response to S. pneumoniae, dendritic cells and MyD88, an important adaptor of innate immunity, play critical functions in IL-22 production by ILC3. |
| 538 | 24577508 | Finally, administration of the Toll-like receptor 5 agonist flagellin during S. pneumoniae challenge exacerbated IL-22 production by ILC3, a process that protects against lethal infection. |
| 539 | 24713322 | In some cases (e.g., tumor necrosis factor alpha [TNF-α], interleukin 22 [IL-22], and granulocyte-macrophage colony-stimulating factor [GM-CSF]), liver cells exhibited even higher relative gene expression, whereas fewer genes exhibited differential expression in lung cells. |
| 540 | 24872512 | While monocyte-derived cytokine (tumor necrosis factor alpha [TNF-α], interleukin-1β [IL-1β], and IL-6) production was rarely affected, 30% of all included patients had deficient production of interferon gamma (IFN-γ), IL-17A, or IL-22. |
| 541 | 24872512 | Defective IL-17A and IL-22 production was mainly confined to ID patients with mucocutaneous fungal infections. |
| 542 | 24872512 | Defective IL-17A and IL-22 production was primarily found in patients with fungal infections, while monocyte-derived cytokine production was unaffected. |
| 543 | 24872512 | While monocyte-derived cytokine (tumor necrosis factor alpha [TNF-α], interleukin-1β [IL-1β], and IL-6) production was rarely affected, 30% of all included patients had deficient production of interferon gamma (IFN-γ), IL-17A, or IL-22. |
| 544 | 24872512 | Defective IL-17A and IL-22 production was mainly confined to ID patients with mucocutaneous fungal infections. |
| 545 | 24872512 | Defective IL-17A and IL-22 production was primarily found in patients with fungal infections, while monocyte-derived cytokine production was unaffected. |
| 546 | 24872512 | While monocyte-derived cytokine (tumor necrosis factor alpha [TNF-α], interleukin-1β [IL-1β], and IL-6) production was rarely affected, 30% of all included patients had deficient production of interferon gamma (IFN-γ), IL-17A, or IL-22. |
| 547 | 24872512 | Defective IL-17A and IL-22 production was mainly confined to ID patients with mucocutaneous fungal infections. |
| 548 | 24872512 | Defective IL-17A and IL-22 production was primarily found in patients with fungal infections, while monocyte-derived cytokine production was unaffected. |
| 549 | 24942687 | Directing traffic: IL-17 and IL-22 coordinate pulmonary immune defense. |
| 550 | 24942687 | Here, we review mechanisms controlling the production and functions of interleukin-17 (IL-17) and IL-22, cytokines that direct several aspects of lung immunity. |
| 551 | 24942687 | Innate lymphocytes (γδ T cells, natural killer cells, innate lymphoid cells) are the major source of IL-17 and IL-22 during acute infections, while CD4(+) T-helper 17 (Th17) cells contribute to vaccine-induced immunity. |
| 552 | 24942687 | CD11b(+) DCs stimulated with bacteria or fungi secrete IL-1β and IL-23, potent inducers of IL-17 and IL-22. |
| 553 | 24942687 | On the other hand, recognition of viruses by plasmacytoid DCs inhibits IL-1β and IL-23 release, increasing susceptibility to bacterial superinfections. |
| 554 | 24942687 | IL-17 and IL-22 primarily act on the lung epithelium, inducing antimicrobial proteins and neutrophil chemoattractants. |
| 555 | 24942687 | Recent studies found that stimulation of macrophages and DCs with IL-17 also contributes to antibacterial immunity, while IL-22 promotes epithelial proliferation and repair following injury. |
| 556 | 24942687 | Chronic diseases such as asthma and chronic obstructive pulmonary disease have been associated with IL-17 and IL-22 responses directed against innocuous antigens. |
| 557 | 24942687 | Future studies will evaluate the therapeutic efficacy of targeting the IL-17/IL-22 pathway in pulmonary inflammation. |
| 558 | 24942687 | Directing traffic: IL-17 and IL-22 coordinate pulmonary immune defense. |
| 559 | 24942687 | Here, we review mechanisms controlling the production and functions of interleukin-17 (IL-17) and IL-22, cytokines that direct several aspects of lung immunity. |
| 560 | 24942687 | Innate lymphocytes (γδ T cells, natural killer cells, innate lymphoid cells) are the major source of IL-17 and IL-22 during acute infections, while CD4(+) T-helper 17 (Th17) cells contribute to vaccine-induced immunity. |
| 561 | 24942687 | CD11b(+) DCs stimulated with bacteria or fungi secrete IL-1β and IL-23, potent inducers of IL-17 and IL-22. |
| 562 | 24942687 | On the other hand, recognition of viruses by plasmacytoid DCs inhibits IL-1β and IL-23 release, increasing susceptibility to bacterial superinfections. |
| 563 | 24942687 | IL-17 and IL-22 primarily act on the lung epithelium, inducing antimicrobial proteins and neutrophil chemoattractants. |
| 564 | 24942687 | Recent studies found that stimulation of macrophages and DCs with IL-17 also contributes to antibacterial immunity, while IL-22 promotes epithelial proliferation and repair following injury. |
| 565 | 24942687 | Chronic diseases such as asthma and chronic obstructive pulmonary disease have been associated with IL-17 and IL-22 responses directed against innocuous antigens. |
| 566 | 24942687 | Future studies will evaluate the therapeutic efficacy of targeting the IL-17/IL-22 pathway in pulmonary inflammation. |
| 567 | 24942687 | Directing traffic: IL-17 and IL-22 coordinate pulmonary immune defense. |
| 568 | 24942687 | Here, we review mechanisms controlling the production and functions of interleukin-17 (IL-17) and IL-22, cytokines that direct several aspects of lung immunity. |
| 569 | 24942687 | Innate lymphocytes (γδ T cells, natural killer cells, innate lymphoid cells) are the major source of IL-17 and IL-22 during acute infections, while CD4(+) T-helper 17 (Th17) cells contribute to vaccine-induced immunity. |
| 570 | 24942687 | CD11b(+) DCs stimulated with bacteria or fungi secrete IL-1β and IL-23, potent inducers of IL-17 and IL-22. |
| 571 | 24942687 | On the other hand, recognition of viruses by plasmacytoid DCs inhibits IL-1β and IL-23 release, increasing susceptibility to bacterial superinfections. |
| 572 | 24942687 | IL-17 and IL-22 primarily act on the lung epithelium, inducing antimicrobial proteins and neutrophil chemoattractants. |
| 573 | 24942687 | Recent studies found that stimulation of macrophages and DCs with IL-17 also contributes to antibacterial immunity, while IL-22 promotes epithelial proliferation and repair following injury. |
| 574 | 24942687 | Chronic diseases such as asthma and chronic obstructive pulmonary disease have been associated with IL-17 and IL-22 responses directed against innocuous antigens. |
| 575 | 24942687 | Future studies will evaluate the therapeutic efficacy of targeting the IL-17/IL-22 pathway in pulmonary inflammation. |
| 576 | 24942687 | Directing traffic: IL-17 and IL-22 coordinate pulmonary immune defense. |
| 577 | 24942687 | Here, we review mechanisms controlling the production and functions of interleukin-17 (IL-17) and IL-22, cytokines that direct several aspects of lung immunity. |
| 578 | 24942687 | Innate lymphocytes (γδ T cells, natural killer cells, innate lymphoid cells) are the major source of IL-17 and IL-22 during acute infections, while CD4(+) T-helper 17 (Th17) cells contribute to vaccine-induced immunity. |
| 579 | 24942687 | CD11b(+) DCs stimulated with bacteria or fungi secrete IL-1β and IL-23, potent inducers of IL-17 and IL-22. |
| 580 | 24942687 | On the other hand, recognition of viruses by plasmacytoid DCs inhibits IL-1β and IL-23 release, increasing susceptibility to bacterial superinfections. |
| 581 | 24942687 | IL-17 and IL-22 primarily act on the lung epithelium, inducing antimicrobial proteins and neutrophil chemoattractants. |
| 582 | 24942687 | Recent studies found that stimulation of macrophages and DCs with IL-17 also contributes to antibacterial immunity, while IL-22 promotes epithelial proliferation and repair following injury. |
| 583 | 24942687 | Chronic diseases such as asthma and chronic obstructive pulmonary disease have been associated with IL-17 and IL-22 responses directed against innocuous antigens. |
| 584 | 24942687 | Future studies will evaluate the therapeutic efficacy of targeting the IL-17/IL-22 pathway in pulmonary inflammation. |
| 585 | 24942687 | Directing traffic: IL-17 and IL-22 coordinate pulmonary immune defense. |
| 586 | 24942687 | Here, we review mechanisms controlling the production and functions of interleukin-17 (IL-17) and IL-22, cytokines that direct several aspects of lung immunity. |
| 587 | 24942687 | Innate lymphocytes (γδ T cells, natural killer cells, innate lymphoid cells) are the major source of IL-17 and IL-22 during acute infections, while CD4(+) T-helper 17 (Th17) cells contribute to vaccine-induced immunity. |
| 588 | 24942687 | CD11b(+) DCs stimulated with bacteria or fungi secrete IL-1β and IL-23, potent inducers of IL-17 and IL-22. |
| 589 | 24942687 | On the other hand, recognition of viruses by plasmacytoid DCs inhibits IL-1β and IL-23 release, increasing susceptibility to bacterial superinfections. |
| 590 | 24942687 | IL-17 and IL-22 primarily act on the lung epithelium, inducing antimicrobial proteins and neutrophil chemoattractants. |
| 591 | 24942687 | Recent studies found that stimulation of macrophages and DCs with IL-17 also contributes to antibacterial immunity, while IL-22 promotes epithelial proliferation and repair following injury. |
| 592 | 24942687 | Chronic diseases such as asthma and chronic obstructive pulmonary disease have been associated with IL-17 and IL-22 responses directed against innocuous antigens. |
| 593 | 24942687 | Future studies will evaluate the therapeutic efficacy of targeting the IL-17/IL-22 pathway in pulmonary inflammation. |
| 594 | 24942687 | Directing traffic: IL-17 and IL-22 coordinate pulmonary immune defense. |
| 595 | 24942687 | Here, we review mechanisms controlling the production and functions of interleukin-17 (IL-17) and IL-22, cytokines that direct several aspects of lung immunity. |
| 596 | 24942687 | Innate lymphocytes (γδ T cells, natural killer cells, innate lymphoid cells) are the major source of IL-17 and IL-22 during acute infections, while CD4(+) T-helper 17 (Th17) cells contribute to vaccine-induced immunity. |
| 597 | 24942687 | CD11b(+) DCs stimulated with bacteria or fungi secrete IL-1β and IL-23, potent inducers of IL-17 and IL-22. |
| 598 | 24942687 | On the other hand, recognition of viruses by plasmacytoid DCs inhibits IL-1β and IL-23 release, increasing susceptibility to bacterial superinfections. |
| 599 | 24942687 | IL-17 and IL-22 primarily act on the lung epithelium, inducing antimicrobial proteins and neutrophil chemoattractants. |
| 600 | 24942687 | Recent studies found that stimulation of macrophages and DCs with IL-17 also contributes to antibacterial immunity, while IL-22 promotes epithelial proliferation and repair following injury. |
| 601 | 24942687 | Chronic diseases such as asthma and chronic obstructive pulmonary disease have been associated with IL-17 and IL-22 responses directed against innocuous antigens. |
| 602 | 24942687 | Future studies will evaluate the therapeutic efficacy of targeting the IL-17/IL-22 pathway in pulmonary inflammation. |
| 603 | 24942687 | Directing traffic: IL-17 and IL-22 coordinate pulmonary immune defense. |
| 604 | 24942687 | Here, we review mechanisms controlling the production and functions of interleukin-17 (IL-17) and IL-22, cytokines that direct several aspects of lung immunity. |
| 605 | 24942687 | Innate lymphocytes (γδ T cells, natural killer cells, innate lymphoid cells) are the major source of IL-17 and IL-22 during acute infections, while CD4(+) T-helper 17 (Th17) cells contribute to vaccine-induced immunity. |
| 606 | 24942687 | CD11b(+) DCs stimulated with bacteria or fungi secrete IL-1β and IL-23, potent inducers of IL-17 and IL-22. |
| 607 | 24942687 | On the other hand, recognition of viruses by plasmacytoid DCs inhibits IL-1β and IL-23 release, increasing susceptibility to bacterial superinfections. |
| 608 | 24942687 | IL-17 and IL-22 primarily act on the lung epithelium, inducing antimicrobial proteins and neutrophil chemoattractants. |
| 609 | 24942687 | Recent studies found that stimulation of macrophages and DCs with IL-17 also contributes to antibacterial immunity, while IL-22 promotes epithelial proliferation and repair following injury. |
| 610 | 24942687 | Chronic diseases such as asthma and chronic obstructive pulmonary disease have been associated with IL-17 and IL-22 responses directed against innocuous antigens. |
| 611 | 24942687 | Future studies will evaluate the therapeutic efficacy of targeting the IL-17/IL-22 pathway in pulmonary inflammation. |
| 612 | 24942687 | Directing traffic: IL-17 and IL-22 coordinate pulmonary immune defense. |
| 613 | 24942687 | Here, we review mechanisms controlling the production and functions of interleukin-17 (IL-17) and IL-22, cytokines that direct several aspects of lung immunity. |
| 614 | 24942687 | Innate lymphocytes (γδ T cells, natural killer cells, innate lymphoid cells) are the major source of IL-17 and IL-22 during acute infections, while CD4(+) T-helper 17 (Th17) cells contribute to vaccine-induced immunity. |
| 615 | 24942687 | CD11b(+) DCs stimulated with bacteria or fungi secrete IL-1β and IL-23, potent inducers of IL-17 and IL-22. |
| 616 | 24942687 | On the other hand, recognition of viruses by plasmacytoid DCs inhibits IL-1β and IL-23 release, increasing susceptibility to bacterial superinfections. |
| 617 | 24942687 | IL-17 and IL-22 primarily act on the lung epithelium, inducing antimicrobial proteins and neutrophil chemoattractants. |
| 618 | 24942687 | Recent studies found that stimulation of macrophages and DCs with IL-17 also contributes to antibacterial immunity, while IL-22 promotes epithelial proliferation and repair following injury. |
| 619 | 24942687 | Chronic diseases such as asthma and chronic obstructive pulmonary disease have been associated with IL-17 and IL-22 responses directed against innocuous antigens. |
| 620 | 24942687 | Future studies will evaluate the therapeutic efficacy of targeting the IL-17/IL-22 pathway in pulmonary inflammation. |
| 621 | 24957984 | In vivo analysis of helper T cell responses in patients with autoimmune polyendocrinopathy - candidiasis - ectodermal dystrophy provides evidence in support of an IL-22 defect. |
| 622 | 24957984 | Our in vivo data are compatible with a selective IL-22 defect in the activated CD4(+) T cells of APECED patients, affecting also unexposed skin in steady-state conditions. |
| 623 | 24957984 | In vivo analysis of helper T cell responses in patients with autoimmune polyendocrinopathy - candidiasis - ectodermal dystrophy provides evidence in support of an IL-22 defect. |
| 624 | 24957984 | Our in vivo data are compatible with a selective IL-22 defect in the activated CD4(+) T cells of APECED patients, affecting also unexposed skin in steady-state conditions. |
| 625 | 25141829 | Treatment with IL-17A/IL-17F or IL-22 expanded phosphoantigen 4-hydroxy-3-methyl-but-enyl pyrophosphate (HMBPP)-stimulated Vγ2Vδ2 T cells from BCG-vaccinated macaques but not from naïve animals, and IL-23 induced greater expansion than the other Th17-related cytokines. |
| 626 | 25141829 | Consistently, Mtb infection of macaques also enhanced the ability of IL-17/IL-22 or IL-23 to expand HMBPP-stimulated Vγ2Vδ2 T cells. |
| 627 | 25141829 | When evaluating IL-23 signaling as a prototype, we found that HMBPP/IL-23-expanded Vγ2Vδ2 T cells from macaques infected with Mtb or vaccinated with BCG or Listeria ΔactA prfA*-ESAT6/Ag85B produced IL-17, IL-22, IL-2, and IFN-γ. |
| 628 | 25141829 | Furthermore, HMBPP/IL-23-induced proliferation of Vγ2Vδ2 T cells appeared to require APC contact and involve the conventional and novel protein kinase C signaling pathways. |
| 629 | 25141829 | Treatment with IL-17A/IL-17F or IL-22 expanded phosphoantigen 4-hydroxy-3-methyl-but-enyl pyrophosphate (HMBPP)-stimulated Vγ2Vδ2 T cells from BCG-vaccinated macaques but not from naïve animals, and IL-23 induced greater expansion than the other Th17-related cytokines. |
| 630 | 25141829 | Consistently, Mtb infection of macaques also enhanced the ability of IL-17/IL-22 or IL-23 to expand HMBPP-stimulated Vγ2Vδ2 T cells. |
| 631 | 25141829 | When evaluating IL-23 signaling as a prototype, we found that HMBPP/IL-23-expanded Vγ2Vδ2 T cells from macaques infected with Mtb or vaccinated with BCG or Listeria ΔactA prfA*-ESAT6/Ag85B produced IL-17, IL-22, IL-2, and IFN-γ. |
| 632 | 25141829 | Furthermore, HMBPP/IL-23-induced proliferation of Vγ2Vδ2 T cells appeared to require APC contact and involve the conventional and novel protein kinase C signaling pathways. |
| 633 | 25141829 | Treatment with IL-17A/IL-17F or IL-22 expanded phosphoantigen 4-hydroxy-3-methyl-but-enyl pyrophosphate (HMBPP)-stimulated Vγ2Vδ2 T cells from BCG-vaccinated macaques but not from naïve animals, and IL-23 induced greater expansion than the other Th17-related cytokines. |
| 634 | 25141829 | Consistently, Mtb infection of macaques also enhanced the ability of IL-17/IL-22 or IL-23 to expand HMBPP-stimulated Vγ2Vδ2 T cells. |
| 635 | 25141829 | When evaluating IL-23 signaling as a prototype, we found that HMBPP/IL-23-expanded Vγ2Vδ2 T cells from macaques infected with Mtb or vaccinated with BCG or Listeria ΔactA prfA*-ESAT6/Ag85B produced IL-17, IL-22, IL-2, and IFN-γ. |
| 636 | 25141829 | Furthermore, HMBPP/IL-23-induced proliferation of Vγ2Vδ2 T cells appeared to require APC contact and involve the conventional and novel protein kinase C signaling pathways. |
| 637 | 25192550 | Administration of neutralizing antibodies to IL-17 or IL-22 in rAg85B-treated mice revealed that IL-17 induced the infiltration of neutrophils in BAL fluid and that allergen-induced bronchial eosinophilia was inhibited by IL-22. |
| 638 | 25214209 | Secretion of biologically active human interleukin 22 (IL-22) by Lactococcus lactis. |
| 639 | 25214209 | Interleukin-22 (IL-22) participates in the modulation of innate immunity and inflammation. |
| 640 | 25214209 | We generated a Lactococcus lactis strain that secretes human IL-22 under the regulation of the nisin-inducible promoter. |
| 641 | 25214209 | Identification and secretion of this cytokine was demonstrated using western blots of culture supernatants from IL-22-expressing bacteria. |
| 642 | 25214209 | The recombinant IL-22 protein produced by L. lactis was biologically active as determined by its ability to induce IL-10 secretion when co-cultured with a colon epithelial cell line in vitro. |
| 643 | 25214209 | Secretion of biologically active human interleukin 22 (IL-22) by Lactococcus lactis. |
| 644 | 25214209 | Interleukin-22 (IL-22) participates in the modulation of innate immunity and inflammation. |
| 645 | 25214209 | We generated a Lactococcus lactis strain that secretes human IL-22 under the regulation of the nisin-inducible promoter. |
| 646 | 25214209 | Identification and secretion of this cytokine was demonstrated using western blots of culture supernatants from IL-22-expressing bacteria. |
| 647 | 25214209 | The recombinant IL-22 protein produced by L. lactis was biologically active as determined by its ability to induce IL-10 secretion when co-cultured with a colon epithelial cell line in vitro. |
| 648 | 25214209 | Secretion of biologically active human interleukin 22 (IL-22) by Lactococcus lactis. |
| 649 | 25214209 | Interleukin-22 (IL-22) participates in the modulation of innate immunity and inflammation. |
| 650 | 25214209 | We generated a Lactococcus lactis strain that secretes human IL-22 under the regulation of the nisin-inducible promoter. |
| 651 | 25214209 | Identification and secretion of this cytokine was demonstrated using western blots of culture supernatants from IL-22-expressing bacteria. |
| 652 | 25214209 | The recombinant IL-22 protein produced by L. lactis was biologically active as determined by its ability to induce IL-10 secretion when co-cultured with a colon epithelial cell line in vitro. |
| 653 | 25214209 | Secretion of biologically active human interleukin 22 (IL-22) by Lactococcus lactis. |
| 654 | 25214209 | Interleukin-22 (IL-22) participates in the modulation of innate immunity and inflammation. |
| 655 | 25214209 | We generated a Lactococcus lactis strain that secretes human IL-22 under the regulation of the nisin-inducible promoter. |
| 656 | 25214209 | Identification and secretion of this cytokine was demonstrated using western blots of culture supernatants from IL-22-expressing bacteria. |
| 657 | 25214209 | The recombinant IL-22 protein produced by L. lactis was biologically active as determined by its ability to induce IL-10 secretion when co-cultured with a colon epithelial cell line in vitro. |
| 658 | 25214209 | Secretion of biologically active human interleukin 22 (IL-22) by Lactococcus lactis. |
| 659 | 25214209 | Interleukin-22 (IL-22) participates in the modulation of innate immunity and inflammation. |
| 660 | 25214209 | We generated a Lactococcus lactis strain that secretes human IL-22 under the regulation of the nisin-inducible promoter. |
| 661 | 25214209 | Identification and secretion of this cytokine was demonstrated using western blots of culture supernatants from IL-22-expressing bacteria. |
| 662 | 25214209 | The recombinant IL-22 protein produced by L. lactis was biologically active as determined by its ability to induce IL-10 secretion when co-cultured with a colon epithelial cell line in vitro. |
| 663 | 25253667 | Interleukin-10- and transforming growth factor β-independent regulation of CD8⁺ T cells expressing type 1 and type 2 cytokines in human lymphatic filariasis. |
| 664 | 25253667 | INF individuals exhibited significant decreases in the frequencies of CD8⁺ T cells expressing tumor necrosis factor alpha (TNF-α), gamma interferon (IFN-γ), and interleukin-22 (IL-22) at baseline and/or in response to filarial antigens, compared with CP and EN individuals. |
| 665 | 25253667 | In contrast, the same individuals exhibited significant increases in the frequencies of CD8⁺ T cells expressing IL-4, IL-5, IL-9, IL-13, and IL-21, compared with CP and/or EN individuals. |
| 666 | 25253667 | Finally, the regulation of these responses appears to be independent of IL-10 and transforming growth factor β (TGF-β), since blockade of IL-10 or TGF-β signaling did not significantly alter the frequencies of type 1 or type 2 cytokine-expressing CD8⁺ T cells. |
| 667 | 25346485 | Interleukin-27 (IL-27) is a unique cytokine that has both inflammatory and immune suppressive activities. |
| 668 | 25346485 | However, the specific effect of IL-27 during DC differentiation and how that may change the nature of the antigen-presenting cell has not been investigated. |
| 669 | 25346485 | In this report, we show that IL-27 treatment during monocyte-derived DC differentiation enhanced the ability to process antigens and stimulate T-cell activity. |
| 670 | 25346485 | DCs differentiated in the presence of IL-27 showed enhanced acidification of latex bead-containing phagosomes that was consistent with elevated expression of vacuolar-ATPases. |
| 671 | 25346485 | In addition, the levels of MHC class II surface expression were higher in DCs differentiated in the presence of IL-27. |
| 672 | 25346485 | Production of IL-12 was also significantly increased during S. aureus infection of IL-27-differentiated DCs. |
| 673 | 25346485 | Interleukin-27 (IL-27) is a unique cytokine that has both inflammatory and immune suppressive activities. |
| 674 | 25346485 | However, the specific effect of IL-27 during DC differentiation and how that may change the nature of the antigen-presenting cell has not been investigated. |
| 675 | 25346485 | In this report, we show that IL-27 treatment during monocyte-derived DC differentiation enhanced the ability to process antigens and stimulate T-cell activity. |
| 676 | 25346485 | DCs differentiated in the presence of IL-27 showed enhanced acidification of latex bead-containing phagosomes that was consistent with elevated expression of vacuolar-ATPases. |
| 677 | 25346485 | In addition, the levels of MHC class II surface expression were higher in DCs differentiated in the presence of IL-27. |
| 678 | 25346485 | Production of IL-12 was also significantly increased during S. aureus infection of IL-27-differentiated DCs. |
| 679 | 25346485 | Interleukin-27 (IL-27) is a unique cytokine that has both inflammatory and immune suppressive activities. |
| 680 | 25346485 | However, the specific effect of IL-27 during DC differentiation and how that may change the nature of the antigen-presenting cell has not been investigated. |
| 681 | 25346485 | In this report, we show that IL-27 treatment during monocyte-derived DC differentiation enhanced the ability to process antigens and stimulate T-cell activity. |
| 682 | 25346485 | DCs differentiated in the presence of IL-27 showed enhanced acidification of latex bead-containing phagosomes that was consistent with elevated expression of vacuolar-ATPases. |
| 683 | 25346485 | In addition, the levels of MHC class II surface expression were higher in DCs differentiated in the presence of IL-27. |
| 684 | 25346485 | Production of IL-12 was also significantly increased during S. aureus infection of IL-27-differentiated DCs. |
| 685 | 25346485 | Interleukin-27 (IL-27) is a unique cytokine that has both inflammatory and immune suppressive activities. |
| 686 | 25346485 | However, the specific effect of IL-27 during DC differentiation and how that may change the nature of the antigen-presenting cell has not been investigated. |
| 687 | 25346485 | In this report, we show that IL-27 treatment during monocyte-derived DC differentiation enhanced the ability to process antigens and stimulate T-cell activity. |
| 688 | 25346485 | DCs differentiated in the presence of IL-27 showed enhanced acidification of latex bead-containing phagosomes that was consistent with elevated expression of vacuolar-ATPases. |
| 689 | 25346485 | In addition, the levels of MHC class II surface expression were higher in DCs differentiated in the presence of IL-27. |
| 690 | 25346485 | Production of IL-12 was also significantly increased during S. aureus infection of IL-27-differentiated DCs. |
| 691 | 25346485 | Interleukin-27 (IL-27) is a unique cytokine that has both inflammatory and immune suppressive activities. |
| 692 | 25346485 | However, the specific effect of IL-27 during DC differentiation and how that may change the nature of the antigen-presenting cell has not been investigated. |
| 693 | 25346485 | In this report, we show that IL-27 treatment during monocyte-derived DC differentiation enhanced the ability to process antigens and stimulate T-cell activity. |
| 694 | 25346485 | DCs differentiated in the presence of IL-27 showed enhanced acidification of latex bead-containing phagosomes that was consistent with elevated expression of vacuolar-ATPases. |
| 695 | 25346485 | In addition, the levels of MHC class II surface expression were higher in DCs differentiated in the presence of IL-27. |
| 696 | 25346485 | Production of IL-12 was also significantly increased during S. aureus infection of IL-27-differentiated DCs. |
| 697 | 25489065 | NDV-3 induced increases in CD3+ T-cell and neutrophil infiltration and IL-17A, IL-22, and host defense peptide expression in local settings of SSSI abscesses. |
| 698 | 25489065 | By comparison, protection against hematogenous dissemination required the induction of IL-17A and IL-22 by NDV-3. |
| 699 | 25489065 | NDV-3 induced increases in CD3+ T-cell and neutrophil infiltration and IL-17A, IL-22, and host defense peptide expression in local settings of SSSI abscesses. |
| 700 | 25489065 | By comparison, protection against hematogenous dissemination required the induction of IL-17A and IL-22 by NDV-3. |
| 701 | 25520147 | The CD4 T cell cytokine response (IFN-γ, interleukin-2 [IL-2], interleukin-17A [IL-17A], interleukin-22 [IL-22], granulocyte-macrophage colony-stimulating factor [GM-CSF], and tumor necrosis factor alpha [TNF-α]) and surface marker expression (CD27, CXCR3, and CD154) were then measured. |
| 702 | 25520147 | We found that the proportion of PPD-specific CD4 T cells, defined as CD154(+) TNF-α(+) cells that were negative for CD27 and positive for GM-CSF, gave the strongest discrimination between subjects with latent and those with active TB (area under the receiver operator characteristic [ROC] curve of 0.9277; P < 0.0001). |
| 703 | 25520147 | Also, the proportions and absolute numbers of HBHA-specific CD4 T cells were significantly higher in those with latent TB infection, particularly CD154(+) TNF-α(+) IFN-γ(+) IL-2(+) and CD154(+) TNF-α(+) CXCR3(+). |
| 704 | 25614966 | An IL-27/NFIL3 signalling axis drives Tim-3 and IL-10 expression and T-cell dysfunction. |
| 705 | 25614966 | The inhibitory receptor T-cell immunoglobulin and mucin domain-3 (Tim-3) has emerged as a critical regulator of the T-cell dysfunction that develops in chronic viral infections and cancers. |
| 706 | 25614966 | Here, we demonstrate that interleukin (IL)-27 induces nuclear factor, interleukin 3 regulated (NFIL3), which promotes permissive chromatin remodelling of the Tim-3 locus and induces Tim-3 expression together with the immunosuppressive cytokine IL-10. |
| 707 | 25614966 | We further show that the IL-27/NFIL3 signalling axis is crucial for the induction of Tim-3 in vivo. |
| 708 | 25614966 | In contrast, tumour-infiltrating lymphocytes from IL-27R(-/-) mice exhibit reduced NFIL3, less Tim-3 expression and failure to develop dysfunctional phenotype, resulting in better tumour growth control. |
| 709 | 25614966 | Thus, our data identify an IL-27/NFIL3 signalling axis as a key regulator of effector T-cell responses via induction of Tim-3, IL-10 and T-cell dysfunction. |
| 710 | 25614966 | An IL-27/NFIL3 signalling axis drives Tim-3 and IL-10 expression and T-cell dysfunction. |
| 711 | 25614966 | The inhibitory receptor T-cell immunoglobulin and mucin domain-3 (Tim-3) has emerged as a critical regulator of the T-cell dysfunction that develops in chronic viral infections and cancers. |
| 712 | 25614966 | Here, we demonstrate that interleukin (IL)-27 induces nuclear factor, interleukin 3 regulated (NFIL3), which promotes permissive chromatin remodelling of the Tim-3 locus and induces Tim-3 expression together with the immunosuppressive cytokine IL-10. |
| 713 | 25614966 | We further show that the IL-27/NFIL3 signalling axis is crucial for the induction of Tim-3 in vivo. |
| 714 | 25614966 | In contrast, tumour-infiltrating lymphocytes from IL-27R(-/-) mice exhibit reduced NFIL3, less Tim-3 expression and failure to develop dysfunctional phenotype, resulting in better tumour growth control. |
| 715 | 25614966 | Thus, our data identify an IL-27/NFIL3 signalling axis as a key regulator of effector T-cell responses via induction of Tim-3, IL-10 and T-cell dysfunction. |
| 716 | 25614966 | An IL-27/NFIL3 signalling axis drives Tim-3 and IL-10 expression and T-cell dysfunction. |
| 717 | 25614966 | The inhibitory receptor T-cell immunoglobulin and mucin domain-3 (Tim-3) has emerged as a critical regulator of the T-cell dysfunction that develops in chronic viral infections and cancers. |
| 718 | 25614966 | Here, we demonstrate that interleukin (IL)-27 induces nuclear factor, interleukin 3 regulated (NFIL3), which promotes permissive chromatin remodelling of the Tim-3 locus and induces Tim-3 expression together with the immunosuppressive cytokine IL-10. |
| 719 | 25614966 | We further show that the IL-27/NFIL3 signalling axis is crucial for the induction of Tim-3 in vivo. |
| 720 | 25614966 | In contrast, tumour-infiltrating lymphocytes from IL-27R(-/-) mice exhibit reduced NFIL3, less Tim-3 expression and failure to develop dysfunctional phenotype, resulting in better tumour growth control. |
| 721 | 25614966 | Thus, our data identify an IL-27/NFIL3 signalling axis as a key regulator of effector T-cell responses via induction of Tim-3, IL-10 and T-cell dysfunction. |
| 722 | 25716231 | The Transforming Growth Factor β1/Interleukin-31 Pathway Is Upregulated in Patients with Hepatitis B Virus-Related Acute-on-Chronic Liver Failure and Is Associated with Disease Severity and Survival. |
| 723 | 25716231 | The transforming growth factor β1/interleukin-31 (TGF-β1/IL-31) pathway plays an important role in the process of cell injury and inflammation. |
| 724 | 25716231 | The quantitative serum levels of TGF-β1, IL-9, IL-10, IL-17, IL-22, IL-23, IL-31, IL-33, and IL-35 were analyzed among chronic hepatitis B (CHB) patients (n = 17), ACLF patients (n = 18), and normal control (NC) subjects (n = 18). |
| 725 | 25716231 | Serum TGF-β1 levels were strongly positively correlated with IL-31 in all subjects, and both of them were positively correlated with IL-17, IL-22, and IL-33. |
| 726 | 25716231 | In CHB and ACLF patients, serum levels of TGF-β1 and IL-31 were both increased significantly compared with those in NC subjects and positively correlated with total bilirubin (TBil) and alpha-fetoprotein (AFP) levels. |
| 727 | 25716231 | The Transforming Growth Factor β1/Interleukin-31 Pathway Is Upregulated in Patients with Hepatitis B Virus-Related Acute-on-Chronic Liver Failure and Is Associated with Disease Severity and Survival. |
| 728 | 25716231 | The transforming growth factor β1/interleukin-31 (TGF-β1/IL-31) pathway plays an important role in the process of cell injury and inflammation. |
| 729 | 25716231 | The quantitative serum levels of TGF-β1, IL-9, IL-10, IL-17, IL-22, IL-23, IL-31, IL-33, and IL-35 were analyzed among chronic hepatitis B (CHB) patients (n = 17), ACLF patients (n = 18), and normal control (NC) subjects (n = 18). |
| 730 | 25716231 | Serum TGF-β1 levels were strongly positively correlated with IL-31 in all subjects, and both of them were positively correlated with IL-17, IL-22, and IL-33. |
| 731 | 25716231 | In CHB and ACLF patients, serum levels of TGF-β1 and IL-31 were both increased significantly compared with those in NC subjects and positively correlated with total bilirubin (TBil) and alpha-fetoprotein (AFP) levels. |
| 732 | 25930741 | Interleukin-10, IL-12 and IL-27 were produced in vitro by Conj-stimulated bone marrow dendritic cells, whereas IL-10 and IFN-γ were up-regulated in co-cultures of CD11c(+) and CD4(+) T cells from Conj-treated mice stimulated with allergen. |
| 733 | 25930741 | The Conj effects on IL-10(-/-) and IL-12(-/-) mice confirmed the role of IL-10 and IFN-γ in inducing a protective and balanced redirection the T helper type 2-mediated airway inflammation. |
| 734 | 26069966 | Preclinical studies have found that IL-17 secreting CD4+ Th17 cells in reducing pneumococcal colonisation. |
| 735 | 26069966 | Th17 cytokines assayed included IL-17A, IL-21, IL-22 as well as TNF-α, IL-10, TGF-β, IL-6, IL-23 and IFNγ. |
| 736 | 26069966 | Cytokine levels were significantly lower in children with high density pneumococcal carriage compared with children with low density carriage for IL-17A (p=0.002) and IL-23 (p=0.04). |
| 737 | 26069966 | There was a trend towards significance for IL-22 (p=0.057) while no difference was observed for the other cytokines. |
| 738 | 26069966 | Preclinical studies have found that IL-17 secreting CD4+ Th17 cells in reducing pneumococcal colonisation. |
| 739 | 26069966 | Th17 cytokines assayed included IL-17A, IL-21, IL-22 as well as TNF-α, IL-10, TGF-β, IL-6, IL-23 and IFNγ. |
| 740 | 26069966 | Cytokine levels were significantly lower in children with high density pneumococcal carriage compared with children with low density carriage for IL-17A (p=0.002) and IL-23 (p=0.04). |
| 741 | 26069966 | There was a trend towards significance for IL-22 (p=0.057) while no difference was observed for the other cytokines. |
| 742 | 25503054 | Th17 cells were defined as IL-17+ CD4+ T cells and their function was assessed by the co-expression of IL-22, IL-2 and IFNγ. |