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Gene Information
Gene symbol: TGFB1
Gene name: transforming growth factor, beta 1
HGNC ID: 11766
Synonyms: CED, TGFbeta
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 2017199 | --is stimulated by PRFs such as interferon-gamma, IL-1, TNF, GM-CSF and IL-4. |
| 2 | 2017199 | The activation and expansion of T-lymphocytes requires IL-1, IL-2, IL-4, interferon-gamma, IL-6 and probably IL-7. |
| 3 | 2017199 | Likewise, the activation and expansion of B-lymphocytes is regulated by PRFs such as IL-1, IL-2, IL-4, IL-5, IL-6, IL-7 and interferon-gamma. |
| 4 | 2017199 | Antibody class is critically influenced by particular PRFs, e.g. interferon-gamma regulates IgG2a; IL-4, IgE and IgG1; IL-5 and TGF-beta, IgA. |
| 5 | 2017199 | The recruitment and enhanced production and function of granulocytic and phagocytic cells involves a number of T-lymphocyte PRFs including GM-CSF, IL-3, IL-5, IL-4, and IL-6. |
| 6 | 2017199 | IL-3 induces a mastocytosis and IL-5 an eosinophilia. |
| 7 | 7537721 | L. major induced the production of two competing cytokines in infected macrophages: (1) the parasite activated the gene for tumor necrosis factor (TNF), and production of TNF protein was enhanced by the presence of interferon-gamma (IFN-gamma). |
| 8 | 7537721 | TNF then acted as a autocrine signal to amplify IFN-gamma-induced production of NO; and (2) the parasite upregulated production of transforming growth factor-beta (TGF-beta), which blocked IFN-gamma-induced production of NO. |
| 9 | 7537721 | Whether parasite-induced TNF (parasite destruction) or TGF-beta (parasite survival) prevailed depended upon the presence and quantity of IFN-gamma at the time of infection. |
| 10 | 7537721 | L. major induced the production of two competing cytokines in infected macrophages: (1) the parasite activated the gene for tumor necrosis factor (TNF), and production of TNF protein was enhanced by the presence of interferon-gamma (IFN-gamma). |
| 11 | 7537721 | TNF then acted as a autocrine signal to amplify IFN-gamma-induced production of NO; and (2) the parasite upregulated production of transforming growth factor-beta (TGF-beta), which blocked IFN-gamma-induced production of NO. |
| 12 | 7537721 | Whether parasite-induced TNF (parasite destruction) or TGF-beta (parasite survival) prevailed depended upon the presence and quantity of IFN-gamma at the time of infection. |
| 13 | 7636200 | Although not affecting the outcome of primary challenge, serologic ablation of TGF-beta in the former animals abrogated development of acquired resistance and resulted in impaired production of IL-12/IFN-gamma and higher expression of IL-4/IL-10 at the time of reinfection with virulent yeast. |
| 14 | 7636200 | In addition to previous evidence for an obligatory role of IFN-gamma and IL-12 in Candida-driven Th1 cell differentiation in vivo, the present data establish TGF-beta as a third cytokine, the presence of which may be required for optimal Th1 development leading to long-lived anticandidal resistance. |
| 15 | 8011155 | Suppression can be adoptively transferred by CD8+ T lymphocytes which act by releasing TGF-beta and IL-4 following antigen-specific triggering. |
| 16 | 8027551 | IL-10, TGF-beta 1, and IFN-alpha (cytokines known to regulate effector functions of activated macrophages) also did not block anti-F. tularensis activity of IFN-gamma-stimulated AM. |
| 17 | 8027551 | Reactive oxygen metabolites, depletion of tryptophan, and sequestration of iron did not contribute to anti-F. tularensis activity because addition of superoxide dismutase or catalase, excess iron, or tryptophan to IFN-gamma-treated AM did not reverse the anti-F. tularensis activity observed in these cells. |
| 18 | 8960825 | At 70 days of age mononuclear infiltration of islets had begun and was associated with upregulation of interferon gamma (IFN gamma) and iNOS, but downregulation of interleukin-10 and transforming growth factor beta mRNA (p < 0.001). |
| 19 | 8960825 | Oral lipopolysaccharide (LPS) from E. coli and OM-89, an endotoxin free extract containing immunostimulatory glycolipopeptides and heat shock protein (hsp) 65, both downregulated IFN gamma mRNA while only OM-89 in addition suppressed iNOS mRNA and enhanced Th2 cytokine gene expression (p < 0.001). |
| 20 | 9449788 | Cells containing TGF-beta or IL-8 were not found in human PBMC stimulated with B. firmus. |
| 21 | 9467982 | The antigen now interacts with macrophages or CD4+ cells, and go on to the Peyer's patch where B cells undergo a transforming growth factor beta (TGF-beta)-mediated isotope switch to immunoglobulin (Ig) A. |
| 22 | 9467982 | CD8+ T-cell activation is favoured over CD4+ T-cell activation due to the size of the antigenic binding peptide. |
| 23 | 9472560 | Of the many cytokines available for gene transfer, IL-7 was chosen for these studies because it both stimulates CTL responses and down-regulates tumor production of the immunosuppressive peptide TGF-beta. |
| 24 | 9486394 | High percentages of monocytes were associated with a decreased HIV-1 replication and proliferation that could not be reversed by addition of antibodies against the cytokines IL-1, transforming growth factor-beta (TGF-beta) or indomethacin. |
| 25 | 9498757 | Further, the inhibitory effect of mIEC was not restored by antibodies to TGF-beta, CD1d, E-cadherin, or MHC class I or II. |
| 26 | 9498757 | This inhibitory effect was noted for both gammadelta and alphabeta T cell subsets from IELs, and mRNA levels were reduced for both Th1 (IL-2 and IFN-gamma) and Th2 (IL-4 and IL-5) cytokines in gammadelta and alphabeta IELs. |
| 27 | 9665972 | Inhibition of Mycobacterium bovis BCG-induced tumor necrosis factor alpha secretion in human cells by transforming growth factor beta. |
| 28 | 9665972 | The effect of exogenous transforming growth factor beta (TGF-beta) on Mycobacterium bovis BCG-induced tumor necrosis factor alpha (TNF-alpha) production by human mononuclear cells was studied. |
| 29 | 9665972 | It was found that TNF-alpha production by human cells stimulated with BCG was significantly inhibited by TGF-beta. |
| 30 | 9665972 | Furthermore, the suppressive effect of TGF-beta on TNF-alpha secretion in this system was not due to a direct cytotoxic effect, since cell viability was comparable in the presence or absence of TGF-beta. |
| 31 | 9665972 | Interestingly, our results demonstrated comparative suppressive effects of TGF-beta and interleukin-10 on BCG-induced TNF-alpha secretion. |
| 32 | 9665972 | Together, the data demonstrate, for the first time, that TGF-beta inhibits BCG-induced TNF-alpha secretion by human cells. |
| 33 | 9665972 | Inhibition of Mycobacterium bovis BCG-induced tumor necrosis factor alpha secretion in human cells by transforming growth factor beta. |
| 34 | 9665972 | The effect of exogenous transforming growth factor beta (TGF-beta) on Mycobacterium bovis BCG-induced tumor necrosis factor alpha (TNF-alpha) production by human mononuclear cells was studied. |
| 35 | 9665972 | It was found that TNF-alpha production by human cells stimulated with BCG was significantly inhibited by TGF-beta. |
| 36 | 9665972 | Furthermore, the suppressive effect of TGF-beta on TNF-alpha secretion in this system was not due to a direct cytotoxic effect, since cell viability was comparable in the presence or absence of TGF-beta. |
| 37 | 9665972 | Interestingly, our results demonstrated comparative suppressive effects of TGF-beta and interleukin-10 on BCG-induced TNF-alpha secretion. |
| 38 | 9665972 | Together, the data demonstrate, for the first time, that TGF-beta inhibits BCG-induced TNF-alpha secretion by human cells. |
| 39 | 9665972 | Inhibition of Mycobacterium bovis BCG-induced tumor necrosis factor alpha secretion in human cells by transforming growth factor beta. |
| 40 | 9665972 | The effect of exogenous transforming growth factor beta (TGF-beta) on Mycobacterium bovis BCG-induced tumor necrosis factor alpha (TNF-alpha) production by human mononuclear cells was studied. |
| 41 | 9665972 | It was found that TNF-alpha production by human cells stimulated with BCG was significantly inhibited by TGF-beta. |
| 42 | 9665972 | Furthermore, the suppressive effect of TGF-beta on TNF-alpha secretion in this system was not due to a direct cytotoxic effect, since cell viability was comparable in the presence or absence of TGF-beta. |
| 43 | 9665972 | Interestingly, our results demonstrated comparative suppressive effects of TGF-beta and interleukin-10 on BCG-induced TNF-alpha secretion. |
| 44 | 9665972 | Together, the data demonstrate, for the first time, that TGF-beta inhibits BCG-induced TNF-alpha secretion by human cells. |
| 45 | 9665972 | Inhibition of Mycobacterium bovis BCG-induced tumor necrosis factor alpha secretion in human cells by transforming growth factor beta. |
| 46 | 9665972 | The effect of exogenous transforming growth factor beta (TGF-beta) on Mycobacterium bovis BCG-induced tumor necrosis factor alpha (TNF-alpha) production by human mononuclear cells was studied. |
| 47 | 9665972 | It was found that TNF-alpha production by human cells stimulated with BCG was significantly inhibited by TGF-beta. |
| 48 | 9665972 | Furthermore, the suppressive effect of TGF-beta on TNF-alpha secretion in this system was not due to a direct cytotoxic effect, since cell viability was comparable in the presence or absence of TGF-beta. |
| 49 | 9665972 | Interestingly, our results demonstrated comparative suppressive effects of TGF-beta and interleukin-10 on BCG-induced TNF-alpha secretion. |
| 50 | 9665972 | Together, the data demonstrate, for the first time, that TGF-beta inhibits BCG-induced TNF-alpha secretion by human cells. |
| 51 | 9665972 | Inhibition of Mycobacterium bovis BCG-induced tumor necrosis factor alpha secretion in human cells by transforming growth factor beta. |
| 52 | 9665972 | The effect of exogenous transforming growth factor beta (TGF-beta) on Mycobacterium bovis BCG-induced tumor necrosis factor alpha (TNF-alpha) production by human mononuclear cells was studied. |
| 53 | 9665972 | It was found that TNF-alpha production by human cells stimulated with BCG was significantly inhibited by TGF-beta. |
| 54 | 9665972 | Furthermore, the suppressive effect of TGF-beta on TNF-alpha secretion in this system was not due to a direct cytotoxic effect, since cell viability was comparable in the presence or absence of TGF-beta. |
| 55 | 9665972 | Interestingly, our results demonstrated comparative suppressive effects of TGF-beta and interleukin-10 on BCG-induced TNF-alpha secretion. |
| 56 | 9665972 | Together, the data demonstrate, for the first time, that TGF-beta inhibits BCG-induced TNF-alpha secretion by human cells. |
| 57 | 9665972 | Inhibition of Mycobacterium bovis BCG-induced tumor necrosis factor alpha secretion in human cells by transforming growth factor beta. |
| 58 | 9665972 | The effect of exogenous transforming growth factor beta (TGF-beta) on Mycobacterium bovis BCG-induced tumor necrosis factor alpha (TNF-alpha) production by human mononuclear cells was studied. |
| 59 | 9665972 | It was found that TNF-alpha production by human cells stimulated with BCG was significantly inhibited by TGF-beta. |
| 60 | 9665972 | Furthermore, the suppressive effect of TGF-beta on TNF-alpha secretion in this system was not due to a direct cytotoxic effect, since cell viability was comparable in the presence or absence of TGF-beta. |
| 61 | 9665972 | Interestingly, our results demonstrated comparative suppressive effects of TGF-beta and interleukin-10 on BCG-induced TNF-alpha secretion. |
| 62 | 9665972 | Together, the data demonstrate, for the first time, that TGF-beta inhibits BCG-induced TNF-alpha secretion by human cells. |
| 63 | 9667667 | Analysis of the autologous tumour cell vaccines regarding IL-7 secretion after gene transfer, HLA class I and class II cell surface expression, secretion of immunosuppressive mediators (TGF-beta1, IL-10) and various melanoma-associated tumour antigens revealed a very diverse expression profile. |
| 64 | 9673234 | Protein malnutrition also impaired the abilities of cells from vaccinated LP guinea pigs to produce cytokines, including interferon, tumor necrosis factor alpha (TNF-alpha) and transforming growth factor beta (TGF-beta), in response to PPD, despite the demonstration of higher serum levels of TNF-alpha and TGF-beta after an intravenous injection of PPD into LP guinea pigs. |
| 65 | 9686186 | We have shown that IL-12, a powerful inducer of IFN-gamma production by NK cells, is synthesized soon after trypomastigote-macrophage interaction. |
| 66 | 9686186 | Also, treatment of infected mice with mAb specific for IFN-gamma or TNF-alpha inhibited the protective effect of exogenous IL-12. |
| 67 | 9686186 | On the other hand, TGF-beta and IL-10 produced by infected macrophages inhibited the induction and effects of IL-12. |
| 68 | 9686186 | Therefore, while IL-12, TNF-alpha and IFN-gamma correlate with resistance to T. cruzi infection, TGF-beta and IL-10 promote susceptibility. |
| 69 | 9686186 | We have shown that IL-12, a powerful inducer of IFN-gamma production by NK cells, is synthesized soon after trypomastigote-macrophage interaction. |
| 70 | 9686186 | Also, treatment of infected mice with mAb specific for IFN-gamma or TNF-alpha inhibited the protective effect of exogenous IL-12. |
| 71 | 9686186 | On the other hand, TGF-beta and IL-10 produced by infected macrophages inhibited the induction and effects of IL-12. |
| 72 | 9686186 | Therefore, while IL-12, TNF-alpha and IFN-gamma correlate with resistance to T. cruzi infection, TGF-beta and IL-10 promote susceptibility. |
| 73 | 9724878 | In comparative studies of coccidiosis in chickens, in-vivo and in-vitro studies revealed that interferon-gamma, tumor necrosis factor and transforming growth factor-beta are induced following Eimeria infection. |
| 74 | 9737670 | In this study, we show that proinflammatory stimuli induce the expression of other cytokines such as IL-6, transforming growth factor-beta (TGF-beta), and granulocyte-macrophage colony-stimulating factor (GM-CSF) by muscle cells themselves, as well as the up-regulation of human leucocyte antigen (HLA) class I, class II and intercellular adhesion molecule-1 (ICAM-1). |
| 75 | 9737670 | The levels of HLA class I, class II and ICAM-1 in inflamed muscle may be affected by the secreted products of the stimulation. |
| 76 | 9806041 | Regulation of interleukin-12 by interleukin-10, transforming growth factor-beta, tumor necrosis factor-alpha, and interferon-gamma in human monocytes infected with Mycobacterium tuberculosis H37Ra. |
| 77 | 9806041 | Regulation of interleukin (IL)-12 production by coexpression of tumor necrosis factor (TNF)-alpha, IL-10, and transforming growth factor (TGF)-beta in human monocytes infected with Mycobacterium tuberculosis H37Ra was analyzed. |
| 78 | 9806041 | Also, since IL-12 induces interferon (IFN)-gamma, the effect of IFN-gamma on IL-12 expression was examined. |
| 79 | 9806041 | IL-12 p70 protein paralleled IL-12 p40 protein expression. |
| 80 | 9806041 | TNF-alpha protein expression occurred earlier than IL-12 p40 protein but was not required for IL-12 induction. |
| 81 | 9806041 | Addition or neutralization of TGF-beta did not significantly alter IL-12 induction. |
| 82 | 9806041 | In contrast, recombinant IL-10 reduced IL-12 and neutralization of IL-10 minimally enhanced IL-12. |
| 83 | 9806041 | A pronounced increase in IL-12 followed IFN-gamma pretreatment, which selectively up-regulated IL-12 p35 mRNA. |
| 84 | 9806041 | Regulation of interleukin-12 by interleukin-10, transforming growth factor-beta, tumor necrosis factor-alpha, and interferon-gamma in human monocytes infected with Mycobacterium tuberculosis H37Ra. |
| 85 | 9806041 | Regulation of interleukin (IL)-12 production by coexpression of tumor necrosis factor (TNF)-alpha, IL-10, and transforming growth factor (TGF)-beta in human monocytes infected with Mycobacterium tuberculosis H37Ra was analyzed. |
| 86 | 9806041 | Also, since IL-12 induces interferon (IFN)-gamma, the effect of IFN-gamma on IL-12 expression was examined. |
| 87 | 9806041 | IL-12 p70 protein paralleled IL-12 p40 protein expression. |
| 88 | 9806041 | TNF-alpha protein expression occurred earlier than IL-12 p40 protein but was not required for IL-12 induction. |
| 89 | 9806041 | Addition or neutralization of TGF-beta did not significantly alter IL-12 induction. |
| 90 | 9806041 | In contrast, recombinant IL-10 reduced IL-12 and neutralization of IL-10 minimally enhanced IL-12. |
| 91 | 9806041 | A pronounced increase in IL-12 followed IFN-gamma pretreatment, which selectively up-regulated IL-12 p35 mRNA. |
| 92 | 9826461 | Combination of transforming growth factor beta antisense and interleukin-2 gene therapy in the murine ovarian teratoma model. |
| 93 | 9826461 | The immunosuppressive protein transforming growth factor beta (TGF-beta) inhibits the activation of various immune effector cells including cytotoxic T lymphocytes and may therefore inhibit the efficacy of immunostimulatory interleukin-2 (IL-2) gene therapy. |
| 94 | 9826461 | In this study, we investigated the effect of TGF-beta downregulation on IL-2 gene therapy in the intraperitoneal model of murine ovarian teratoma (MOT). |
| 95 | 9826461 | Subcutaneous immunization of C3H mice with a mixture of IL-2 gene-transduced fibroblasts and TGF-beta antisense-modified MOT cells induced significantly better protection against a subsequent intraperitoneal tumor challenge compared with immunization with unmodified MOT cells alone [11/16 (69%) vs 4/21 (19%) tumor-free animals, P < 0.01]. |
| 96 | 9826461 | Immunization with either a mixture of IL-2 gene modified fibroblasts and unmodified MOT cells [2/12 (17%) tumor-free animals] or TGF-beta antisense-modified MOT cells alone (0/13 tumor free animals) failed to induce significant protection compared with immunization with unmodified MOT cells. |
| 97 | 9826461 | These data show that combined TGF-beta antisense and IL-2 gene therapy is required to generate effective antitumor responses in the MOT model. |
| 98 | 9826461 | Combination of transforming growth factor beta antisense and interleukin-2 gene therapy in the murine ovarian teratoma model. |
| 99 | 9826461 | The immunosuppressive protein transforming growth factor beta (TGF-beta) inhibits the activation of various immune effector cells including cytotoxic T lymphocytes and may therefore inhibit the efficacy of immunostimulatory interleukin-2 (IL-2) gene therapy. |
| 100 | 9826461 | In this study, we investigated the effect of TGF-beta downregulation on IL-2 gene therapy in the intraperitoneal model of murine ovarian teratoma (MOT). |
| 101 | 9826461 | Subcutaneous immunization of C3H mice with a mixture of IL-2 gene-transduced fibroblasts and TGF-beta antisense-modified MOT cells induced significantly better protection against a subsequent intraperitoneal tumor challenge compared with immunization with unmodified MOT cells alone [11/16 (69%) vs 4/21 (19%) tumor-free animals, P < 0.01]. |
| 102 | 9826461 | Immunization with either a mixture of IL-2 gene modified fibroblasts and unmodified MOT cells [2/12 (17%) tumor-free animals] or TGF-beta antisense-modified MOT cells alone (0/13 tumor free animals) failed to induce significant protection compared with immunization with unmodified MOT cells. |
| 103 | 9826461 | These data show that combined TGF-beta antisense and IL-2 gene therapy is required to generate effective antitumor responses in the MOT model. |
| 104 | 9826461 | Combination of transforming growth factor beta antisense and interleukin-2 gene therapy in the murine ovarian teratoma model. |
| 105 | 9826461 | The immunosuppressive protein transforming growth factor beta (TGF-beta) inhibits the activation of various immune effector cells including cytotoxic T lymphocytes and may therefore inhibit the efficacy of immunostimulatory interleukin-2 (IL-2) gene therapy. |
| 106 | 9826461 | In this study, we investigated the effect of TGF-beta downregulation on IL-2 gene therapy in the intraperitoneal model of murine ovarian teratoma (MOT). |
| 107 | 9826461 | Subcutaneous immunization of C3H mice with a mixture of IL-2 gene-transduced fibroblasts and TGF-beta antisense-modified MOT cells induced significantly better protection against a subsequent intraperitoneal tumor challenge compared with immunization with unmodified MOT cells alone [11/16 (69%) vs 4/21 (19%) tumor-free animals, P < 0.01]. |
| 108 | 9826461 | Immunization with either a mixture of IL-2 gene modified fibroblasts and unmodified MOT cells [2/12 (17%) tumor-free animals] or TGF-beta antisense-modified MOT cells alone (0/13 tumor free animals) failed to induce significant protection compared with immunization with unmodified MOT cells. |
| 109 | 9826461 | These data show that combined TGF-beta antisense and IL-2 gene therapy is required to generate effective antitumor responses in the MOT model. |
| 110 | 9826461 | Combination of transforming growth factor beta antisense and interleukin-2 gene therapy in the murine ovarian teratoma model. |
| 111 | 9826461 | The immunosuppressive protein transforming growth factor beta (TGF-beta) inhibits the activation of various immune effector cells including cytotoxic T lymphocytes and may therefore inhibit the efficacy of immunostimulatory interleukin-2 (IL-2) gene therapy. |
| 112 | 9826461 | In this study, we investigated the effect of TGF-beta downregulation on IL-2 gene therapy in the intraperitoneal model of murine ovarian teratoma (MOT). |
| 113 | 9826461 | Subcutaneous immunization of C3H mice with a mixture of IL-2 gene-transduced fibroblasts and TGF-beta antisense-modified MOT cells induced significantly better protection against a subsequent intraperitoneal tumor challenge compared with immunization with unmodified MOT cells alone [11/16 (69%) vs 4/21 (19%) tumor-free animals, P < 0.01]. |
| 114 | 9826461 | Immunization with either a mixture of IL-2 gene modified fibroblasts and unmodified MOT cells [2/12 (17%) tumor-free animals] or TGF-beta antisense-modified MOT cells alone (0/13 tumor free animals) failed to induce significant protection compared with immunization with unmodified MOT cells. |
| 115 | 9826461 | These data show that combined TGF-beta antisense and IL-2 gene therapy is required to generate effective antitumor responses in the MOT model. |
| 116 | 9826461 | Combination of transforming growth factor beta antisense and interleukin-2 gene therapy in the murine ovarian teratoma model. |
| 117 | 9826461 | The immunosuppressive protein transforming growth factor beta (TGF-beta) inhibits the activation of various immune effector cells including cytotoxic T lymphocytes and may therefore inhibit the efficacy of immunostimulatory interleukin-2 (IL-2) gene therapy. |
| 118 | 9826461 | In this study, we investigated the effect of TGF-beta downregulation on IL-2 gene therapy in the intraperitoneal model of murine ovarian teratoma (MOT). |
| 119 | 9826461 | Subcutaneous immunization of C3H mice with a mixture of IL-2 gene-transduced fibroblasts and TGF-beta antisense-modified MOT cells induced significantly better protection against a subsequent intraperitoneal tumor challenge compared with immunization with unmodified MOT cells alone [11/16 (69%) vs 4/21 (19%) tumor-free animals, P < 0.01]. |
| 120 | 9826461 | Immunization with either a mixture of IL-2 gene modified fibroblasts and unmodified MOT cells [2/12 (17%) tumor-free animals] or TGF-beta antisense-modified MOT cells alone (0/13 tumor free animals) failed to induce significant protection compared with immunization with unmodified MOT cells. |
| 121 | 9826461 | These data show that combined TGF-beta antisense and IL-2 gene therapy is required to generate effective antitumor responses in the MOT model. |
| 122 | 9826461 | Combination of transforming growth factor beta antisense and interleukin-2 gene therapy in the murine ovarian teratoma model. |
| 123 | 9826461 | The immunosuppressive protein transforming growth factor beta (TGF-beta) inhibits the activation of various immune effector cells including cytotoxic T lymphocytes and may therefore inhibit the efficacy of immunostimulatory interleukin-2 (IL-2) gene therapy. |
| 124 | 9826461 | In this study, we investigated the effect of TGF-beta downregulation on IL-2 gene therapy in the intraperitoneal model of murine ovarian teratoma (MOT). |
| 125 | 9826461 | Subcutaneous immunization of C3H mice with a mixture of IL-2 gene-transduced fibroblasts and TGF-beta antisense-modified MOT cells induced significantly better protection against a subsequent intraperitoneal tumor challenge compared with immunization with unmodified MOT cells alone [11/16 (69%) vs 4/21 (19%) tumor-free animals, P < 0.01]. |
| 126 | 9826461 | Immunization with either a mixture of IL-2 gene modified fibroblasts and unmodified MOT cells [2/12 (17%) tumor-free animals] or TGF-beta antisense-modified MOT cells alone (0/13 tumor free animals) failed to induce significant protection compared with immunization with unmodified MOT cells. |
| 127 | 9826461 | These data show that combined TGF-beta antisense and IL-2 gene therapy is required to generate effective antitumor responses in the MOT model. |
| 128 | 9927516 | IL-12 p70 production by stimulated human monocytes was inhibited by CT in a dose-dependent manner. |
| 129 | 9927516 | CT also inhibited the production of IL-12 p70 by monocyte-derived dendritic cells, as well as the production of tumor necrosis factor alpha, but not IL-10, IL-6, or transforming growth factor (TGF)-beta1, by stimulated monocytes. |
| 130 | 9927516 | The effects of CT were not due to autocrine production of IL-10, TGF-beta1, or prostaglandin E2. |
| 131 | 9927516 | CT inhibited the production of IFN-gamma by anti-CD3-stimulated human peripheral blood mononuclear cell, due in part to suppression of IL-12 production, but also to the inhibition of expression of the beta1 and beta2 chains of the IL-12 receptor on T cells. |
| 132 | 9927516 | In vivo, mice given CT before systemic challenge with lipopolysaccharide had markedly reduced serum levels of IL-12 p40 and interferon gamma. |
| 133 | 10477566 | DCs incubated with recombinant S. gordonii were much more efficient than DCs pulsed with soluble C-fragment of tetanus toxin at stimulating specific CD4+ T cells as determined by cell proliferation and IFN-gamma release. |
| 134 | 10477566 | In particular, S. gordonii dose-dependently up-regulated expression of membrane molecules (MHC I and II, CD80, CD86, CD54, CD40, CD83) and reduced both phagocytic and endocytic activities. |
| 135 | 10477566 | Furthermore, bacteria promoted in a dose-dependent manner DC release of cytokines (IL-6, TNF-alpha, IL-1beta, IL-12, TGF-beta, and IL-10) and of the chemokines IL-8, RANTES, IFN-gamma-inducible protein-10, and monokine induced by IFN-gamma. |
| 136 | 10601552 | Human tumor antigens when presented appropriately (with costimulatory molecules and with IL-2, IL-12) break the host's natural tolerance toward its tumor and induce rejection strength immune reactions even in patients with metastatic disease. |
| 137 | 10601552 | For successful active specific immunization against human cancers the understanding of the immunoevasive maneuvers of the tumor cell (through FasL --> Fas; TRAIL; CD40L --> CD40; TGFbeta etc. systems) is essential. |
| 138 | 10614503 | With respect to IgA antibody production in the gut whereas IL-4 and TGF-beta have been implicated in isotype switching of precursor cells to IgA commitment, their subsequent localisation, proliferation and effector activity expression is dependent on IL-5 and IL-6 expression locally. |
| 139 | 10614503 | Whereas IgA+ cells of the B2 lineage are IL-6 dependent but IL-5 independent, B1-derived IgA+ cells are IL-5 dependent and IL-6 independent. |
| 140 | 10757348 | This study examines how large tumors might suppress the T cell functions and escape from the immune responses elicited by a granulocyte-macrophage colony-stimulating factor (GM-CSF)-secreting tumor vaccine. |
| 141 | 10757348 | Expression of transforming growth factor beta (TGF-beta) and interleukin 10 (IL-10), the potent immunosuppressive factors, was detected in the parental tumor cell line RLmale 1 (a murine T leukemia cell line), as well as in the tumor region, the levels of which correlated with tumor progression. |
| 142 | 10757348 | The immunosuppressive activity of IL-10 was also signified by the findings that administration of the conditioned medium of RLmale 1 cultured in a serum-free medium, in which the TGF-beta activity was then lost while the IL-10 activity still remained, or of recombinant IL-10 to the early-treated group of mice abrogated the known efficacy of tumor vaccine on the small tumors. |
| 143 | 10757348 | This study examines how large tumors might suppress the T cell functions and escape from the immune responses elicited by a granulocyte-macrophage colony-stimulating factor (GM-CSF)-secreting tumor vaccine. |
| 144 | 10757348 | Expression of transforming growth factor beta (TGF-beta) and interleukin 10 (IL-10), the potent immunosuppressive factors, was detected in the parental tumor cell line RLmale 1 (a murine T leukemia cell line), as well as in the tumor region, the levels of which correlated with tumor progression. |
| 145 | 10757348 | The immunosuppressive activity of IL-10 was also signified by the findings that administration of the conditioned medium of RLmale 1 cultured in a serum-free medium, in which the TGF-beta activity was then lost while the IL-10 activity still remained, or of recombinant IL-10 to the early-treated group of mice abrogated the known efficacy of tumor vaccine on the small tumors. |
| 146 | 10878341 | Addition of neutralizing Abs to the cultures showed that the suppression was mediated by TGF-beta but not by IL-10 or IFN-gamma. |
| 147 | 10878341 | The self-MHC-reactive clones also inhibited proliferation of primary CD4+ T cells and TT-specific T cell clones, but in this case the inhibition was mediated by both IL-10 and TGF-beta. |
| 148 | 10878341 | We found that prestimulation of non-T cells for 8 h with PWM or for 48 h for rCD40L results in non-T cells capable of inducing self-MHC-reactive T cell to produce high levels of TGF-beta and IL-10. |
| 149 | 10878341 | Finally, addition of CTLA-4/Fc or blocking F(ab')2 anti-CTLA-4 mAb, plus optimally stimulated non-T cells, to cultures of self-MHC-reactive clones inhibited the induction of TGF-beta but not IL-10 or IFN-gamma production. |
| 150 | 10878341 | Addition of neutralizing Abs to the cultures showed that the suppression was mediated by TGF-beta but not by IL-10 or IFN-gamma. |
| 151 | 10878341 | The self-MHC-reactive clones also inhibited proliferation of primary CD4+ T cells and TT-specific T cell clones, but in this case the inhibition was mediated by both IL-10 and TGF-beta. |
| 152 | 10878341 | We found that prestimulation of non-T cells for 8 h with PWM or for 48 h for rCD40L results in non-T cells capable of inducing self-MHC-reactive T cell to produce high levels of TGF-beta and IL-10. |
| 153 | 10878341 | Finally, addition of CTLA-4/Fc or blocking F(ab')2 anti-CTLA-4 mAb, plus optimally stimulated non-T cells, to cultures of self-MHC-reactive clones inhibited the induction of TGF-beta but not IL-10 or IFN-gamma production. |
| 154 | 10900489 | Naturally acquired versus vaccine-induced immunity to malaria: a dual role for TGF-beta and IL-12? |
| 155 | 10928070 | Immunization with TGF-beta antisense oligonucleotide-modified autologous tumor vaccine enhances the antitumor immunity of MBT-2 tumor-bearing mice through upregulation of MHC class I and Fas expressions. |
| 156 | 10928070 | The result of flow cytometry analysis reveals that decreased production of TGF-beta led to the increased expressions of MHC class I molecule and Fas on the surface of MBT-2 tumor cells. |
| 157 | 10928070 | Our result implies that decreasing the amount of TGF-beta secreted from the autologous tumor vaccine by antisense strategy may significantly improve its immunogenicity through up-regulation of both MHC class I and Fas expressions. |
| 158 | 10928070 | Immunization with TGF-beta antisense oligonucleotide-modified autologous tumor vaccine enhances the antitumor immunity of MBT-2 tumor-bearing mice through upregulation of MHC class I and Fas expressions. |
| 159 | 10928070 | The result of flow cytometry analysis reveals that decreased production of TGF-beta led to the increased expressions of MHC class I molecule and Fas on the surface of MBT-2 tumor cells. |
| 160 | 10928070 | Our result implies that decreasing the amount of TGF-beta secreted from the autologous tumor vaccine by antisense strategy may significantly improve its immunogenicity through up-regulation of both MHC class I and Fas expressions. |
| 161 | 10928070 | Immunization with TGF-beta antisense oligonucleotide-modified autologous tumor vaccine enhances the antitumor immunity of MBT-2 tumor-bearing mice through upregulation of MHC class I and Fas expressions. |
| 162 | 10928070 | The result of flow cytometry analysis reveals that decreased production of TGF-beta led to the increased expressions of MHC class I molecule and Fas on the surface of MBT-2 tumor cells. |
| 163 | 10928070 | Our result implies that decreasing the amount of TGF-beta secreted from the autologous tumor vaccine by antisense strategy may significantly improve its immunogenicity through up-regulation of both MHC class I and Fas expressions. |
| 164 | 10950804 | Reduced interleukin-12 and transforming growth factor-beta1 in severe childhood malaria: relationship of cytokine balance with disease severity. |
| 165 | 10950804 | IL-12 and TGF-beta1 were significantly lower, whereas tumor necrosis factor (TNF)-alpha and IL-10 were significantly higher in children with severe malaria. |
| 166 | 10950804 | The ratios of TGF-beta1/IL-12 and IL-10/IL-12 were significantly higher in the severe, compared with the mild, malaria group. |
| 167 | 10950804 | In contrast, ratios of TGF-beta1/TNF-alpha and IL-10/TNF-alpha were significantly lower in the severe malaria group. |
| 168 | 10950804 | These results suggest that the inflammatory cascade in severe malaria is characterized by suppression of the protective effects of TGF-beta1 and IL-12, and that overproduction of TNF-alpha may promote deleterious effects, such as severe anemia. |
| 169 | 10950804 | Reduced interleukin-12 and transforming growth factor-beta1 in severe childhood malaria: relationship of cytokine balance with disease severity. |
| 170 | 10950804 | IL-12 and TGF-beta1 were significantly lower, whereas tumor necrosis factor (TNF)-alpha and IL-10 were significantly higher in children with severe malaria. |
| 171 | 10950804 | The ratios of TGF-beta1/IL-12 and IL-10/IL-12 were significantly higher in the severe, compared with the mild, malaria group. |
| 172 | 10950804 | In contrast, ratios of TGF-beta1/TNF-alpha and IL-10/TNF-alpha were significantly lower in the severe malaria group. |
| 173 | 10950804 | These results suggest that the inflammatory cascade in severe malaria is characterized by suppression of the protective effects of TGF-beta1 and IL-12, and that overproduction of TNF-alpha may promote deleterious effects, such as severe anemia. |
| 174 | 10950804 | Reduced interleukin-12 and transforming growth factor-beta1 in severe childhood malaria: relationship of cytokine balance with disease severity. |
| 175 | 10950804 | IL-12 and TGF-beta1 were significantly lower, whereas tumor necrosis factor (TNF)-alpha and IL-10 were significantly higher in children with severe malaria. |
| 176 | 10950804 | The ratios of TGF-beta1/IL-12 and IL-10/IL-12 were significantly higher in the severe, compared with the mild, malaria group. |
| 177 | 10950804 | In contrast, ratios of TGF-beta1/TNF-alpha and IL-10/TNF-alpha were significantly lower in the severe malaria group. |
| 178 | 10950804 | These results suggest that the inflammatory cascade in severe malaria is characterized by suppression of the protective effects of TGF-beta1 and IL-12, and that overproduction of TNF-alpha may promote deleterious effects, such as severe anemia. |
| 179 | 10950804 | Reduced interleukin-12 and transforming growth factor-beta1 in severe childhood malaria: relationship of cytokine balance with disease severity. |
| 180 | 10950804 | IL-12 and TGF-beta1 were significantly lower, whereas tumor necrosis factor (TNF)-alpha and IL-10 were significantly higher in children with severe malaria. |
| 181 | 10950804 | The ratios of TGF-beta1/IL-12 and IL-10/IL-12 were significantly higher in the severe, compared with the mild, malaria group. |
| 182 | 10950804 | In contrast, ratios of TGF-beta1/TNF-alpha and IL-10/TNF-alpha were significantly lower in the severe malaria group. |
| 183 | 10950804 | These results suggest that the inflammatory cascade in severe malaria is characterized by suppression of the protective effects of TGF-beta1 and IL-12, and that overproduction of TNF-alpha may promote deleterious effects, such as severe anemia. |
| 184 | 10950804 | Reduced interleukin-12 and transforming growth factor-beta1 in severe childhood malaria: relationship of cytokine balance with disease severity. |
| 185 | 10950804 | IL-12 and TGF-beta1 were significantly lower, whereas tumor necrosis factor (TNF)-alpha and IL-10 were significantly higher in children with severe malaria. |
| 186 | 10950804 | The ratios of TGF-beta1/IL-12 and IL-10/IL-12 were significantly higher in the severe, compared with the mild, malaria group. |
| 187 | 10950804 | In contrast, ratios of TGF-beta1/TNF-alpha and IL-10/TNF-alpha were significantly lower in the severe malaria group. |
| 188 | 10950804 | These results suggest that the inflammatory cascade in severe malaria is characterized by suppression of the protective effects of TGF-beta1 and IL-12, and that overproduction of TNF-alpha may promote deleterious effects, such as severe anemia. |
| 189 | 11499806 | Comparative analysis of IFN-gamma B7.1 and antisense TGF-beta gene transfer on the tumorigenicity of a poorly immunogenic metastatic mammary carcinoma. |
| 190 | 11499806 | Gene therapy has been employed to counter these mechanisms of immune evasion by transference of B7.1, IFN-gamma or antisense TGF-beta genes into tumor cells, resulting in cell surface expression of B7.1, upregulation of MHC class I and class II molecules, or elimination of tumor-derived TGF-beta, respectively. |
| 191 | 11499806 | In this study, we have employed a very aggressive, poorly immunogenic and highly metastatic mammary model, 4T1, to compare the efficacy of B7.1, IFN-gamma and antisense TGF-beta gene transfer in stimulating an anti-tumor response. |
| 192 | 11499806 | We demonstrate that both IFN-gamma and antisense TGF-beta gene expression significantly reduced the tumorigenicity of these cells compared to mock transduced cells, with IFN-gamma having a greater effect. |
| 193 | 11499806 | The anti-tumor response directed against antisense TGF-beta-expressing 4T1 tumors was mediated by CD4+ and CD8+ T cells. |
| 194 | 11499806 | However, CD8+ T cells, and not CD4+ T cells, appeared to mediate the anti-tumor response against IFN-gamma-expressing tumors. |
| 195 | 11499806 | Treatment of tumor-bearing animals with IFN-gamma or antisense TGF-beta gene-modified tumor cell vaccines reduced the number of clonogenic metastases to the lungs and liver compared to treatment with mock-transduced cells. |
| 196 | 11499806 | Finally, in a residual disease model in which the primary tumor was excised and mice were vaccinated with irradiated tumor cells, treatment of mice with vaccinations consisting of 4T1 cells expressing both antisense TGF-beta and IFN-gamma genes was the most effective in prolonging survival. |
| 197 | 11499806 | Comparative analysis of IFN-gamma B7.1 and antisense TGF-beta gene transfer on the tumorigenicity of a poorly immunogenic metastatic mammary carcinoma. |
| 198 | 11499806 | Gene therapy has been employed to counter these mechanisms of immune evasion by transference of B7.1, IFN-gamma or antisense TGF-beta genes into tumor cells, resulting in cell surface expression of B7.1, upregulation of MHC class I and class II molecules, or elimination of tumor-derived TGF-beta, respectively. |
| 199 | 11499806 | In this study, we have employed a very aggressive, poorly immunogenic and highly metastatic mammary model, 4T1, to compare the efficacy of B7.1, IFN-gamma and antisense TGF-beta gene transfer in stimulating an anti-tumor response. |
| 200 | 11499806 | We demonstrate that both IFN-gamma and antisense TGF-beta gene expression significantly reduced the tumorigenicity of these cells compared to mock transduced cells, with IFN-gamma having a greater effect. |
| 201 | 11499806 | The anti-tumor response directed against antisense TGF-beta-expressing 4T1 tumors was mediated by CD4+ and CD8+ T cells. |
| 202 | 11499806 | However, CD8+ T cells, and not CD4+ T cells, appeared to mediate the anti-tumor response against IFN-gamma-expressing tumors. |
| 203 | 11499806 | Treatment of tumor-bearing animals with IFN-gamma or antisense TGF-beta gene-modified tumor cell vaccines reduced the number of clonogenic metastases to the lungs and liver compared to treatment with mock-transduced cells. |
| 204 | 11499806 | Finally, in a residual disease model in which the primary tumor was excised and mice were vaccinated with irradiated tumor cells, treatment of mice with vaccinations consisting of 4T1 cells expressing both antisense TGF-beta and IFN-gamma genes was the most effective in prolonging survival. |
| 205 | 11499806 | Comparative analysis of IFN-gamma B7.1 and antisense TGF-beta gene transfer on the tumorigenicity of a poorly immunogenic metastatic mammary carcinoma. |
| 206 | 11499806 | Gene therapy has been employed to counter these mechanisms of immune evasion by transference of B7.1, IFN-gamma or antisense TGF-beta genes into tumor cells, resulting in cell surface expression of B7.1, upregulation of MHC class I and class II molecules, or elimination of tumor-derived TGF-beta, respectively. |
| 207 | 11499806 | In this study, we have employed a very aggressive, poorly immunogenic and highly metastatic mammary model, 4T1, to compare the efficacy of B7.1, IFN-gamma and antisense TGF-beta gene transfer in stimulating an anti-tumor response. |
| 208 | 11499806 | We demonstrate that both IFN-gamma and antisense TGF-beta gene expression significantly reduced the tumorigenicity of these cells compared to mock transduced cells, with IFN-gamma having a greater effect. |
| 209 | 11499806 | The anti-tumor response directed against antisense TGF-beta-expressing 4T1 tumors was mediated by CD4+ and CD8+ T cells. |
| 210 | 11499806 | However, CD8+ T cells, and not CD4+ T cells, appeared to mediate the anti-tumor response against IFN-gamma-expressing tumors. |
| 211 | 11499806 | Treatment of tumor-bearing animals with IFN-gamma or antisense TGF-beta gene-modified tumor cell vaccines reduced the number of clonogenic metastases to the lungs and liver compared to treatment with mock-transduced cells. |
| 212 | 11499806 | Finally, in a residual disease model in which the primary tumor was excised and mice were vaccinated with irradiated tumor cells, treatment of mice with vaccinations consisting of 4T1 cells expressing both antisense TGF-beta and IFN-gamma genes was the most effective in prolonging survival. |
| 213 | 11499806 | Comparative analysis of IFN-gamma B7.1 and antisense TGF-beta gene transfer on the tumorigenicity of a poorly immunogenic metastatic mammary carcinoma. |
| 214 | 11499806 | Gene therapy has been employed to counter these mechanisms of immune evasion by transference of B7.1, IFN-gamma or antisense TGF-beta genes into tumor cells, resulting in cell surface expression of B7.1, upregulation of MHC class I and class II molecules, or elimination of tumor-derived TGF-beta, respectively. |
| 215 | 11499806 | In this study, we have employed a very aggressive, poorly immunogenic and highly metastatic mammary model, 4T1, to compare the efficacy of B7.1, IFN-gamma and antisense TGF-beta gene transfer in stimulating an anti-tumor response. |
| 216 | 11499806 | We demonstrate that both IFN-gamma and antisense TGF-beta gene expression significantly reduced the tumorigenicity of these cells compared to mock transduced cells, with IFN-gamma having a greater effect. |
| 217 | 11499806 | The anti-tumor response directed against antisense TGF-beta-expressing 4T1 tumors was mediated by CD4+ and CD8+ T cells. |
| 218 | 11499806 | However, CD8+ T cells, and not CD4+ T cells, appeared to mediate the anti-tumor response against IFN-gamma-expressing tumors. |
| 219 | 11499806 | Treatment of tumor-bearing animals with IFN-gamma or antisense TGF-beta gene-modified tumor cell vaccines reduced the number of clonogenic metastases to the lungs and liver compared to treatment with mock-transduced cells. |
| 220 | 11499806 | Finally, in a residual disease model in which the primary tumor was excised and mice were vaccinated with irradiated tumor cells, treatment of mice with vaccinations consisting of 4T1 cells expressing both antisense TGF-beta and IFN-gamma genes was the most effective in prolonging survival. |
| 221 | 11499806 | Comparative analysis of IFN-gamma B7.1 and antisense TGF-beta gene transfer on the tumorigenicity of a poorly immunogenic metastatic mammary carcinoma. |
| 222 | 11499806 | Gene therapy has been employed to counter these mechanisms of immune evasion by transference of B7.1, IFN-gamma or antisense TGF-beta genes into tumor cells, resulting in cell surface expression of B7.1, upregulation of MHC class I and class II molecules, or elimination of tumor-derived TGF-beta, respectively. |
| 223 | 11499806 | In this study, we have employed a very aggressive, poorly immunogenic and highly metastatic mammary model, 4T1, to compare the efficacy of B7.1, IFN-gamma and antisense TGF-beta gene transfer in stimulating an anti-tumor response. |
| 224 | 11499806 | We demonstrate that both IFN-gamma and antisense TGF-beta gene expression significantly reduced the tumorigenicity of these cells compared to mock transduced cells, with IFN-gamma having a greater effect. |
| 225 | 11499806 | The anti-tumor response directed against antisense TGF-beta-expressing 4T1 tumors was mediated by CD4+ and CD8+ T cells. |
| 226 | 11499806 | However, CD8+ T cells, and not CD4+ T cells, appeared to mediate the anti-tumor response against IFN-gamma-expressing tumors. |
| 227 | 11499806 | Treatment of tumor-bearing animals with IFN-gamma or antisense TGF-beta gene-modified tumor cell vaccines reduced the number of clonogenic metastases to the lungs and liver compared to treatment with mock-transduced cells. |
| 228 | 11499806 | Finally, in a residual disease model in which the primary tumor was excised and mice were vaccinated with irradiated tumor cells, treatment of mice with vaccinations consisting of 4T1 cells expressing both antisense TGF-beta and IFN-gamma genes was the most effective in prolonging survival. |
| 229 | 11499806 | Comparative analysis of IFN-gamma B7.1 and antisense TGF-beta gene transfer on the tumorigenicity of a poorly immunogenic metastatic mammary carcinoma. |
| 230 | 11499806 | Gene therapy has been employed to counter these mechanisms of immune evasion by transference of B7.1, IFN-gamma or antisense TGF-beta genes into tumor cells, resulting in cell surface expression of B7.1, upregulation of MHC class I and class II molecules, or elimination of tumor-derived TGF-beta, respectively. |
| 231 | 11499806 | In this study, we have employed a very aggressive, poorly immunogenic and highly metastatic mammary model, 4T1, to compare the efficacy of B7.1, IFN-gamma and antisense TGF-beta gene transfer in stimulating an anti-tumor response. |
| 232 | 11499806 | We demonstrate that both IFN-gamma and antisense TGF-beta gene expression significantly reduced the tumorigenicity of these cells compared to mock transduced cells, with IFN-gamma having a greater effect. |
| 233 | 11499806 | The anti-tumor response directed against antisense TGF-beta-expressing 4T1 tumors was mediated by CD4+ and CD8+ T cells. |
| 234 | 11499806 | However, CD8+ T cells, and not CD4+ T cells, appeared to mediate the anti-tumor response against IFN-gamma-expressing tumors. |
| 235 | 11499806 | Treatment of tumor-bearing animals with IFN-gamma or antisense TGF-beta gene-modified tumor cell vaccines reduced the number of clonogenic metastases to the lungs and liver compared to treatment with mock-transduced cells. |
| 236 | 11499806 | Finally, in a residual disease model in which the primary tumor was excised and mice were vaccinated with irradiated tumor cells, treatment of mice with vaccinations consisting of 4T1 cells expressing both antisense TGF-beta and IFN-gamma genes was the most effective in prolonging survival. |
| 237 | 11499806 | Comparative analysis of IFN-gamma B7.1 and antisense TGF-beta gene transfer on the tumorigenicity of a poorly immunogenic metastatic mammary carcinoma. |
| 238 | 11499806 | Gene therapy has been employed to counter these mechanisms of immune evasion by transference of B7.1, IFN-gamma or antisense TGF-beta genes into tumor cells, resulting in cell surface expression of B7.1, upregulation of MHC class I and class II molecules, or elimination of tumor-derived TGF-beta, respectively. |
| 239 | 11499806 | In this study, we have employed a very aggressive, poorly immunogenic and highly metastatic mammary model, 4T1, to compare the efficacy of B7.1, IFN-gamma and antisense TGF-beta gene transfer in stimulating an anti-tumor response. |
| 240 | 11499806 | We demonstrate that both IFN-gamma and antisense TGF-beta gene expression significantly reduced the tumorigenicity of these cells compared to mock transduced cells, with IFN-gamma having a greater effect. |
| 241 | 11499806 | The anti-tumor response directed against antisense TGF-beta-expressing 4T1 tumors was mediated by CD4+ and CD8+ T cells. |
| 242 | 11499806 | However, CD8+ T cells, and not CD4+ T cells, appeared to mediate the anti-tumor response against IFN-gamma-expressing tumors. |
| 243 | 11499806 | Treatment of tumor-bearing animals with IFN-gamma or antisense TGF-beta gene-modified tumor cell vaccines reduced the number of clonogenic metastases to the lungs and liver compared to treatment with mock-transduced cells. |
| 244 | 11499806 | Finally, in a residual disease model in which the primary tumor was excised and mice were vaccinated with irradiated tumor cells, treatment of mice with vaccinations consisting of 4T1 cells expressing both antisense TGF-beta and IFN-gamma genes was the most effective in prolonging survival. |
| 245 | 11578774 | The lessons learned from these models are of great interest not only for understanding of the role of TGF-beta in AD, but also for future treatments where testing of anti-inflammatory agents such as ibuprofen and an amyloid vaccine hold great promise. |
| 246 | 11585761 | Using HSVtk suicide gene therapy, we showed that macrophages can distinguish between tumor cells dying through classical apoptosis and tumor cells engineered to die through nonapoptotic mechanisms, resulting in secretion of either immunosuppressive cytokines (interleukin 10 and transforming growth factor beta) or inflammatory cytokines (tumor necrosis factor alpha or interleukin 1beta), respectively. |
| 247 | 11709285 | However, the inhibition is not alleviated by blocking with antibodies to IL-4, IL-10 or TGF-beta. |
| 248 | 11709285 | Fractionation of the splenocyte population from S. mansoni-infected mice shows that the suppression is mediated by a non-B, non-T cell that expresses CD16 and Mac-1, but not FcepsilonR or NK1.1. |
| 249 | 11714814 | Depletion of the CD4+ T cell subset considerably reduces the ability of Lm-LLO-E7 to eliminate established TC-1 tumors. |
| 250 | 11714814 | Ab-mediated depletion of TGF-beta and CD25+ cells improves the effectiveness of Lm-E7 treatment, suggesting that TGF-beta and CD25+ cells are in part responsible for this suppressive response. |
| 251 | 11714814 | CD4+ T cells from mice immunized with Lm-E7 are capable of suppressing the ability of Lm-LLO-E7 to induce the regression of TC-1 when transferred to tumor-bearing mice. |
| 252 | 11735339 | Comparison of expression levels of several potential immune inhibitory mediators between the tumors growing in mice and cultured tumor cells demonstrated higher expression of IL-10, GM-CSF, TGF-beta, and NO synthetase in tumors. |
| 253 | 11772233 | Features of the pathophysiology of von Hippel Lindau protein are described, with attention to potential novel therapies targeting HIF-1alpha, VEGF, TGF-beta1 and TGF-alpha pathways. |
| 254 | 11772233 | Most basic are cytokine therapies incorporating new IL-2 and IFN-alpha schedules. |
| 255 | 11826917 | Interleukin-12 and interleukin-18 are macrophage products that favor the development of Th1 type of protective immune response. |
| 256 | 11826917 | The production of anti-inflammatory cytokines such as IL-10, TGF-beta and IL-4 in response to M. tuberculosis may down regulate the immune response and limit tissue injury by inhibiting excessive inflammatory response. |
| 257 | 12007887 | Distinct T (CD4+, CD8+, gammadelta-TCR+) and B (CD21+, CD45R+) lymphocyte staining patterns were observed within and around follicles of the rectal mucosa. |
| 258 | 12007887 | RT-PCR examination of the cytokines expressed in the rectal mucosal tissue revealed consistently high levels of TGFbeta and IL-8 mRNA, low levels of IL-2 mRNA and no detectable IL-4 mRNA. |
| 259 | 12021842 | Female NOD mice were treated orally with ICAM-1, TGF-beta, or control plasmid DNA and received a single injection of cyclophosphamide for synchronization and acceleration of the disease process in the pancreas. |
| 260 | 12021842 | Quantitative RT-PCR analysis of pancreatic mRNA showed that cyclophosphamide induced the expression of Th1 cytokines (IFN-gamma and IL-12p40) in vehicle- or control plasmid-treated mice. |
| 261 | 12021842 | Treatment with ICAM-1 and TGF-beta DNA resulted in increased levels of IL-10 mRNA in the pancreas, indicating an anti-inflammatory regulatory immune response. |
| 262 | 12021842 | We conclude that oral vaccination with DNA encoding immunoregulatory molecules such as ICAM-1 and TGF-beta represents an approach for modulating the ongoing inflammatory process in the pancreas of diabetes prone NOD mice. |
| 263 | 12021842 | Female NOD mice were treated orally with ICAM-1, TGF-beta, or control plasmid DNA and received a single injection of cyclophosphamide for synchronization and acceleration of the disease process in the pancreas. |
| 264 | 12021842 | Quantitative RT-PCR analysis of pancreatic mRNA showed that cyclophosphamide induced the expression of Th1 cytokines (IFN-gamma and IL-12p40) in vehicle- or control plasmid-treated mice. |
| 265 | 12021842 | Treatment with ICAM-1 and TGF-beta DNA resulted in increased levels of IL-10 mRNA in the pancreas, indicating an anti-inflammatory regulatory immune response. |
| 266 | 12021842 | We conclude that oral vaccination with DNA encoding immunoregulatory molecules such as ICAM-1 and TGF-beta represents an approach for modulating the ongoing inflammatory process in the pancreas of diabetes prone NOD mice. |
| 267 | 12021842 | Female NOD mice were treated orally with ICAM-1, TGF-beta, or control plasmid DNA and received a single injection of cyclophosphamide for synchronization and acceleration of the disease process in the pancreas. |
| 268 | 12021842 | Quantitative RT-PCR analysis of pancreatic mRNA showed that cyclophosphamide induced the expression of Th1 cytokines (IFN-gamma and IL-12p40) in vehicle- or control plasmid-treated mice. |
| 269 | 12021842 | Treatment with ICAM-1 and TGF-beta DNA resulted in increased levels of IL-10 mRNA in the pancreas, indicating an anti-inflammatory regulatory immune response. |
| 270 | 12021842 | We conclude that oral vaccination with DNA encoding immunoregulatory molecules such as ICAM-1 and TGF-beta represents an approach for modulating the ongoing inflammatory process in the pancreas of diabetes prone NOD mice. |
| 271 | 12100028 | The cell lines expressed HLA-A2 as well as shared tumour-associated antigens (TAAs) representative of colon carcinomas: CEA, Ep-CAM, MUC1, HER2/neu and MAGE antigens. |
| 272 | 12100028 | They did not secrete high levels of the immunosuppressive factors TGF-beta, IL-10 or prostaglandins. |
| 273 | 12191514 | We have assessed the optimal conditions in terms of dose and kinetics of those cytokines which are released early (TNF-alpha, IL6 and TGF-beta, IL10) or (interferon [IFN]-gamma and IL5) in WB cultures stimulated with mitogens and mycobacterial antigens. |
| 274 | 12191514 | Using unpaired Student's t-tests, pulmonary tuberculosis patients (P.TB; n=11), in response to CFP, showed higher monocyte-derived IL6 (p=0.023) and IL10 (p=0.042) compared to endemic controls (EC; n=13), and significantly suppressed T-cell-derived IFN-gamma (p=0.028) and IL5 (p=0.012) secretion but increased IL10 (p=0.047) on day 5, indicating that CFP is a strong stimulus for IL10 secretion in pulmonary TB patients. |
| 275 | 12191514 | Extrapulmonary TB patients (E.TB; n=6) showed no elevation of early monocyte-derived cytokines to either PPD or CFP, but showed a marked suppression of the T-cell-derived cytokines IFN-gamma (PPD, p=0.015; CFP, p=0.05) and IL5 (PPD, p=0.05; CFP, p=0.015). |
| 276 | 12193750 | In this study, we measured the prevalence of T(reg) that coexpress CD4 and CD25 in the PBLs, tumor-infiltrating lymphocytes, and regional lymph node lymphocytes from 65 patients with either pancreas or breast cancer. |
| 277 | 12193750 | T(reg) constitutively coexpressed CTLA-4 and CD45RO markers, and secreted TGF-beta and IL-10 but did not secrete IFN-gamma. |
| 278 | 12193750 | When cocultured with activated CD8(+) cells or CD4(+)25(-) cells, T(reg) potently suppressed their proliferation and secretion of IFN-gamma. |
| 279 | 12438333 | Dynamics of gamma interferon, interleukin-12 (IL-12), IL-10, and transforming growth factor beta mRNA expression in primary Mycobacterium bovis BCG infection in guinea pigs measured by a real-time fluorogenic reverse transcription-PCR assay. |
| 280 | 12438333 | Initially, we established a quantitative assay using a real-time reverse transcription-PCR (RT-PCR) to measure guinea pig gamma interferon (IFN-gamma), interleukin-12 (IL-12), IL-10, and transforming growth factor beta (TGF-beta) mRNA. |
| 281 | 12438333 | The expression of IL-10 and TGF-beta increased slightly only in PBMCs. |
| 282 | 12438333 | In this study, we quantitatively measured IL-10, IL-12, TGF-beta, and IFN-gamma mRNA in BCG-immunized guinea pigs and showed that the level of IFN-gamma mRNA expression does not necessarily reflect the magnitude of the DTH response, suggesting that there may be an intricate relationship between protective immunity, the level of IFN-gamma, and the DTH response. |
| 283 | 12438333 | Dynamics of gamma interferon, interleukin-12 (IL-12), IL-10, and transforming growth factor beta mRNA expression in primary Mycobacterium bovis BCG infection in guinea pigs measured by a real-time fluorogenic reverse transcription-PCR assay. |
| 284 | 12438333 | Initially, we established a quantitative assay using a real-time reverse transcription-PCR (RT-PCR) to measure guinea pig gamma interferon (IFN-gamma), interleukin-12 (IL-12), IL-10, and transforming growth factor beta (TGF-beta) mRNA. |
| 285 | 12438333 | The expression of IL-10 and TGF-beta increased slightly only in PBMCs. |
| 286 | 12438333 | In this study, we quantitatively measured IL-10, IL-12, TGF-beta, and IFN-gamma mRNA in BCG-immunized guinea pigs and showed that the level of IFN-gamma mRNA expression does not necessarily reflect the magnitude of the DTH response, suggesting that there may be an intricate relationship between protective immunity, the level of IFN-gamma, and the DTH response. |
| 287 | 12438333 | Dynamics of gamma interferon, interleukin-12 (IL-12), IL-10, and transforming growth factor beta mRNA expression in primary Mycobacterium bovis BCG infection in guinea pigs measured by a real-time fluorogenic reverse transcription-PCR assay. |
| 288 | 12438333 | Initially, we established a quantitative assay using a real-time reverse transcription-PCR (RT-PCR) to measure guinea pig gamma interferon (IFN-gamma), interleukin-12 (IL-12), IL-10, and transforming growth factor beta (TGF-beta) mRNA. |
| 289 | 12438333 | The expression of IL-10 and TGF-beta increased slightly only in PBMCs. |
| 290 | 12438333 | In this study, we quantitatively measured IL-10, IL-12, TGF-beta, and IFN-gamma mRNA in BCG-immunized guinea pigs and showed that the level of IFN-gamma mRNA expression does not necessarily reflect the magnitude of the DTH response, suggesting that there may be an intricate relationship between protective immunity, the level of IFN-gamma, and the DTH response. |
| 291 | 12438333 | Dynamics of gamma interferon, interleukin-12 (IL-12), IL-10, and transforming growth factor beta mRNA expression in primary Mycobacterium bovis BCG infection in guinea pigs measured by a real-time fluorogenic reverse transcription-PCR assay. |
| 292 | 12438333 | Initially, we established a quantitative assay using a real-time reverse transcription-PCR (RT-PCR) to measure guinea pig gamma interferon (IFN-gamma), interleukin-12 (IL-12), IL-10, and transforming growth factor beta (TGF-beta) mRNA. |
| 293 | 12438333 | The expression of IL-10 and TGF-beta increased slightly only in PBMCs. |
| 294 | 12438333 | In this study, we quantitatively measured IL-10, IL-12, TGF-beta, and IFN-gamma mRNA in BCG-immunized guinea pigs and showed that the level of IFN-gamma mRNA expression does not necessarily reflect the magnitude of the DTH response, suggesting that there may be an intricate relationship between protective immunity, the level of IFN-gamma, and the DTH response. |
| 295 | 12444136 | B7/CD28-dependent CD4+CD25+ regulatory T cells are essential components of the memory-protective immunity to Candida albicans. |
| 296 | 12444136 | Here we show that CD4(+)CD25(+) T cells, negatively regulating antifungal Th1 reactivity, are generated in mice with candidiasis. |
| 297 | 12444136 | CD4(+)CD25(+) T cells were not generated in B7-2- or CD28-deficient mice or in condition of IL-10 signaling deficiency. |
| 298 | 12444136 | CD4(+)CD25(+) T cells poorly proliferated in vitro; were highly enriched for cells producing IL-4, IL-10, and TGF-beta; and required IL-10-producing, Candida hypha-activated dendritic cells for generation. |
| 299 | 12444136 | Adoptive transfer of CD4(+)CD25(+) T cells or IL-10-producing dendritic cells restored resistance to reinfection and decreased inflammation in B7-2-deficient mice. |
| 300 | 12472671 | Proteasome subunit alpha type 3 (PSMA3), transcription factor EC (TFEC) isoform and BTK region clone 2f10-rpi were transiently upregulated. |
| 301 | 12472671 | Tryptophanyl-tRNA synthetase and CD63 antigen were upregulated for at least 24 h. |
| 302 | 12472671 | Neuronal apoptosis inhibitory protein (NAIP) and transforming growth factor-beta-induced 68 kDa protein were downregulated. |
| 303 | 12472671 | By comparing the expression of NAIP with that of other members of the inhibitor of apoptosis protein (IAP) family and the Bcl-2 family, only NAIP was found to be strongly expressed in iDCs before stimulation by LPS. |
| 304 | 12522049 | Interestingly, the level of epithelial staining for several cytokines, e.g., interleukin-8 (IL-8), transforming growth factor beta (TGF-beta), and gamma interferon (IFN-gamma), was found to be significantly lower in DU patients than in AS carriers and uninfected individuals. |
| 305 | 12522049 | However, larger numbers of IL-8-, IL-6-, TGF-beta-, and IFN-gamma-positive mononuclear cells were observed in the duodenal lamina propria of both DU patients and AS carriers than in that of the uninfected controls. |
| 306 | 12522049 | Interestingly, the level of epithelial staining for several cytokines, e.g., interleukin-8 (IL-8), transforming growth factor beta (TGF-beta), and gamma interferon (IFN-gamma), was found to be significantly lower in DU patients than in AS carriers and uninfected individuals. |
| 307 | 12522049 | However, larger numbers of IL-8-, IL-6-, TGF-beta-, and IFN-gamma-positive mononuclear cells were observed in the duodenal lamina propria of both DU patients and AS carriers than in that of the uninfected controls. |
| 308 | 12641655 | Peripheral blood monocytes were differentiated into immature DCs with interleukin-4 (IL-4) and granulocyte-macrophage colony-stimulating factor, and pulsed with an immunogenic tetanus toxoid peptide. |
| 309 | 12641655 | However, stimulation with antigen-pulsed DCs overexpressing IotakappaBetaalpha, the endogenous inhibitor of NF-kappaB, led to a significant reduction in T-cell proliferation, and decreased production of interferon-gamma, IL-4 and IL-10, whereas transforming growth factor-beta production was low throughout. |
| 310 | 12654790 | Increases in tumor necrosis factor alpha, interleukin-6, transforming growth factor beta, and vascular endothelial growth factor mRNA expression were associated with the enhancement of intracellular BCG growth. |
| 311 | 12654790 | Increases in gamma interferon, FAS, FAS ligand, perforin, granzyme, and granulysin mRNA expression were associated with intracellular BCG inhibition. |
| 312 | 12704173 | The induction of IgA was well correlated with an increased production of transforming growth factor beta1. |
| 313 | 12803883 | Prostaglandins, interleukin-(IL-)10, and transforming growth factor-beta are other players of in vivo endotoxin tolerance. |
| 314 | 12803883 | Cross-tolerance between LPS, TLR2 specific ligands, IL-1 and TNF has been regularly reported. |
| 315 | 12810183 | They appear to exert their effects by producing a Th2 to Th1 shift, as well as inducing regulatory cytokines such as interleukin-10 and transforming growth factor-beta. |
| 316 | 12820727 | The mature CTLs secrete IFN-gamma and are cytolytic against MUC1-expressing tumor cells in vitro. |
| 317 | 12820727 | The pancreas tumor cells secrete immunosuppressive cytokines, including IL-10 and TGF-beta that are partly responsible for the down-regulation of CTL activity. |
| 318 | 12820727 | CD4+ CD25+ T regulatory cells, which secrete IL-10, were also found in the tumor environment. |
| 319 | 12894571 | These problems emanate from the following mechanisms that the tumor cells are employing to avoid detection and destruction by the immune system: (i) Down-regulation of HLA class I expression on the surface of tumor cells; (ii) Down-regulation of tumor antigen expression or selection of negative tumor variants; (iii) Expression of naturally occurring altered peptide ligands by tumor cells; (iv) Lack of costimulatory molecules on tumors cells; (v) Production of immunosuppressive cytokines, such as TGF-beta and IL-10; (vi) Induction of lymphocyte apoptosis by tumor cells using the Fas/Fas L pathway; (vii) Down-regulation or absence of CD3 zeta (zeta) transcripts or protein in tumor-infiltrating lymphocytes (TIL), and others. |
| 320 | 12957792 | To understand the pathogenesis of vaccine-modified measles (VMM), we measured plasma levels of IFN-gamma and IL-2 (Th1 cytokines), IL-4 and IL-10 (Th2 cytokines), IL-12, TNF-alpha and TGF-beta1 in children with uncomplicated measles, who had anti-measles IgG antibodies and with a history of immunization on admission (day 0), day 14 and day 60. |
| 321 | 12957792 | Plasma levels of IFN-gamma, IL-2 and IL-12 were significantly higher in VMM patients on day 0 compared to healthy controls (p = 0.023; p = 0.018; p = 0.001) respectively. |
| 322 | 12957792 | Kinetically, IFN-gamma and IL-10 levels decreased consistently from day 0 to days 14 and 60 in VMM patients. |
| 323 | 14607947 | C57BL/6 mice infected with a nonlethal (Py17X) strain of Plasmodium yoelii produce TGF-beta from 5 days postinfection; this correlates with resolution of parasitemia, down-regulation of TNF-alpha, and full recovery. |
| 324 | 14607947 | In contrast, infection with the lethal strain Py17XL induces high levels of circulating TGF-beta within 24 h; this is associated with delayed and blunted IFN-gamma and TNF-alpha responses, failure to clear parasites, and 100% mortality. |
| 325 | 14607947 | Neutralization of early TGF-beta in Py17XL infection leads to a compensatory increase in IL-10 production, while simultaneous neutralization of TGF-beta and IL-10R signaling leads to up-regulation of TNF-alpha and IFN-gamma, prolonged survival in all, and ultimate resolution of infection in 40% of Py17XL-infected animals. |
| 326 | 14607947 | TGF-beta production can be induced in an Ag-specific manner from splenocytes of infected mice, and by cross-linking surface CTLA-4. |
| 327 | 14607947 | CD25(+) and CD8(+) cells are the primary source of TGF-beta following Py17X stimulation of splenocytes, whereas Py17XL induces significant production of TGF-beta from adherent cells. |
| 328 | 14607947 | In mice immunized against Py17XL, the early TGF-beta response is inhibited and is accompanied by significant up-regulation of IFN-gamma and TNF-alpha and rapid resolution of challenge infections. |
| 329 | 14607947 | C57BL/6 mice infected with a nonlethal (Py17X) strain of Plasmodium yoelii produce TGF-beta from 5 days postinfection; this correlates with resolution of parasitemia, down-regulation of TNF-alpha, and full recovery. |
| 330 | 14607947 | In contrast, infection with the lethal strain Py17XL induces high levels of circulating TGF-beta within 24 h; this is associated with delayed and blunted IFN-gamma and TNF-alpha responses, failure to clear parasites, and 100% mortality. |
| 331 | 14607947 | Neutralization of early TGF-beta in Py17XL infection leads to a compensatory increase in IL-10 production, while simultaneous neutralization of TGF-beta and IL-10R signaling leads to up-regulation of TNF-alpha and IFN-gamma, prolonged survival in all, and ultimate resolution of infection in 40% of Py17XL-infected animals. |
| 332 | 14607947 | TGF-beta production can be induced in an Ag-specific manner from splenocytes of infected mice, and by cross-linking surface CTLA-4. |
| 333 | 14607947 | CD25(+) and CD8(+) cells are the primary source of TGF-beta following Py17X stimulation of splenocytes, whereas Py17XL induces significant production of TGF-beta from adherent cells. |
| 334 | 14607947 | In mice immunized against Py17XL, the early TGF-beta response is inhibited and is accompanied by significant up-regulation of IFN-gamma and TNF-alpha and rapid resolution of challenge infections. |
| 335 | 14607947 | C57BL/6 mice infected with a nonlethal (Py17X) strain of Plasmodium yoelii produce TGF-beta from 5 days postinfection; this correlates with resolution of parasitemia, down-regulation of TNF-alpha, and full recovery. |
| 336 | 14607947 | In contrast, infection with the lethal strain Py17XL induces high levels of circulating TGF-beta within 24 h; this is associated with delayed and blunted IFN-gamma and TNF-alpha responses, failure to clear parasites, and 100% mortality. |
| 337 | 14607947 | Neutralization of early TGF-beta in Py17XL infection leads to a compensatory increase in IL-10 production, while simultaneous neutralization of TGF-beta and IL-10R signaling leads to up-regulation of TNF-alpha and IFN-gamma, prolonged survival in all, and ultimate resolution of infection in 40% of Py17XL-infected animals. |
| 338 | 14607947 | TGF-beta production can be induced in an Ag-specific manner from splenocytes of infected mice, and by cross-linking surface CTLA-4. |
| 339 | 14607947 | CD25(+) and CD8(+) cells are the primary source of TGF-beta following Py17X stimulation of splenocytes, whereas Py17XL induces significant production of TGF-beta from adherent cells. |
| 340 | 14607947 | In mice immunized against Py17XL, the early TGF-beta response is inhibited and is accompanied by significant up-regulation of IFN-gamma and TNF-alpha and rapid resolution of challenge infections. |
| 341 | 14607947 | C57BL/6 mice infected with a nonlethal (Py17X) strain of Plasmodium yoelii produce TGF-beta from 5 days postinfection; this correlates with resolution of parasitemia, down-regulation of TNF-alpha, and full recovery. |
| 342 | 14607947 | In contrast, infection with the lethal strain Py17XL induces high levels of circulating TGF-beta within 24 h; this is associated with delayed and blunted IFN-gamma and TNF-alpha responses, failure to clear parasites, and 100% mortality. |
| 343 | 14607947 | Neutralization of early TGF-beta in Py17XL infection leads to a compensatory increase in IL-10 production, while simultaneous neutralization of TGF-beta and IL-10R signaling leads to up-regulation of TNF-alpha and IFN-gamma, prolonged survival in all, and ultimate resolution of infection in 40% of Py17XL-infected animals. |
| 344 | 14607947 | TGF-beta production can be induced in an Ag-specific manner from splenocytes of infected mice, and by cross-linking surface CTLA-4. |
| 345 | 14607947 | CD25(+) and CD8(+) cells are the primary source of TGF-beta following Py17X stimulation of splenocytes, whereas Py17XL induces significant production of TGF-beta from adherent cells. |
| 346 | 14607947 | In mice immunized against Py17XL, the early TGF-beta response is inhibited and is accompanied by significant up-regulation of IFN-gamma and TNF-alpha and rapid resolution of challenge infections. |
| 347 | 14607947 | C57BL/6 mice infected with a nonlethal (Py17X) strain of Plasmodium yoelii produce TGF-beta from 5 days postinfection; this correlates with resolution of parasitemia, down-regulation of TNF-alpha, and full recovery. |
| 348 | 14607947 | In contrast, infection with the lethal strain Py17XL induces high levels of circulating TGF-beta within 24 h; this is associated with delayed and blunted IFN-gamma and TNF-alpha responses, failure to clear parasites, and 100% mortality. |
| 349 | 14607947 | Neutralization of early TGF-beta in Py17XL infection leads to a compensatory increase in IL-10 production, while simultaneous neutralization of TGF-beta and IL-10R signaling leads to up-regulation of TNF-alpha and IFN-gamma, prolonged survival in all, and ultimate resolution of infection in 40% of Py17XL-infected animals. |
| 350 | 14607947 | TGF-beta production can be induced in an Ag-specific manner from splenocytes of infected mice, and by cross-linking surface CTLA-4. |
| 351 | 14607947 | CD25(+) and CD8(+) cells are the primary source of TGF-beta following Py17X stimulation of splenocytes, whereas Py17XL induces significant production of TGF-beta from adherent cells. |
| 352 | 14607947 | In mice immunized against Py17XL, the early TGF-beta response is inhibited and is accompanied by significant up-regulation of IFN-gamma and TNF-alpha and rapid resolution of challenge infections. |
| 353 | 14607947 | C57BL/6 mice infected with a nonlethal (Py17X) strain of Plasmodium yoelii produce TGF-beta from 5 days postinfection; this correlates with resolution of parasitemia, down-regulation of TNF-alpha, and full recovery. |
| 354 | 14607947 | In contrast, infection with the lethal strain Py17XL induces high levels of circulating TGF-beta within 24 h; this is associated with delayed and blunted IFN-gamma and TNF-alpha responses, failure to clear parasites, and 100% mortality. |
| 355 | 14607947 | Neutralization of early TGF-beta in Py17XL infection leads to a compensatory increase in IL-10 production, while simultaneous neutralization of TGF-beta and IL-10R signaling leads to up-regulation of TNF-alpha and IFN-gamma, prolonged survival in all, and ultimate resolution of infection in 40% of Py17XL-infected animals. |
| 356 | 14607947 | TGF-beta production can be induced in an Ag-specific manner from splenocytes of infected mice, and by cross-linking surface CTLA-4. |
| 357 | 14607947 | CD25(+) and CD8(+) cells are the primary source of TGF-beta following Py17X stimulation of splenocytes, whereas Py17XL induces significant production of TGF-beta from adherent cells. |
| 358 | 14607947 | In mice immunized against Py17XL, the early TGF-beta response is inhibited and is accompanied by significant up-regulation of IFN-gamma and TNF-alpha and rapid resolution of challenge infections. |
| 359 | 14632664 | RNA samples from stimulated and unstimulated chicken thymocytes were assayed for messenger RNA encoding the cytokines interleukin-1beta (IL-1beta), IL-2, interferon-alpha (IFN-alpha), IFN-beta, IFN-gamma and transforming growth factor-beta4 (TGF-beta4), and also components of the major histocompatibility complex (MHC), beta2-microglobulin (beta2M) and the MHC class I alpha-chain (MHC IA). |
| 360 | 14632664 | Mitogen stimulation of embryonic day 18 and day 1 post-hatch thymocytes induced up-regulation of IFN-gamma, IL-1beta and TGF-beta transcripts, and down-regulation of IFN-alpha, IFN-beta and IL-2 transcripts, with a higher induction of IFN-gamma, IL-1beta and TGF-beta transcripts in more immature T-cell-receptor-negative (TCR-) than TCR+ (TCR1+, TCR2+, or TCR3+) subsets. |
| 361 | 14632664 | Thymocytes from embryonic day 14 chicks responded to mitogen with a short burst of unsustained proliferation, and transcriptional down-regulation of the cytokines IL-2, IL-1beta, IFN-alpha, IFN-beta and IFN-gamma. |
| 362 | 14632664 | Transcripts encoding TGF-beta and type I interferons (IFN-alpha and IFN-beta) were constitutively expressed at high levels in very early thymocytes at embryonic day 14. |
| 363 | 14632664 | RNA samples from stimulated and unstimulated chicken thymocytes were assayed for messenger RNA encoding the cytokines interleukin-1beta (IL-1beta), IL-2, interferon-alpha (IFN-alpha), IFN-beta, IFN-gamma and transforming growth factor-beta4 (TGF-beta4), and also components of the major histocompatibility complex (MHC), beta2-microglobulin (beta2M) and the MHC class I alpha-chain (MHC IA). |
| 364 | 14632664 | Mitogen stimulation of embryonic day 18 and day 1 post-hatch thymocytes induced up-regulation of IFN-gamma, IL-1beta and TGF-beta transcripts, and down-regulation of IFN-alpha, IFN-beta and IL-2 transcripts, with a higher induction of IFN-gamma, IL-1beta and TGF-beta transcripts in more immature T-cell-receptor-negative (TCR-) than TCR+ (TCR1+, TCR2+, or TCR3+) subsets. |
| 365 | 14632664 | Thymocytes from embryonic day 14 chicks responded to mitogen with a short burst of unsustained proliferation, and transcriptional down-regulation of the cytokines IL-2, IL-1beta, IFN-alpha, IFN-beta and IFN-gamma. |
| 366 | 14632664 | Transcripts encoding TGF-beta and type I interferons (IFN-alpha and IFN-beta) were constitutively expressed at high levels in very early thymocytes at embryonic day 14. |
| 367 | 14657224 | Transforming growth factor-beta production and myeloid cells are an effector mechanism through which CD1d-restricted T cells block cytotoxic T lymphocyte-mediated tumor immunosurveillance: abrogation prevents tumor recurrence. |
| 368 | 14657224 | Our previous work demonstrated that cytotoxic T lymphocyte (CTL)-mediated tumor immunosurveillance of the 15-12RM tumor could be suppressed by a CD1d-restricted lymphocyte, most likely a natural killer (NK) T cell, which produces interleukin (IL)-13. |
| 369 | 14657224 | T cell-reconstituted recombination activating gene (RAG)2 knockout (KO) and RAG2/IL-4 receptor alpha double KO mice showed that inhibition of immunosurveillance requires IL-13 responsiveness by a non-T non-B cell. |
| 370 | 14657224 | Such nonlymphoid splenocytes from tumor-bearing mice produced more transforming growth factor (TGF)-beta, a potent inhibitor of CTL, ex vivo than such cells from naive mice, and this TGF-beta production was dependent on the presence in vivo of both IL-13 and CD1d-restricted T cells. |
| 371 | 14657224 | Further, blocking TGF-beta or depleting Gr-1+ cells in vivo prevented the tumor recurrence, implying that TGF-beta made by a CD11b+ Gr-1+ myeloid cell, in an IL-13 and CD1d-restricted T cell-dependent mechanism, is necessary for down-regulation of tumor immunosurveillance. |
| 372 | 14657224 | Identification of this stepwise regulation of immunosurveillance, involving CD1-restricted T cells, IL-13, myeloid cells, and TGF-beta, explains previous observations on myeloid suppressor cells or TGF-beta and provides insights for targeted approaches for cancer immunotherapy, including synergistic blockade of TGF-beta and IL-13. |
| 373 | 14657224 | Transforming growth factor-beta production and myeloid cells are an effector mechanism through which CD1d-restricted T cells block cytotoxic T lymphocyte-mediated tumor immunosurveillance: abrogation prevents tumor recurrence. |
| 374 | 14657224 | Our previous work demonstrated that cytotoxic T lymphocyte (CTL)-mediated tumor immunosurveillance of the 15-12RM tumor could be suppressed by a CD1d-restricted lymphocyte, most likely a natural killer (NK) T cell, which produces interleukin (IL)-13. |
| 375 | 14657224 | T cell-reconstituted recombination activating gene (RAG)2 knockout (KO) and RAG2/IL-4 receptor alpha double KO mice showed that inhibition of immunosurveillance requires IL-13 responsiveness by a non-T non-B cell. |
| 376 | 14657224 | Such nonlymphoid splenocytes from tumor-bearing mice produced more transforming growth factor (TGF)-beta, a potent inhibitor of CTL, ex vivo than such cells from naive mice, and this TGF-beta production was dependent on the presence in vivo of both IL-13 and CD1d-restricted T cells. |
| 377 | 14657224 | Further, blocking TGF-beta or depleting Gr-1+ cells in vivo prevented the tumor recurrence, implying that TGF-beta made by a CD11b+ Gr-1+ myeloid cell, in an IL-13 and CD1d-restricted T cell-dependent mechanism, is necessary for down-regulation of tumor immunosurveillance. |
| 378 | 14657224 | Identification of this stepwise regulation of immunosurveillance, involving CD1-restricted T cells, IL-13, myeloid cells, and TGF-beta, explains previous observations on myeloid suppressor cells or TGF-beta and provides insights for targeted approaches for cancer immunotherapy, including synergistic blockade of TGF-beta and IL-13. |
| 379 | 14657224 | Transforming growth factor-beta production and myeloid cells are an effector mechanism through which CD1d-restricted T cells block cytotoxic T lymphocyte-mediated tumor immunosurveillance: abrogation prevents tumor recurrence. |
| 380 | 14657224 | Our previous work demonstrated that cytotoxic T lymphocyte (CTL)-mediated tumor immunosurveillance of the 15-12RM tumor could be suppressed by a CD1d-restricted lymphocyte, most likely a natural killer (NK) T cell, which produces interleukin (IL)-13. |
| 381 | 14657224 | T cell-reconstituted recombination activating gene (RAG)2 knockout (KO) and RAG2/IL-4 receptor alpha double KO mice showed that inhibition of immunosurveillance requires IL-13 responsiveness by a non-T non-B cell. |
| 382 | 14657224 | Such nonlymphoid splenocytes from tumor-bearing mice produced more transforming growth factor (TGF)-beta, a potent inhibitor of CTL, ex vivo than such cells from naive mice, and this TGF-beta production was dependent on the presence in vivo of both IL-13 and CD1d-restricted T cells. |
| 383 | 14657224 | Further, blocking TGF-beta or depleting Gr-1+ cells in vivo prevented the tumor recurrence, implying that TGF-beta made by a CD11b+ Gr-1+ myeloid cell, in an IL-13 and CD1d-restricted T cell-dependent mechanism, is necessary for down-regulation of tumor immunosurveillance. |
| 384 | 14657224 | Identification of this stepwise regulation of immunosurveillance, involving CD1-restricted T cells, IL-13, myeloid cells, and TGF-beta, explains previous observations on myeloid suppressor cells or TGF-beta and provides insights for targeted approaches for cancer immunotherapy, including synergistic blockade of TGF-beta and IL-13. |
| 385 | 14657224 | Transforming growth factor-beta production and myeloid cells are an effector mechanism through which CD1d-restricted T cells block cytotoxic T lymphocyte-mediated tumor immunosurveillance: abrogation prevents tumor recurrence. |
| 386 | 14657224 | Our previous work demonstrated that cytotoxic T lymphocyte (CTL)-mediated tumor immunosurveillance of the 15-12RM tumor could be suppressed by a CD1d-restricted lymphocyte, most likely a natural killer (NK) T cell, which produces interleukin (IL)-13. |
| 387 | 14657224 | T cell-reconstituted recombination activating gene (RAG)2 knockout (KO) and RAG2/IL-4 receptor alpha double KO mice showed that inhibition of immunosurveillance requires IL-13 responsiveness by a non-T non-B cell. |
| 388 | 14657224 | Such nonlymphoid splenocytes from tumor-bearing mice produced more transforming growth factor (TGF)-beta, a potent inhibitor of CTL, ex vivo than such cells from naive mice, and this TGF-beta production was dependent on the presence in vivo of both IL-13 and CD1d-restricted T cells. |
| 389 | 14657224 | Further, blocking TGF-beta or depleting Gr-1+ cells in vivo prevented the tumor recurrence, implying that TGF-beta made by a CD11b+ Gr-1+ myeloid cell, in an IL-13 and CD1d-restricted T cell-dependent mechanism, is necessary for down-regulation of tumor immunosurveillance. |
| 390 | 14657224 | Identification of this stepwise regulation of immunosurveillance, involving CD1-restricted T cells, IL-13, myeloid cells, and TGF-beta, explains previous observations on myeloid suppressor cells or TGF-beta and provides insights for targeted approaches for cancer immunotherapy, including synergistic blockade of TGF-beta and IL-13. |
| 391 | 14670331 | Immunization with FII induced significant production of IFN-gamma and IL-10 associated with high levels of IgG1 and IgG2a. |
| 392 | 14670331 | In contrast, FIII immunized mice develop a progressive disseminated disease to spleen and liver presented significant levels of INF-gamma, IL-10 or TGF-beta associated with high production of IgG1 and IgG2a with low production of IgG2b and IgG3 after challenge infection. |
| 393 | 14671117 | Divergent regions contain gene families, which overall comprise over 49% of the CNPV genome and include genes encoding 51 proteins containing ankyrin repeats, 26 N1R/p28-like proteins, and potential immunomodulatory proteins, including those similar to transforming growth factor beta and beta-nerve growth factor. |
| 394 | 14671117 | CNPV genes lacking homologues in FWPV encode proteins similar to ubiquitin, interleukin-10-like proteins, tumor necrosis factor receptor, PIR1 RNA phosphatase, thioredoxin binding protein, MyD116 domain proteins, circovirus Rep proteins, and the nucleotide metabolism proteins thymidylate kinase and ribonucleotide reductase small subunit. |
| 395 | 14685154 | However, in EBV-positive Hodgkin's disease (HD) the efficacy of adoptively transferred EBV-specific CTL may be limited by tumor-derived immunosuppressive factors, such as T-cell growth factor (TGF) beta, interleukin (IL)13 and the chemokine TARC. |
| 396 | 14685154 | EBV-specific CTL transduced with a retrovirus vector expressing the p40 and p35 subunits of IL12 as a single molecule (Flexi-IL12), produced IL12 following antigenic stimulation. |
| 397 | 14685154 | This resulted in an elevated production of Th1 cytokines, including interferon gamma and tumor necrosis factor alpha, and a reduction in the Th2 cytokines IL4 and IL5. |
| 398 | 14685154 | Flexi-IL12-transduced CTL resisted the antiproliferative and anticytotoxic effects of exogenous TGFbeta, likely by antagonizing the TGFbeta-induced downregulation of the Th1 transcriptional factor T-bet. |
| 399 | 14742545 | The replication-promoting effect of IFN-gamma on amastigotes was independent of the source and genetic background of Mphis, was apparently not affected by surface opsonization of amastigotes, was not mediated by interleukin-10 or transforming growth factor beta, and was observed at different temperatures. |
| 400 | 14742545 | On the other hand, IFN-gamma could stimulate Mphis to limit amastigote replication when it was coupled with lipopolysaccharides but not when it was coupled with tumor necrosis factor alpha. |
| 401 | 14971031 | Dendritic cells generated in the presence of GM-CSF plus IL-15 prime potent CD8+ Tc1 responses in vivo. |
| 402 | 14971031 | DC progenitors can be stimulated to differentiate into immature DC by various growth factors, including GM-CSF and IL-4. |
| 403 | 14971031 | Here we show that IL-15, in combination with GM-CSF, is a growth factor for murine DC. |
| 404 | 14971031 | Murine bone marrow cells, depleted of T cells, B cells, I-A+ cells and Gr-1+ granulocytes, and cultured in the presence of GM-CSF plus IL-15 (IL-15 DC), yielded DC expressing high levels of CD11c and MHC class II molecules, as well as CD11b. |
| 405 | 14971031 | These cells expressed significant levels of CD40, CD80 and CD86, and could stimulate allogeneic CD4+ T cells efficiently. |
| 406 | 14971031 | Interestingly, IL-15 DC were far superior to DC generated with GM-CSF plus IL-4 in stimulating allogeneic CD8+ T cells in vitro. |
| 407 | 14971031 | Consistent with this, IL-15 DC induced much more potent antigen-specific CD8+ T cell responses with high levels of Th1 cytokines in vivo, compared to DC generated with GM-CSF plus IL-4, or with GM-CSF plus TGF-beta, or with GM-CSF alone. |
| 408 | 14971031 | Together, these data suggest that IL-15 promotes the development of DC, which induce potent Th1 and Tc1 responses in vivo. |
| 409 | 15064826 | Resistance in visceral leishmaniasis involves both CD4+ and CD8+ T cells, and interleukin (IL)-2, interferon (IFN)-gamma, and IL-12, the latter in a mechanism independent of IFN-gamma and linked to transforming growth factor (TGF)-beta production. |
| 410 | 15064826 | Susceptibility involves IL-10 but not IL-4, and B cells. |
| 411 | 15064826 | In immune animals, upon re-infection, the elements involved in resistance are different, i.e., CD8+ T cells and IL-2. |
| 412 | 15064826 | Interactions of the co-stimulatory molecule family B7-CTLA-4 leading to increased level of TGF-beta as well as apoptosis of CD4+ T cells and inhibition of macrophage apoptosis by Leishmania infection are other components participating in immunosuppression. |
| 413 | 15102698 | DC-AdCCL21 administration led to increases in the CD4(+), CD8(+), and CD3(+)CXCR3(+) T cells, as well as DC expressing CD11c(+) DEC205(+). |
| 414 | 15102698 | CD4(+)CD25(+) T-regulatory cells infiltrating the tumors were markedly reduced after DC-AdCCL21 therapy. |
| 415 | 15102698 | The tumor site cellular infiltrates were accompanied by the enhanced elaboration of granulocyte macrophage colony-stimulating factor, IFN-gamma, MIG/CXCL9, IP-10/CXCL10, and interleukin 12, but decreases in the immunosuppressive mediators transforming growth factor beta and prostaglandin E(2). |
| 416 | 15102698 | In vivo depletion of IP-10/CXCL10, MIG/CXCL9, or IFN-gamma significantly reduced the antitumor efficacy of DC-AdCCL21. |
| 417 | 15128839 | The Dsg3-specific Tr1 cells secreted IL-10, TGF-beta, and IL-5 upon Ag stimulation, proliferated in response to IL-2 but not to Dsg3 or mitogenic stimuli, and inhibited the proliferative response of Dsg3- and tetanus toxoid-responsive Th clones in an Ag-specific (Dsg3) and cell number-dependent manner. |
| 418 | 15128839 | Moreover, their inhibitory effect was blocked by Ab against IL-10, TGF-beta, and by paraformaldehyde fixation. |
| 419 | 15128839 | These observations strongly suggest that 1) Dsg3-responsive Tr1 cells predominate in healthy individuals, 2) their growth requires the presence of IL-2, and 3) they exert their Dsg3-dependent inhibitory function by the secretion of IL-10 and TGF-beta. |
| 420 | 15128839 | The Dsg3-specific Tr1 cells secreted IL-10, TGF-beta, and IL-5 upon Ag stimulation, proliferated in response to IL-2 but not to Dsg3 or mitogenic stimuli, and inhibited the proliferative response of Dsg3- and tetanus toxoid-responsive Th clones in an Ag-specific (Dsg3) and cell number-dependent manner. |
| 421 | 15128839 | Moreover, their inhibitory effect was blocked by Ab against IL-10, TGF-beta, and by paraformaldehyde fixation. |
| 422 | 15128839 | These observations strongly suggest that 1) Dsg3-responsive Tr1 cells predominate in healthy individuals, 2) their growth requires the presence of IL-2, and 3) they exert their Dsg3-dependent inhibitory function by the secretion of IL-10 and TGF-beta. |
| 423 | 15128839 | The Dsg3-specific Tr1 cells secreted IL-10, TGF-beta, and IL-5 upon Ag stimulation, proliferated in response to IL-2 but not to Dsg3 or mitogenic stimuli, and inhibited the proliferative response of Dsg3- and tetanus toxoid-responsive Th clones in an Ag-specific (Dsg3) and cell number-dependent manner. |
| 424 | 15128839 | Moreover, their inhibitory effect was blocked by Ab against IL-10, TGF-beta, and by paraformaldehyde fixation. |
| 425 | 15128839 | These observations strongly suggest that 1) Dsg3-responsive Tr1 cells predominate in healthy individuals, 2) their growth requires the presence of IL-2, and 3) they exert their Dsg3-dependent inhibitory function by the secretion of IL-10 and TGF-beta. |
| 426 | 15239136 | We investigated the importance of HSP70 and TGF-beta expression in apoptotic cells used in the treatment of an established and nonimmunogenic rat carcinoma. |
| 427 | 15270841 | However, DNA vaccination encoding microbial or reporter antigens is known to induce specific long-lasting CD4 Th1 and strong cytolytic CD8 T cell responses. |
| 428 | 15270841 | Simultaneously, DNA immunization induced GAD-specific CD4 T cells secreting interleukin (IL)-4 (P < 0.05) and transforming growth factor (TGF)-beta (P = 0.03). |
| 429 | 15270841 | Furthermore, vaccination produced high amounts of Th2 cytokine-related IgG1 (P < 3.10(-3)) and TGF-beta-related IgG2b to GAD (P = 0.015). |
| 430 | 15270841 | Surprisingly, diabetes onset was correlated positively with Th2-related GAD-specific IgG1 (P < 10(-4)) and TGF-beta-related IgG2b (P < 3.10(-3)). |
| 431 | 15270841 | However, DNA vaccination encoding microbial or reporter antigens is known to induce specific long-lasting CD4 Th1 and strong cytolytic CD8 T cell responses. |
| 432 | 15270841 | Simultaneously, DNA immunization induced GAD-specific CD4 T cells secreting interleukin (IL)-4 (P < 0.05) and transforming growth factor (TGF)-beta (P = 0.03). |
| 433 | 15270841 | Furthermore, vaccination produced high amounts of Th2 cytokine-related IgG1 (P < 3.10(-3)) and TGF-beta-related IgG2b to GAD (P = 0.015). |
| 434 | 15270841 | Surprisingly, diabetes onset was correlated positively with Th2-related GAD-specific IgG1 (P < 10(-4)) and TGF-beta-related IgG2b (P < 3.10(-3)). |
| 435 | 15277580 | Immunosuppressive factors, such as vascular endothelial growth factor, transforming growth factor-beta, prostaglandin E2, interleukin (IL)-10, and IL-6, are made frequently by cancer cells. |
| 436 | 15277580 | However, a number of factors appear to be made directly in response to signaling molecules, such as RAS, AKT, and signal transducer and activator of transcription 3, which are activated as a result of genetic events that occur during oncogenesis. |
| 437 | 15308777 | We shall describe here two such examples: a copolymer of amino acids related to myelin basic protein, in the case of multiple sclerosis, and a peptide derived from the nicotinic acetylcholine receptor (AChR), in the case of myasthenia gravis (MG). |
| 438 | 15308777 | The active suppression is mediated by the CD4(+)CD25(+) immunoregulatory cells and is associated with the down-regulation of Th1-type cytokines and the up-regulation of the secretion of IL-10 and the immunosuppressive cytokine, transforming growth factor beta. |
| 439 | 15313511 | The target genes included Mx-1, viral haemorrhagic septicaemia virus induced gene 8 (Vig-8), TNF-alpha1, TNF-alpha2, IL-1beta1, IL-8, TGF-beta1 and Hsp70. |
| 440 | 15314542 | CD4+CD25+ regulatory T cells that secrete TGFbeta and IL-10 are preferentially induced by a vaccine vector. |
| 441 | 15314542 | The authors confirm that these increased numbers of CD4CD25 T cells are indeed suppressor in function by in vitro suppression assays and that the mechanism of action of the tumor-infiltrating cells involves the production of suppressor cytokines interleukin-10 and transforming growth factor beta. |
| 442 | 15314542 | CD4+CD25+ regulatory T cells that secrete TGFbeta and IL-10 are preferentially induced by a vaccine vector. |
| 443 | 15314542 | The authors confirm that these increased numbers of CD4CD25 T cells are indeed suppressor in function by in vitro suppression assays and that the mechanism of action of the tumor-infiltrating cells involves the production of suppressor cytokines interleukin-10 and transforming growth factor beta. |
| 444 | 15331781 | Dual effect of CD4+CD25+ regulatory T cells in neurodegeneration: a dialogue with microglia. |
| 445 | 15331781 | Here we show that the ability to spontaneously manifest a T cell-dependent protective response is restricted by naturally occurring CD4(+)CD25(+) regulatory T cells (Treg); depletion of Treg was beneficial in two mouse strains (C57BL/6J and BALB/c/OLA) differing in their spontaneous T cell-dependent ability to withstand the consequences of optic nerve injury. |
| 446 | 15331781 | We attribute these disparate effects of Treg to their differential interaction (in part via IL-10 and transforming growth factor beta) with local innate immune cells (microglia) in the presence and in the absence of effector T cells. |
| 447 | 15553669 | Monocytes were separated from the peripheral blood collected by leukapheresis, and were cultured with GM-CSF and IL-4 for 6 days. |
| 448 | 15553669 | Then, TNF-alpha, IL-1beta, IL-6 and PGE2 were added for maturation of DC. |
| 449 | 15553669 | Th1/Th2 and Tc1/Tc2 balances improved in six of the nine patients after vaccination. |
| 450 | 15553669 | In this study, it was shown that immunosuppressive factors, such as IAP and TGF-beta, and Th1 balance are useful as markers of immunomonitoring for tumor-DC fusion vaccine in patients with advanced or recurrent gastrointestinal patients. |
| 451 | 15626469 | A panel of three CpG-oligodeoxynucleotides (ODN) and three eukaryotic expression vectors currently used in experimental DNA vaccines in pigs (pcDNA1, pcDNA3.1 and pCI) were screened for their immunostimulatory activity on porcine PBMC by evaluating in vitro the lymphocyte proliferative responses and cytokine profiles (IL-1alpha, IL-2, IL-4, IL-6, IL-10, IFN-gamma, TGF-beta, TNF-alpha). |
| 452 | 15626469 | Furthermore, CpG-ODN A significantly induced IL-6 and TNF-alpha together with elevated levels of IFN-gamma and IL-2 mRNA expression even though considerable heterogeneity was observed in the response of individual pigs. |
| 453 | 15626469 | For pcDNA1, proliferation was absent together with significantly decreased levels of IL-6 and IFN-gamma. |
| 454 | 15650885 | It also enhances cell-mediated immunity by targeting antigen delivery in antigen-presenting cells to both the MHC class I pathway of exogenous presentation that activates CD8 T cells and the MHC class II pathway that processes antigen endogenously and presents it to CD4 T cells. |
| 455 | 15650885 | In particular, we describe the effect on tumor angiogenesis, induction of antitumor suppressor factors like CD4+CD25+ T cells and regulatory cytokines TGF-beta and IL-10, homing and infiltration of antigen-specific CD8+ T cells to the tumor, and also effects of the vaccines on antigen-presenting cells, especially focusing on dendritic cell maturation and ability to influence tumor regression. |
| 456 | 15735048 | CD4(+) Treg cells do not secrete interleukin (IL)-10 and transforming growth factor beta cytokines but express CD25, the glucocorticoid-induced tumor necrosis factor receptor-related protein (GITR), and Forkhead Box P3 (Foxp3), and are capable of suppressing the proliferative responses of naive CD4(+) and CD8(+) T cells to stimulation with mitogenic anti-CD3 antibody. |
| 457 | 15735048 | Importantly, these Treg cells suppress IL-2 secretion by CD4(+) effector T cells specific for either EBNA1 or a melanoma antigen, suggesting that these CD4(+) Treg cells induce immune suppression. |
| 458 | 15750831 | In this study, we investigated the feasibility of using a plasmid DNA encoding Xenopus laevis transforming growth factor-beta 5 (aTGF-beta5) as an immunogen to induce neutralizing antibodies against murine TGF-beta1 (mTGF-beta1) and thus enhance the efficacy of plasmid DNA vaccine encoding murine tyrosinase-related protein 2 (mTRP-2) through neutralization of TGF-beta. |
| 459 | 15750831 | Moreover, immunization of C57BL/6 wild-type mice with a combination of aTGF-beta5 and mTRP-2 induced the protective and therapeutic antitumor immunity to B16F10 melanoma, whereas the antitumor activity was abrogated in both CD4-deficient mice and CD8-deficient mice on the C57BL/6 background. |
| 460 | 15750831 | Neutralization of TGF-beta can enhance the efficacy of DNA vaccine encoding mTRP-2 and the induction of antitumor immunity by this immunization strategy is associated with CD4+ and CD8+ T cells. |
| 461 | 15750831 | In this study, we investigated the feasibility of using a plasmid DNA encoding Xenopus laevis transforming growth factor-beta 5 (aTGF-beta5) as an immunogen to induce neutralizing antibodies against murine TGF-beta1 (mTGF-beta1) and thus enhance the efficacy of plasmid DNA vaccine encoding murine tyrosinase-related protein 2 (mTRP-2) through neutralization of TGF-beta. |
| 462 | 15750831 | Moreover, immunization of C57BL/6 wild-type mice with a combination of aTGF-beta5 and mTRP-2 induced the protective and therapeutic antitumor immunity to B16F10 melanoma, whereas the antitumor activity was abrogated in both CD4-deficient mice and CD8-deficient mice on the C57BL/6 background. |
| 463 | 15750831 | Neutralization of TGF-beta can enhance the efficacy of DNA vaccine encoding mTRP-2 and the induction of antitumor immunity by this immunization strategy is associated with CD4+ and CD8+ T cells. |
| 464 | 15797470 | We generated a mammalian expression system for recombinant cytokines using the equine IgG1 heavy chain constant region as a tag for detection and purification of the expressed cytokine, demonstrated here using equine interferon-gamma (IFN-gamma), interleukin-2 (IL-2), interleukin-4 (IL4) and transforming growth factor-beta1 (TGF-beta1). |
| 465 | 15797470 | The purification of the fusion protein by protein G affinity columns, the enterokinase digestion of the cytokine from the IgG1 heavy chain region after or during purification, and the biological activity of the cytokine within the fusion protein or after its isolation was demonstrated in detail for equine IFN-gamma/IgG1 by up-regulation of major histocompatibility complex (MHC) class II expression on horse lymphocytes. |
| 466 | 15797470 | Biological activity could also be confirmed for the IL-2 and IL-4/IgG1 fusion proteins. |
| 467 | 15797470 | To test the crossreactivity and specificity of anti-human TGF-beta1, and anti-bovine and anti-canine IFN-gamma antibodies to respective horse cytokines, the four cytokine/IgG1 fusion proteins were successfully used in ELISA, flow cytometry and/or Western blotting. |
| 468 | 15797470 | We generated a mammalian expression system for recombinant cytokines using the equine IgG1 heavy chain constant region as a tag for detection and purification of the expressed cytokine, demonstrated here using equine interferon-gamma (IFN-gamma), interleukin-2 (IL-2), interleukin-4 (IL4) and transforming growth factor-beta1 (TGF-beta1). |
| 469 | 15797470 | The purification of the fusion protein by protein G affinity columns, the enterokinase digestion of the cytokine from the IgG1 heavy chain region after or during purification, and the biological activity of the cytokine within the fusion protein or after its isolation was demonstrated in detail for equine IFN-gamma/IgG1 by up-regulation of major histocompatibility complex (MHC) class II expression on horse lymphocytes. |
| 470 | 15797470 | Biological activity could also be confirmed for the IL-2 and IL-4/IgG1 fusion proteins. |
| 471 | 15797470 | To test the crossreactivity and specificity of anti-human TGF-beta1, and anti-bovine and anti-canine IFN-gamma antibodies to respective horse cytokines, the four cytokine/IgG1 fusion proteins were successfully used in ELISA, flow cytometry and/or Western blotting. |
| 472 | 15879099 | Tat-induced TGF-beta mRNA synthesis is also blocked by the ERK1 inhibitor PD98059, suggesting that ERK1 is needed for TGF-beta production. |
| 473 | 15879099 | Moreover, Tat strongly activates the c-Jun component of the multimolecular complex AP-1, whereas TGF-beta triggers c-Fos and c-Jun. |
| 474 | 15879099 | Of note, treatment of NK cells with PTX-B or PT9K/129G inhibits Tat- and TGF-beta-induced activation of AP-1. |
| 475 | 15879099 | TGF-beta enhances starvation-induced NK cell apoptosis, significantly reduces transcription of the antiapoptotic protein Bcl-2, and inhibits Akt phosphorylation induced by oligomerization of the triggering NK cell receptor NKG2D. |
| 476 | 15879099 | It is of note that in NK cells from patients with early HIV-1 infection, mRNA expression of Bcl-2 and Bcl-x(L) was consistently lower than that in healthy donors; interestingly, TGF-beta and Tat were detected in the sera of these patients. |
| 477 | 15879099 | Tat-induced TGF-beta mRNA synthesis is also blocked by the ERK1 inhibitor PD98059, suggesting that ERK1 is needed for TGF-beta production. |
| 478 | 15879099 | Moreover, Tat strongly activates the c-Jun component of the multimolecular complex AP-1, whereas TGF-beta triggers c-Fos and c-Jun. |
| 479 | 15879099 | Of note, treatment of NK cells with PTX-B or PT9K/129G inhibits Tat- and TGF-beta-induced activation of AP-1. |
| 480 | 15879099 | TGF-beta enhances starvation-induced NK cell apoptosis, significantly reduces transcription of the antiapoptotic protein Bcl-2, and inhibits Akt phosphorylation induced by oligomerization of the triggering NK cell receptor NKG2D. |
| 481 | 15879099 | It is of note that in NK cells from patients with early HIV-1 infection, mRNA expression of Bcl-2 and Bcl-x(L) was consistently lower than that in healthy donors; interestingly, TGF-beta and Tat were detected in the sera of these patients. |
| 482 | 15879099 | Tat-induced TGF-beta mRNA synthesis is also blocked by the ERK1 inhibitor PD98059, suggesting that ERK1 is needed for TGF-beta production. |
| 483 | 15879099 | Moreover, Tat strongly activates the c-Jun component of the multimolecular complex AP-1, whereas TGF-beta triggers c-Fos and c-Jun. |
| 484 | 15879099 | Of note, treatment of NK cells with PTX-B or PT9K/129G inhibits Tat- and TGF-beta-induced activation of AP-1. |
| 485 | 15879099 | TGF-beta enhances starvation-induced NK cell apoptosis, significantly reduces transcription of the antiapoptotic protein Bcl-2, and inhibits Akt phosphorylation induced by oligomerization of the triggering NK cell receptor NKG2D. |
| 486 | 15879099 | It is of note that in NK cells from patients with early HIV-1 infection, mRNA expression of Bcl-2 and Bcl-x(L) was consistently lower than that in healthy donors; interestingly, TGF-beta and Tat were detected in the sera of these patients. |
| 487 | 15879099 | Tat-induced TGF-beta mRNA synthesis is also blocked by the ERK1 inhibitor PD98059, suggesting that ERK1 is needed for TGF-beta production. |
| 488 | 15879099 | Moreover, Tat strongly activates the c-Jun component of the multimolecular complex AP-1, whereas TGF-beta triggers c-Fos and c-Jun. |
| 489 | 15879099 | Of note, treatment of NK cells with PTX-B or PT9K/129G inhibits Tat- and TGF-beta-induced activation of AP-1. |
| 490 | 15879099 | TGF-beta enhances starvation-induced NK cell apoptosis, significantly reduces transcription of the antiapoptotic protein Bcl-2, and inhibits Akt phosphorylation induced by oligomerization of the triggering NK cell receptor NKG2D. |
| 491 | 15879099 | It is of note that in NK cells from patients with early HIV-1 infection, mRNA expression of Bcl-2 and Bcl-x(L) was consistently lower than that in healthy donors; interestingly, TGF-beta and Tat were detected in the sera of these patients. |
| 492 | 15905510 | CD4(+)CD25(+) T cells and cytokines IL-10 and TGF-beta1 did not increase after challenge. |
| 493 | 15919138 | However, it was not known if B7-1/Ig acted only by binding CD28 (amplifying a stimulatory signal) or by blocking CTLA-4 on T cells (removing inhibitory signals). |
| 494 | 15919138 | Here, we aimed to determine this using a plasmid encoding mutant B7-1/Ig (B7-1wa/Ig), which binds only to CTLA-4 but not to CD28. |
| 495 | 15919138 | We found that, in vitro, a significant fraction of CD3/CD28-activated T cells (in the absence of DCs) expressed CTLA-4 and B7-1. |
| 496 | 15919138 | Primed T cells of CTLA-4(+)B7-1(+/-) phenotype acted as regulatory T cells by inhibiting IFNgamma production by re-stimulated CTLA-4(-)B7-1(-) cells, and this was reversed by antibodies against IL-10 or TGF-beta1. |
| 497 | 15919138 | Both B7-1wa/Ig and CTLA-4/Ig, which bind to CTLA-4 and B7-1/B7-2 respectively, enhanced IFNgamma production, but not the proliferation or IL-4 release in mixed T-cell populations containing these two cell types. |
| 498 | 15919138 | In contrast, CTLA-4(-)B7-1(-) T cells produced IFNgamma which was not affected by B7-1wa/Ig or CTLA-4/Ig. |
| 499 | 15966311 | Chicken cytokine genes that have been cloned to date include ChIFN-gamma, ChIL-1beta, ChIFN-alpha, ChIL-15, ChIL-18, ChIL-8, ChIL-2, ChIL-6, ChIL-16, SCF, MGF, TGFbeta, Lymphotactin, MIP-1beta, CXC and CC chemokines, so the use of cytokines in poultry has become more feasible with the discovery of a number of avian cytokine genes. |
| 500 | 16041007 | Mucosal type 2/3 responses (producing interleukin-4 [IL-4], IL-6 and/or transforming growth factor beta) could be necessary for optimal induction of protective secretory immunoglobulin A responses. |
| 501 | 16041007 | On the other hand, systemic type 1 responses (including gamma interferon [IFN-gamma], tumor necrosis factor alpha, and optimal cytotoxic T-cell responses) are likely to be critical for protection against the disseminated intracellular replication that occurs after mucosal invasion. |
| 502 | 16041007 | T. cruzi infection followed by nifurtimox treatment rescue was used to immunize CD4, CD8, beta2-microglobulin, inducible nitric oxide synthase (iNOS), IL-12, IFN-gamma, and IL-4 knockout mice. |
| 503 | 16041007 | Despite the previously demonstrated importance of CD4(+) T cells, CD8(+) T cells, and nitric oxide for T. cruzi immunity, CD4, CD8, and iNOS knockout mice developed mucosal and systemic protective immunity. |
| 504 | 16041007 | However, IL-12, IFN-gamma, and beta2-microglobulin-deficient mice failed to develop mucosal or systemic protection. |
| 505 | 16175400 | Furthermore, many cancer patients exhibit a cytokine profile skewed toward IL10 and TGFbeta. |
| 506 | 16175400 | IL12 and IFNgamma were expressed by CD40L-engineered DCs, while TNFalpha-matured DCs lacked IFNgamma and exhibited low IL12 expression. |
| 507 | 16175400 | We further demonstrate that the resistance of CD40L-expressing DCs to TGFbeta and IL10 may be due to decreased levels of TGFbeta and IL10 receptors. |
| 508 | 16175400 | Thus, CD40L-engineered DCs are robust Th1-promoting ones that are resistant to Tr1/Th3-signaling via IL10 and TGFbeta. |
| 509 | 16175400 | Furthermore, many cancer patients exhibit a cytokine profile skewed toward IL10 and TGFbeta. |
| 510 | 16175400 | IL12 and IFNgamma were expressed by CD40L-engineered DCs, while TNFalpha-matured DCs lacked IFNgamma and exhibited low IL12 expression. |
| 511 | 16175400 | We further demonstrate that the resistance of CD40L-expressing DCs to TGFbeta and IL10 may be due to decreased levels of TGFbeta and IL10 receptors. |
| 512 | 16175400 | Thus, CD40L-engineered DCs are robust Th1-promoting ones that are resistant to Tr1/Th3-signaling via IL10 and TGFbeta. |
| 513 | 16175400 | Furthermore, many cancer patients exhibit a cytokine profile skewed toward IL10 and TGFbeta. |
| 514 | 16175400 | IL12 and IFNgamma were expressed by CD40L-engineered DCs, while TNFalpha-matured DCs lacked IFNgamma and exhibited low IL12 expression. |
| 515 | 16175400 | We further demonstrate that the resistance of CD40L-expressing DCs to TGFbeta and IL10 may be due to decreased levels of TGFbeta and IL10 receptors. |
| 516 | 16175400 | Thus, CD40L-engineered DCs are robust Th1-promoting ones that are resistant to Tr1/Th3-signaling via IL10 and TGFbeta. |
| 517 | 16213184 | Gastric IL-10 and TGFbeta transcripts were found only at relatively low levels. |
| 518 | 16216395 | CP-deficient L. mexicana elicited significantly lower levels of Th2-associated cytokines IL-10 and TGF-beta than the WT in the primary lesion of hamsters. |
| 519 | 16291589 | Tumor evasion of the immune system: inhibiting p38 MAPK signaling restores the function of dendritic cells in multiple myeloma. |
| 520 | 16291589 | Neutralizing antibodies against IL-6, IL-10, and TGF-beta partially abrogated the effects. |
| 521 | 16291589 | TCCM treatment activated p38 mitogen-activated protein kinase (MAPK) and Janus kinase (JNK) but inhibited extracellular regulated kinase (ERK). |
| 522 | 16291589 | Inhibiting p38 MAPK restored the phenotype, cytokine secretion, and function of TCCM-treated BMDCs. |
| 523 | 16291589 | Thus, our results suggested that tumor-induced p38 MAPK activation and ERK inhibition in DCs may be a new mechanism for tumor evasion and that regulating these pathways during DC differentiation provides new strategies for generating potent DC vaccines for immunotherapy in patients with cancer. |
| 524 | 16294321 | We compared the levels of expression of a number of molecules involved in tumor metastasis, which included transforming growth factor-beta1 (TGF-beta1), E-cadherin, matrix metalloproteinases (MMPs): MT1-MMP, MMP-2, MMP-9, their tissue inhibitors (TIMPs): TIMP-1/TIMP-2, and pro-angiogenic factors CD31, VEGF-R2, and iNOS between primary and metastatic tumors by real-time RT-PCR and immunohistochemistry. |
| 525 | 16294321 | In the metastatic tumors, levels of MT1-MMP, MMP-2, and MMP-9 were significantly elevated (P < 0.001), while levels of TIMP-1/TIMP-2 and E-cadherin were decreased (P < 0.001) compared to control or primary tumors. |
| 526 | 16294321 | Levels of CD31, VEGF-R2, and iNOS were also significantly elevated in the metastatic lesions (P < 0.001). |
| 527 | 16352562 | To understand the role of cytokines during rotavirus infection, we assessed the kinetics of tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) (proinflammatory), IL-12 (Th1 inducer), gamma interferon (IFN-gamma) (Th1), IL-4 and IL-10 (Th2), and transforming growth factor beta (Th3) cytokine responses by enzyme-linked immunosorbent assay in serum and intestinal contents of neonatal gnotobiotic pigs and IL-12, IFN-gamma, IL-4, and IL-10 cytokine-secreting cell (CSC) responses of mononuclear cells from ileum, spleen, and blood by ELISPOT. |
| 528 | 16352562 | In serum, IL-6 was significantly elevated at postinoculation day (PID) 1 in the VirHRV group and at PID 3 in both HRV groups. |
| 529 | 16352562 | A significantly higher percentage of pigs had IFN-gamma and IL-10 responses in serum after VirHRV infection than after AttHRV infection or in controls. |
| 530 | 16352562 | Higher protection rates may be associated with more balanced Th1- and Th2-type responses, but induction of higher earlier IFN-gamma (Th1) and proinflammatory cytokines triggered by VirHRV may also play an important role in the higher intestinal immunoglobulin A responses and protection rates induced by VirHRV. |
| 531 | 16409190 | Whereas a central paradigm for successful immunotherapy has been to reorient the pattern of allergen-specific T-cell responses in atopic patients from a T helper (Th)2 to Th1 profile, there is currently a growing interest in eliciting regulatory T cells, capable of downregulating both Th1 and Th2 responses through the production of interleukin (IL)-10 and/or transforming growth factor (TGF)-beta. |
| 532 | 16409190 | During SLIT, the allergen is captured within the oral mucosa by Langerhans-like dendritic cells expressing high-affinity IgE receptors, producing IL-10 and TGF-beta, and upregulating indoleamine dioxygenase (IDO), suggesting that such cells are prone to induce tolerance. |
| 533 | 16415106 | Transfer of regulatory T cells generated ex vivo modifies graft rejection through induction of tolerogenic CD4+CD25+ cells in the recipient. |
| 534 | 16415106 | Certain CD4+CD25+ T cells can induce and maintain T-cell non-responsiveness to donor alloantigens and have therapeutic potential in solid organ transplantation. |
| 535 | 16415106 | Peripheral CD4+CD25- cells alloactivated with IL-2 and transforming growth factor beta (TGF-beta) ex vivo express the transcription factor FoxP3, and become potent antigen-specific CD4+CD25- suppressor cells. |
| 536 | 16415106 | Here we report that the transfer of TGF-beta-induced regulatory CD4+ and CD8+ T cells (Tregs) co-incident with transplantation of a histoincompatible heart resulted in extended allograft survival. |
| 537 | 16415106 | To account for this result, we injected non-transplanted mice with a single dose of CD4+ and CD8+ Tregs and transferred donor cells every 2 weeks to mimic the continuous stimulation of a transplant. |
| 538 | 16415106 | We observed increased splenic CD4+CD25+ cells that were of recipient origin. |
| 539 | 16415106 | Both the increased number of CD4+CD25+ cells and their tolerogenic effect were dependent on continued donor antigen boosting. |
| 540 | 16415106 | Transfer of regulatory T cells generated ex vivo modifies graft rejection through induction of tolerogenic CD4+CD25+ cells in the recipient. |
| 541 | 16415106 | Certain CD4+CD25+ T cells can induce and maintain T-cell non-responsiveness to donor alloantigens and have therapeutic potential in solid organ transplantation. |
| 542 | 16415106 | Peripheral CD4+CD25- cells alloactivated with IL-2 and transforming growth factor beta (TGF-beta) ex vivo express the transcription factor FoxP3, and become potent antigen-specific CD4+CD25- suppressor cells. |
| 543 | 16415106 | Here we report that the transfer of TGF-beta-induced regulatory CD4+ and CD8+ T cells (Tregs) co-incident with transplantation of a histoincompatible heart resulted in extended allograft survival. |
| 544 | 16415106 | To account for this result, we injected non-transplanted mice with a single dose of CD4+ and CD8+ Tregs and transferred donor cells every 2 weeks to mimic the continuous stimulation of a transplant. |
| 545 | 16415106 | We observed increased splenic CD4+CD25+ cells that were of recipient origin. |
| 546 | 16415106 | Both the increased number of CD4+CD25+ cells and their tolerogenic effect were dependent on continued donor antigen boosting. |
| 547 | 16446177 | Lately, the existence of subpopulations of regulatory T lymphocytes (RTL) able to limit the immune response in a specific form has been established, specially inhibiting the proliferation and activity of CD4+ and CD8+ effector T lymphocytes. |
| 548 | 16446177 | These cellular subpopulations, mostly CD4+/CD25+/Foxp3+ T lymphocytes (Treg) of thymic origin, or TR1 lymphocytes able to release IL-10, and tumour growth factor beta (TGF-beta) producing TH3 lymphocytes, would be accumulated in the body during tumour growth, inhibiting the immune response. |
| 549 | 16540176 | Expression of interferon-gamma (IFN-gamma), transforming growth factor-beta (TGF-beta), type I procollagen and cell marker identification of T cells, B cells, macrophages and WC1(+)gammadelta TCR+ cells were assessed. |
| 550 | 16552043 | In response to nematode and malarial antigens, spleen cells from immunized nematode-infected mice produced significantly lower levels of gamma interferon but more interleukin-4 (IL-4), IL-13, and IL-10 in vitro than spleen cells from immunized nematode-free mice produced. |
| 551 | 16552043 | Furthermore, H. polygyrus infection also induced a strong transforming growth factor beta1 response in vivo and in vitro. |
| 552 | 16585215 | CD1d-restricted natural killer T cells can down-regulate tumor immunosurveillance independent of interleukin-4 receptor-signal transducer and activator of transcription 6 or transforming growth factor-beta. |
| 553 | 16585215 | Further, we examined the role of CD4(+) and/or CD8(+) cells by depleting the cells in vivo and measuring CTL activity in vitro. |
| 554 | 16585215 | We also asked the role of interleukin (IL)-4 receptor alpha (IL-4Ralpha)-signal transducer and activator of transcription 6 (STAT6) signaling, including IL-13, and transforming growth factor beta (TGF-beta) by using gene-disrupted mice or treating mice with cytokine antagonists. |
| 555 | 16585215 | Further studies suggested that the rejection of tumor in CD1d KO mice was dependent on CD8(+) lymphocytes. |
| 556 | 16585215 | Distinct from other murine tumor models, the negative regulation induced by CD1d-restricted NKT cells was not dependent on IL-4Ralpha-STAT6 signaling, including IL-13, or on TGF-beta. |
| 557 | 16585215 | CD1d-restricted natural killer T cells can down-regulate tumor immunosurveillance independent of interleukin-4 receptor-signal transducer and activator of transcription 6 or transforming growth factor-beta. |
| 558 | 16585215 | Further, we examined the role of CD4(+) and/or CD8(+) cells by depleting the cells in vivo and measuring CTL activity in vitro. |
| 559 | 16585215 | We also asked the role of interleukin (IL)-4 receptor alpha (IL-4Ralpha)-signal transducer and activator of transcription 6 (STAT6) signaling, including IL-13, and transforming growth factor beta (TGF-beta) by using gene-disrupted mice or treating mice with cytokine antagonists. |
| 560 | 16585215 | Further studies suggested that the rejection of tumor in CD1d KO mice was dependent on CD8(+) lymphocytes. |
| 561 | 16585215 | Distinct from other murine tumor models, the negative regulation induced by CD1d-restricted NKT cells was not dependent on IL-4Ralpha-STAT6 signaling, including IL-13, or on TGF-beta. |
| 562 | 16585215 | CD1d-restricted natural killer T cells can down-regulate tumor immunosurveillance independent of interleukin-4 receptor-signal transducer and activator of transcription 6 or transforming growth factor-beta. |
| 563 | 16585215 | Further, we examined the role of CD4(+) and/or CD8(+) cells by depleting the cells in vivo and measuring CTL activity in vitro. |
| 564 | 16585215 | We also asked the role of interleukin (IL)-4 receptor alpha (IL-4Ralpha)-signal transducer and activator of transcription 6 (STAT6) signaling, including IL-13, and transforming growth factor beta (TGF-beta) by using gene-disrupted mice or treating mice with cytokine antagonists. |
| 565 | 16585215 | Further studies suggested that the rejection of tumor in CD1d KO mice was dependent on CD8(+) lymphocytes. |
| 566 | 16585215 | Distinct from other murine tumor models, the negative regulation induced by CD1d-restricted NKT cells was not dependent on IL-4Ralpha-STAT6 signaling, including IL-13, or on TGF-beta. |
| 567 | 16603614 | These antigen-specific immunoproteins are thought to have immunoregulatory properties in the suppression of cell-mediated immunity (CMI) because they often associate with interleukin-10 (IL-10) and transforming growth factor beta. |
| 568 | 16603614 | For 14 participants, the effect of mannan stimulation on TABM production and gamma interferon (IFN-gamma) and IL-4 mRNA expression by peripheral blood lymphocytes was also studied. |
| 569 | 16603614 | In addition, the CAM-TABM level was directly related to mRNA expression for IL-4 but not IFN-gamma. |
| 570 | 16608409 | The active suppression is mediated by the CD4+ CD25+ immunoregulatory cells and is associated with the downregulation of Th1-type cytokines and upregulation of the secretion of IL-10 and the immunosuppressive cytokine transforming growth factor beta. |
| 571 | 16700620 | Convection-enhanced delivery of interleukin-13 receptor-directed cytotoxin for malignant glioma therapy. |
| 572 | 16700620 | To target these IL-13R, we generated a chimeric fusion protein, composed of human IL-13 and mutated Pseudomonas exotoxin (PE), termed IL-13 cytotoxin (IL13-PE), and tested its cytotoxicity to IL-13R-expressing GBM cells. |
| 573 | 16700620 | IL-13 cytotoxin was highly potent and selective in killing IL-13R-expressing GBM cells. |
| 574 | 16700620 | These clinical trials involved convection-enhanced delivery (CED) of IL-13 cytotoxin either intratumoral or intraparenchymal after resection of tumor. |
| 575 | 16712895 | Levels of interleukin-10 (IL-10) produced by peripheral blood mononuclear cells (PBMC) seemed to inversely correlate with interferon-gamma responses. |
| 576 | 16712895 | IL-2, IL-4 or transforming growth factor-beta responses were not detected at any time for neither of the vaccines. |
| 577 | 16712895 | These results indicated a strong involvement of IFN-gamma, and maybe IL-10, in the development of immunity against PRRS virus. |
| 578 | 16725233 | We have studied the effect of pIL8+ co-administration on the expression of two pro-inflammatory cytokines, such as IL-1beta and tumour necrosis factor alpha (TNF-alpha); cytokines that have mainly an inhibitory role, IL-11 and transforming growth factor beta (TGF-beta); and a Th1 type cytokine, IL-18. |
| 579 | 16757067 | Specific IgG and cell mediated immune responses (cellular proliferation) including release of tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), transforming growth factor-beta (TGF-beta) and nitric oxide (NO) from host's cells stimulated with BmAFII or lipopolysaccharide (LPS)/concanavalin A (Con A) in vitro were determined. |
| 580 | 16757067 | Immunization alone resulted in downregulation of responses of cellular proliferation, IFN-gamma, TNF-alpha and NO production (P<0.01) but increased TGF-beta release (P<0.001) whereas the converse was seen after L3 inoculation in these animals. |
| 581 | 16757067 | Specific IgG and cell mediated immune responses (cellular proliferation) including release of tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), transforming growth factor-beta (TGF-beta) and nitric oxide (NO) from host's cells stimulated with BmAFII or lipopolysaccharide (LPS)/concanavalin A (Con A) in vitro were determined. |
| 582 | 16757067 | Immunization alone resulted in downregulation of responses of cellular proliferation, IFN-gamma, TNF-alpha and NO production (P<0.01) but increased TGF-beta release (P<0.001) whereas the converse was seen after L3 inoculation in these animals. |
| 583 | 16760321 | Peripheral blood leukocytes (PBL) from infected WTD expressed more gamma interferon (IFN-gamma), interleukin-12p40 (IL-12p40), granulocyte-monocyte colony-stimulating factor, and IL-4 mRNA than did PBL from uninfected deer; however, differences were not detected in expression of IL-10 and transforming growth factor-beta mRNA. |
| 584 | 16790365 | However, in this study, we demonstrate protection against disease by covaccination with a mutant B7-1 molecule (B7-1wa) that binds the negative T cell regulator CTLA-4 (CD152), but not CD28. |
| 585 | 16790365 | In vitro, the T cells of covaccinated mice had negative responses to both insulin and GAD65, and this was restored by adding blocking antibodies to transforming growth factor beta1 (TGF-beta1), suggesting a role for this cytokine. |
| 586 | 16790365 | Furthermore, vaccinated mice had increased numbers of T cells with Tr-associated markers, such as CTLA-4, Foxp3, and membrane-bound TGF-beta1. |
| 587 | 16790365 | However, in this study, we demonstrate protection against disease by covaccination with a mutant B7-1 molecule (B7-1wa) that binds the negative T cell regulator CTLA-4 (CD152), but not CD28. |
| 588 | 16790365 | In vitro, the T cells of covaccinated mice had negative responses to both insulin and GAD65, and this was restored by adding blocking antibodies to transforming growth factor beta1 (TGF-beta1), suggesting a role for this cytokine. |
| 589 | 16790365 | Furthermore, vaccinated mice had increased numbers of T cells with Tr-associated markers, such as CTLA-4, Foxp3, and membrane-bound TGF-beta1. |
| 590 | 16790792 | In order to quantify in vivo the mRNAs of cytokines which play important roles in leptospirosis, we have developed quantitative real-time PCR assays for interleukin-2 (IL-2), IL-4, IL-10, IL-12p40, tumor necrosis factor alpha (TNF-alpha), gamma interferon (IFN-gamma), transforming growth factor beta, and two housekeeping genes (encoding beta-actin and hypoxanthine phosphoribosyltransferase). |
| 591 | 16790792 | In this kinetic study, there was pronounced expression of Th1 cytokine mRNA (TNF-alpha, IFN-gamma, and IL-12), with transcripts being detected as early as 1 h postinfection. |
| 592 | 16790792 | Expression of anti-inflammatory cytokines, such as IL-4 and IL-10, was prominent in delayed samples from 1 to 4 days postinfection in response to infection with Leptospira interrogans. |
| 593 | 16814903 | The increased resistance was accompanied by a markedly lower antigen-driven TGF-beta and IL-10 responses in the lesion-draining lymph nodes, concomitant with significantly higher IFN-gamma production. |
| 594 | 16814903 | In both cases, similarly slower lesion growth and lower parasite burden were found that was associated with increased IFN-gamma and IL-10 responses in the lesion-draining lymph nodes. |
| 595 | 16862213 | In fact, a legumain-based DNA vaccine served as a tool to prove this point, as it induced a robust CD8+ T cell response against TAMs, which dramatically reduced their density in tumor tissues and resulted in a marked decrease in proangiogenic factors released by TAMs such as TGF-beta, TNF-alpha, MMP-9, and VEGF. |
| 596 | 16896154 | CTLA-4 blockade decreases TGF-beta, IDO, and viral RNA expression in tissues of SIVmac251-infected macaques. |
| 597 | 16896154 | Regulatory T (T(reg)) cells are a subset of CD25(+)CD4(+) T cells that constitutively express high levels of cytotoxic T lymphocyte antigen-4 (CTLA-4) and suppress T-cell activation and effector functions. |
| 598 | 16896154 | CTLA-4 blockade decreased expression of the tryptophan-depleting enzyme IDO and the level of the suppressive cytokine transforming growth factor-beta (TGF-beta) in tissues. |
| 599 | 16896154 | CTLA-4 blockade was associated with decreased viral RNA levels in lymph nodes and an increase in the effector function of both SIV-specific CD4(+) and CD8(+) T cells. |
| 600 | 16896154 | CTLA-4 blockade decreases TGF-beta, IDO, and viral RNA expression in tissues of SIVmac251-infected macaques. |
| 601 | 16896154 | Regulatory T (T(reg)) cells are a subset of CD25(+)CD4(+) T cells that constitutively express high levels of cytotoxic T lymphocyte antigen-4 (CTLA-4) and suppress T-cell activation and effector functions. |
| 602 | 16896154 | CTLA-4 blockade decreased expression of the tryptophan-depleting enzyme IDO and the level of the suppressive cytokine transforming growth factor-beta (TGF-beta) in tissues. |
| 603 | 16896154 | CTLA-4 blockade was associated with decreased viral RNA levels in lymph nodes and an increase in the effector function of both SIV-specific CD4(+) and CD8(+) T cells. |
| 604 | 16918694 | Sublingual tolerance induction with antigen conjugated to cholera toxin B subunit induces Foxp3+CD25+CD4+ regulatory T cells and suppresses delayed-type hypersensitivity reactions. |
| 605 | 16918694 | -induced tolerance be explained by the generation of Foxp3+CD25+CD4+ regulatory T cells (T(reg))? |
| 606 | 16918694 | The intracellular expression of Foxp3 was strongly increased in OVA-specific (KJ1-26+) CD4+ T cells from OVA/CTB-treated mice. |
| 607 | 16918694 | Thus, s.l. administration of CTB-conjugated Ag can efficiently induce peripheral T-cell tolerance associated with strong increases in serum TGF-beta levels and in Ag-specific Foxp3+CD25+CD4+ T(reg) cells. |
| 608 | 16938461 | The genes investigated were those that code for interleukin (IL)-1alpha, IL-1beta, IL-1R, IL-1RA, IL-4RA, IL-2, IL-4, IL-6, IL-10, IL-12, interferon-gamma (IFN-gamma), transforming growth factor-beta (TGF-beta), and tumor necrosis factor-alpha (TNF-alpha). |
| 609 | 16938461 | Analyses of the data identified TGF-beta codon 25 GG (92.85% vs. 64.44%, p=0.04, OR=7.17), IL-4 -1098 GG (16.6% vs. 0.0%, p=0.05, OR=18.33), IL-10 -1082 GG (28.5% vs. 6.8%, p=0.05, OR=5.47), and IL-10 -1082 GCC/GCC (28.57% vs. 4.5%, p=0.025, OR=8.4) polymorphisms as risk factors for progression of bladder cancer. |
| 610 | 16938461 | The genes investigated were those that code for interleukin (IL)-1alpha, IL-1beta, IL-1R, IL-1RA, IL-4RA, IL-2, IL-4, IL-6, IL-10, IL-12, interferon-gamma (IFN-gamma), transforming growth factor-beta (TGF-beta), and tumor necrosis factor-alpha (TNF-alpha). |
| 611 | 16938461 | Analyses of the data identified TGF-beta codon 25 GG (92.85% vs. 64.44%, p=0.04, OR=7.17), IL-4 -1098 GG (16.6% vs. 0.0%, p=0.05, OR=18.33), IL-10 -1082 GG (28.5% vs. 6.8%, p=0.05, OR=5.47), and IL-10 -1082 GCC/GCC (28.57% vs. 4.5%, p=0.025, OR=8.4) polymorphisms as risk factors for progression of bladder cancer. |
| 612 | 16956640 | Profiles of cytokines such as IFN-gamma, IL-2, IL-4, IL-5 and TGF-beta in immunized mice showed a naive T-cells bias to Th1 and Th3 polarization. |
| 613 | 17079673 | Increased T cell recruitment to the CNS after amyloid beta 1-42 immunization in Alzheimer's mice overproducing transforming growth factor-beta 1. |
| 614 | 17079673 | Immunotherapy targeting the amyloid beta (Abeta) peptide is a novel therapy under investigation for the treatment of Alzheimer's disease (AD). |
| 615 | 17079673 | Furthermore, TGF-beta1 overexpression in a mouse model for AD [amyloid precursor protein (APP) mice] leads to development of additional T cell infiltrates when mice were immunized at a young but not old age with AN1792. |
| 616 | 17079673 | Notably, only mice overproducing both Abeta (APP mice) and TGF-beta1 experienced a rise in T lymphocyte number after immunization. |
| 617 | 17079673 | These results demonstrate that TGF-beta1 overproduction in the brain can promote T cell infiltration, in particular after Abeta(1-42) immunization. |
| 618 | 17079673 | Likewise, levels of TGF-beta1 or other immune factors in brains of AD patients may influence the response to Abeta(1-42) immunization. |
| 619 | 17079673 | Increased T cell recruitment to the CNS after amyloid beta 1-42 immunization in Alzheimer's mice overproducing transforming growth factor-beta 1. |
| 620 | 17079673 | Immunotherapy targeting the amyloid beta (Abeta) peptide is a novel therapy under investigation for the treatment of Alzheimer's disease (AD). |
| 621 | 17079673 | Furthermore, TGF-beta1 overexpression in a mouse model for AD [amyloid precursor protein (APP) mice] leads to development of additional T cell infiltrates when mice were immunized at a young but not old age with AN1792. |
| 622 | 17079673 | Notably, only mice overproducing both Abeta (APP mice) and TGF-beta1 experienced a rise in T lymphocyte number after immunization. |
| 623 | 17079673 | These results demonstrate that TGF-beta1 overproduction in the brain can promote T cell infiltration, in particular after Abeta(1-42) immunization. |
| 624 | 17079673 | Likewise, levels of TGF-beta1 or other immune factors in brains of AD patients may influence the response to Abeta(1-42) immunization. |
| 625 | 17079673 | Increased T cell recruitment to the CNS after amyloid beta 1-42 immunization in Alzheimer's mice overproducing transforming growth factor-beta 1. |
| 626 | 17079673 | Immunotherapy targeting the amyloid beta (Abeta) peptide is a novel therapy under investigation for the treatment of Alzheimer's disease (AD). |
| 627 | 17079673 | Furthermore, TGF-beta1 overexpression in a mouse model for AD [amyloid precursor protein (APP) mice] leads to development of additional T cell infiltrates when mice were immunized at a young but not old age with AN1792. |
| 628 | 17079673 | Notably, only mice overproducing both Abeta (APP mice) and TGF-beta1 experienced a rise in T lymphocyte number after immunization. |
| 629 | 17079673 | These results demonstrate that TGF-beta1 overproduction in the brain can promote T cell infiltration, in particular after Abeta(1-42) immunization. |
| 630 | 17079673 | Likewise, levels of TGF-beta1 or other immune factors in brains of AD patients may influence the response to Abeta(1-42) immunization. |
| 631 | 17079673 | Increased T cell recruitment to the CNS after amyloid beta 1-42 immunization in Alzheimer's mice overproducing transforming growth factor-beta 1. |
| 632 | 17079673 | Immunotherapy targeting the amyloid beta (Abeta) peptide is a novel therapy under investigation for the treatment of Alzheimer's disease (AD). |
| 633 | 17079673 | Furthermore, TGF-beta1 overexpression in a mouse model for AD [amyloid precursor protein (APP) mice] leads to development of additional T cell infiltrates when mice were immunized at a young but not old age with AN1792. |
| 634 | 17079673 | Notably, only mice overproducing both Abeta (APP mice) and TGF-beta1 experienced a rise in T lymphocyte number after immunization. |
| 635 | 17079673 | These results demonstrate that TGF-beta1 overproduction in the brain can promote T cell infiltration, in particular after Abeta(1-42) immunization. |
| 636 | 17079673 | Likewise, levels of TGF-beta1 or other immune factors in brains of AD patients may influence the response to Abeta(1-42) immunization. |
| 637 | 17079673 | Increased T cell recruitment to the CNS after amyloid beta 1-42 immunization in Alzheimer's mice overproducing transforming growth factor-beta 1. |
| 638 | 17079673 | Immunotherapy targeting the amyloid beta (Abeta) peptide is a novel therapy under investigation for the treatment of Alzheimer's disease (AD). |
| 639 | 17079673 | Furthermore, TGF-beta1 overexpression in a mouse model for AD [amyloid precursor protein (APP) mice] leads to development of additional T cell infiltrates when mice were immunized at a young but not old age with AN1792. |
| 640 | 17079673 | Notably, only mice overproducing both Abeta (APP mice) and TGF-beta1 experienced a rise in T lymphocyte number after immunization. |
| 641 | 17079673 | These results demonstrate that TGF-beta1 overproduction in the brain can promote T cell infiltration, in particular after Abeta(1-42) immunization. |
| 642 | 17079673 | Likewise, levels of TGF-beta1 or other immune factors in brains of AD patients may influence the response to Abeta(1-42) immunization. |
| 643 | 17082610 | Distinct molecular program imposed on CD4+ T cell targets by CD4+CD25+ regulatory T cells. |
| 644 | 17082610 | CD4+CD25+ regulatory T cells (Tregs) are key modulators of immunity, but their mechanism of action is unclear. |
| 645 | 17082610 | To elucidate the molecular consequences of Treg encounter, we analyzed changes in gene expression in CD4+ T cell targets activated in the presence or absence of CD4+CD25+ Tregs. |
| 646 | 17082610 | Therefore, we compared the gene profile of T cells following Treg encounter with that of T cells made anergic, TGF-beta-treated, or IL-2-deprived; all possible modes of Treg action. |
| 647 | 17106649 | Flow cytometric analyses showed that TGF-beta2 does not suppress the upregulation of MHC (major histocompatibility complex) class II molecules and the T cell stimulatory capacity of human DC that were stimulated with a strong cytokine cocktail containing tumor necrosis factor alpha (TNF-alpha), IL-1beta, IL-6 and prostaglandin E2 (PGE2). |
| 648 | 17106649 | Although both mature and immature DC expressed comparable amounts of the TGF-beta receptor type II, Smad2 phosphorylation and subsequent upregulation of Smad7 was inhibited in mature DC, but not immature DC. |
| 649 | 17106649 | However, further analysis revealed that mature DC alone are not sufficient to mediate full T cell activation in the presence of TGF-beta2, unless IL-12 is added to the DC/T-cell coculture. |
| 650 | 17106649 | Finally, we demonstrate that MHC class II expression and IL-12 secretion by DC are not disturbed by TGF-beta2 after DC stimulation with a modified maturation cocktail containing the Toll-like receptor (TLR)-ligands Poly I:C or R848, TNF-alpha, IL-1beta and INF-gamma. |
| 651 | 17163448 | The effect of T(reg) cells was largely dependent on cell-cell contact, but not on IL-10 or TGF-beta. |
| 652 | 17215847 | It can be used to deliver protein drugs such as glucagon-like peptide 1 (GLP-1), leptin or transforming growth factor beta (TGF-beta). |
| 653 | 17217432 | Levels of IL-12p40, TNFalpha, TGFbeta, IFNgamma and IL-10 mRNA were assessed by laser capture microdissection followed by quantitative real-time PCR in the pulmonary granulomas of unimmunized and BCG-vaccinated guinea pigs infected by aerosol with virulent Mycobacterium tuberculosis. |
| 654 | 17217432 | The cytokine profile of granulomas from vaccinated guinea pigs shifted from type 1 cytokine mRNA (IFNgamma and IL-12p40) at 3 weeks to a predominantly anti-inflammatory environment (TGFbeta mRNA) at 6 weeks. |
| 655 | 17217432 | Levels of IL-12p40, TNFalpha, TGFbeta, IFNgamma and IL-10 mRNA were assessed by laser capture microdissection followed by quantitative real-time PCR in the pulmonary granulomas of unimmunized and BCG-vaccinated guinea pigs infected by aerosol with virulent Mycobacterium tuberculosis. |
| 656 | 17217432 | The cytokine profile of granulomas from vaccinated guinea pigs shifted from type 1 cytokine mRNA (IFNgamma and IL-12p40) at 3 weeks to a predominantly anti-inflammatory environment (TGFbeta mRNA) at 6 weeks. |
| 657 | 17275522 | DC were propagated from C3H (H2(k)) bone marrow (BM) using granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin-4 (IL-4). |
| 658 | 17275522 | Expression of major histocompatibility complex (MHC) class I and II was not affected, while CD40, CD80, and CD86 costimulatory molecules on DC were significantly inhibited by treatment with TGF-beta. |
| 659 | 17275522 | This observation correlated with reduced interferon-gamma (IFN-gamma) and increased IL-10 production. |
| 660 | 17293100 | This paradox has been partially resolved by data clarifying the immunoregulatory role of skin cytokines (e.g. transforming growth factor-beta and interleukin-10) and the consequences of antigen presentation by subsets of skin-associated antigen-presenting cells. |
| 661 | 17299718 | Immunosuppression during active tuberculosis is characterized by decreased interferon- gamma production and CD25 expression with elevated forkhead box P3, transforming growth factor- beta , and interleukin-4 mRNA levels. |
| 662 | 17299718 | All 3 groups displayed BCG-induced increases in effector and regulatory T cell phenotypes as defined by CD4(+)CD25(lo) and CD4(+)CD25(hi) T cells, respectively. |
| 663 | 17299718 | In case patients with active disease, BCG stimulation induced the lowest increase of CD25, CD4(+)CD25(hi), CTLA-4, and interferon- gamma . |
| 664 | 17299718 | However, these case patients expressed the highest mRNA levels of forkhead box P3, transforming growth factor (TGF)- beta , and interleukin (IL)-4 and a lower T-bet : GATA-3 ratio. |
| 665 | 17299718 | There were no significant differences in IL-4 delta 2, IL-10, or TGF- beta receptor-II mRNA expression between groups. |
| 666 | 17299718 | Immunosuppression during active tuberculosis is characterized by decreased interferon- gamma production and CD25 expression with elevated forkhead box P3, transforming growth factor- beta , and interleukin-4 mRNA levels. |
| 667 | 17299718 | All 3 groups displayed BCG-induced increases in effector and regulatory T cell phenotypes as defined by CD4(+)CD25(lo) and CD4(+)CD25(hi) T cells, respectively. |
| 668 | 17299718 | In case patients with active disease, BCG stimulation induced the lowest increase of CD25, CD4(+)CD25(hi), CTLA-4, and interferon- gamma . |
| 669 | 17299718 | However, these case patients expressed the highest mRNA levels of forkhead box P3, transforming growth factor (TGF)- beta , and interleukin (IL)-4 and a lower T-bet : GATA-3 ratio. |
| 670 | 17299718 | There were no significant differences in IL-4 delta 2, IL-10, or TGF- beta receptor-II mRNA expression between groups. |
| 671 | 17339357 | Supernatants were assayed for interleukin-12p70 (IL-12p70), IL-10, IL-6, transforming growth factor beta (TGF-beta), NO, and tumor necrosis factor alpha (TNF-alpha). |
| 672 | 17339357 | Our results indicate that the addition of MAX upregulates the cytokines associated with a type 2 response (IL-10, IL-6, and TGF-beta) but downregulates type 1 cytokines (IL-12p70 and TNF-alpha) and NO. |
| 673 | 17339357 | Supernatants were assayed for interleukin-12p70 (IL-12p70), IL-10, IL-6, transforming growth factor beta (TGF-beta), NO, and tumor necrosis factor alpha (TNF-alpha). |
| 674 | 17339357 | Our results indicate that the addition of MAX upregulates the cytokines associated with a type 2 response (IL-10, IL-6, and TGF-beta) but downregulates type 1 cytokines (IL-12p70 and TNF-alpha) and NO. |
| 675 | 17473921 | Tumor lysate-pulsed DCs were rendered TGF-beta insensitive by dominant-negative TGF-beta type II receptor (TbetaRIIDN), leading to the blockade of TGF-beta signals to members of the Smad family, which are the principal cytoplasmic intermediates involved in the transduction of signals from TGF-beta receptors to the nucleus. |
| 676 | 17473921 | Phosphorylated Smad-2 was undetectable and expression of surface co-stimulatory molecules (CD80/CD86) were upregulated in TbetaRIIDN DCs after antigen and TGF-beta1 stimulation. |
| 677 | 17473921 | Vaccination of C57BL/6 tumor-bearing mice with the TbetaRIIDN DC vaccine induced potent tumor-specific cytotoxic T lymphocyte responses against TRAMP-C2 tumors, increased serum IFN-gamma and IL-12 level, inhibited tumor growth and increased mouse survival. |
| 678 | 17473921 | Tumor lysate-pulsed DCs were rendered TGF-beta insensitive by dominant-negative TGF-beta type II receptor (TbetaRIIDN), leading to the blockade of TGF-beta signals to members of the Smad family, which are the principal cytoplasmic intermediates involved in the transduction of signals from TGF-beta receptors to the nucleus. |
| 679 | 17473921 | Phosphorylated Smad-2 was undetectable and expression of surface co-stimulatory molecules (CD80/CD86) were upregulated in TbetaRIIDN DCs after antigen and TGF-beta1 stimulation. |
| 680 | 17473921 | Vaccination of C57BL/6 tumor-bearing mice with the TbetaRIIDN DC vaccine induced potent tumor-specific cytotoxic T lymphocyte responses against TRAMP-C2 tumors, increased serum IFN-gamma and IL-12 level, inhibited tumor growth and increased mouse survival. |
| 681 | 17475646 | Functional Foxp3+ CD4+ CD25(Bright+) "natural" regulatory T cells are abundant in rabbit conjunctiva and suppress virus-specific CD4+ and CD8+ effector T cells during ocular herpes infection. |
| 682 | 17475646 | We studied the phenotype and distribution of "naturally" occurring CD4(+) CD25(+) T regulatory cells (CD4(+) CD25(+) nT(reg) cells) resident in rabbit conjunctiva, the main T-cell inductive site of the ocular mucosal immune system, and we investigated their suppressive capacities using herpes simplex virus type 1 (HSV-1)-specific effector T (T(eff)) cells induced during ocular infection. |
| 683 | 17475646 | The expression of CD4, CD25, CTLA4, GITR, and Foxp3 was examined by reverse transcription-PCR, Western blotting, and fluorescence-activated cell sorter analysis in CD45(+) pan-leukocytes isolated from conjunctiva, spleen, and peripheral blood monocyte cells (PBMC) of HSV-1-infected and uninfected rabbits. |
| 684 | 17475646 | Normal conjunctiva showed a higher frequency of CD4(+) CD25((Bright+)) T cells than did spleen and PBMC. |
| 685 | 17475646 | These cells expressed high levels of Foxp3, GITR, and CTLA4 molecules. |
| 686 | 17475646 | CD4(+) CD25((Bright+)) T cells were localized continuously along the upper and lower palpebral and bulbar conjunctiva, throughout the epithelium and substantia propria. |
| 687 | 17475646 | Conjunctiva-derived CD4(+) CD25((Bright+)) T cells, but not CD4(+) CD25((low)) T cells, efficiently suppressed HSV-specific CD4(+) and CD8(+) T(eff) cells. |
| 688 | 17475646 | The CD4(+) CD25((Bright+)) T-cell-mediated suppression was effective on both peripheral blood and conjunctiva infiltrating T(eff) cells and was cell-cell contact dependent but independent of interleukin-10 and transforming growth factor beta. |
| 689 | 17475646 | Interestingly, during an ocular herpes infection, there was a selective increase in the frequency and suppressive capacity of Foxp3(+) CD4(+) CD25((Bright+)) T cells in conjunctiva but not in the spleen or in peripheral blood. |
| 690 | 17475646 | Altogether, these results provide the first evidence that functional Foxp3(+) CD4(+) CD25((Bright+)) T(reg) cells accumulate in the conjunctiva. |
| 691 | 17475646 | It remains to be determined whether conjunctiva CD4(+) CD25(+) nT(reg) cells affect the topical/mucosal delivery of subunit vaccines that stimulate the ocular mucosal immune system. |
| 692 | 17505023 | Induction of a distinct CD8 Tnc17 subset by transforming growth factor-beta and interleukin-6. |
| 693 | 17505023 | Cross-talk between TGF-beta and IL-6 has been shown to direct the differentiation of CD4(+) cells into special IL-17-secreting cells, which are termed Th17 cells. |
| 694 | 17505023 | In this study, we demonstrated that TGF-beta and IL-6 could stimulate CD8(+) cells to differentiate into noncytotoxic, IL-17-producing cells in MLC. |
| 695 | 17505023 | These IL-17-producing CD8(+) cells exhibit a unique granzyme B(-)IFN-gamma(-)IL-10(-) phenotype. |
| 696 | 17505023 | The mRNA level of Th2/T cytotoxic 2 (Tc2) transcription factors GATA3 and Th1/Tc1 transcription factors T-box expressed in T cell (T-bet) as well as its target H2.O-like homeobox (Hlx) is decreased in CD8(+) cells from TGF-beta- and IL-6-treated MLC. |
| 697 | 17505023 | In addition, these CD8(+) cells display a marked up-regulation of retinoic acid-related orphan receptor-gammat, a key IL-17 transcription factor. |
| 698 | 17505023 | These results demonstrate that the existence of an IL-17-producing CD8(+) subset belongs to neither the Tc1 nor the Tc2 subset and can be categorized as a T noncytotoxic 17 (Tnc17) subset. |
| 699 | 17505023 | Induction of a distinct CD8 Tnc17 subset by transforming growth factor-beta and interleukin-6. |
| 700 | 17505023 | Cross-talk between TGF-beta and IL-6 has been shown to direct the differentiation of CD4(+) cells into special IL-17-secreting cells, which are termed Th17 cells. |
| 701 | 17505023 | In this study, we demonstrated that TGF-beta and IL-6 could stimulate CD8(+) cells to differentiate into noncytotoxic, IL-17-producing cells in MLC. |
| 702 | 17505023 | These IL-17-producing CD8(+) cells exhibit a unique granzyme B(-)IFN-gamma(-)IL-10(-) phenotype. |
| 703 | 17505023 | The mRNA level of Th2/T cytotoxic 2 (Tc2) transcription factors GATA3 and Th1/Tc1 transcription factors T-box expressed in T cell (T-bet) as well as its target H2.O-like homeobox (Hlx) is decreased in CD8(+) cells from TGF-beta- and IL-6-treated MLC. |
| 704 | 17505023 | In addition, these CD8(+) cells display a marked up-regulation of retinoic acid-related orphan receptor-gammat, a key IL-17 transcription factor. |
| 705 | 17505023 | These results demonstrate that the existence of an IL-17-producing CD8(+) subset belongs to neither the Tc1 nor the Tc2 subset and can be categorized as a T noncytotoxic 17 (Tnc17) subset. |
| 706 | 17505023 | Induction of a distinct CD8 Tnc17 subset by transforming growth factor-beta and interleukin-6. |
| 707 | 17505023 | Cross-talk between TGF-beta and IL-6 has been shown to direct the differentiation of CD4(+) cells into special IL-17-secreting cells, which are termed Th17 cells. |
| 708 | 17505023 | In this study, we demonstrated that TGF-beta and IL-6 could stimulate CD8(+) cells to differentiate into noncytotoxic, IL-17-producing cells in MLC. |
| 709 | 17505023 | These IL-17-producing CD8(+) cells exhibit a unique granzyme B(-)IFN-gamma(-)IL-10(-) phenotype. |
| 710 | 17505023 | The mRNA level of Th2/T cytotoxic 2 (Tc2) transcription factors GATA3 and Th1/Tc1 transcription factors T-box expressed in T cell (T-bet) as well as its target H2.O-like homeobox (Hlx) is decreased in CD8(+) cells from TGF-beta- and IL-6-treated MLC. |
| 711 | 17505023 | In addition, these CD8(+) cells display a marked up-regulation of retinoic acid-related orphan receptor-gammat, a key IL-17 transcription factor. |
| 712 | 17505023 | These results demonstrate that the existence of an IL-17-producing CD8(+) subset belongs to neither the Tc1 nor the Tc2 subset and can be categorized as a T noncytotoxic 17 (Tnc17) subset. |
| 713 | 17505023 | Induction of a distinct CD8 Tnc17 subset by transforming growth factor-beta and interleukin-6. |
| 714 | 17505023 | Cross-talk between TGF-beta and IL-6 has been shown to direct the differentiation of CD4(+) cells into special IL-17-secreting cells, which are termed Th17 cells. |
| 715 | 17505023 | In this study, we demonstrated that TGF-beta and IL-6 could stimulate CD8(+) cells to differentiate into noncytotoxic, IL-17-producing cells in MLC. |
| 716 | 17505023 | These IL-17-producing CD8(+) cells exhibit a unique granzyme B(-)IFN-gamma(-)IL-10(-) phenotype. |
| 717 | 17505023 | The mRNA level of Th2/T cytotoxic 2 (Tc2) transcription factors GATA3 and Th1/Tc1 transcription factors T-box expressed in T cell (T-bet) as well as its target H2.O-like homeobox (Hlx) is decreased in CD8(+) cells from TGF-beta- and IL-6-treated MLC. |
| 718 | 17505023 | In addition, these CD8(+) cells display a marked up-regulation of retinoic acid-related orphan receptor-gammat, a key IL-17 transcription factor. |
| 719 | 17505023 | These results demonstrate that the existence of an IL-17-producing CD8(+) subset belongs to neither the Tc1 nor the Tc2 subset and can be categorized as a T noncytotoxic 17 (Tnc17) subset. |
| 720 | 17570105 | This pathway involves enhanced induction of CD8(+) cytotoxic T lymphocytes (CTLs) and down-regulation of interleukin-4 and transforming growth factor- beta , leading to further enhancement of the activity of CD8(+) CTLs and of other microbicidal pathways. |
| 721 | 17724448 | In view of this, several approaches are being studied to inhibit TGF-beta activity, including neutralizing antibodies, soluble receptors, receptor kinase antagonist drugs, antisense reagents and a number of less specific drugs such as angiotensin II antagonists and tranilast. |
| 722 | 17785784 | In this study, we show that monocyte-derived DCs pretreated with the vitamin A derivative all-trans retinoic acid (RA) indeed acquired several attributes characteristic of mucosal DC: secretion of TGF-beta and IL-6 and the capacity to augment mucosal homing receptor expression and IgA responses in cocultured lymphocytes. |
| 723 | 17786327 | Benefits of gene transduction of granulocyte macrophage colony-stimulating factor in cancer vaccine using genetically modified dendritic cells. |
| 724 | 17786327 | Granulocyte macrophage colony-stimulating factor (GM-CSF) is a key cytokine for the generation and stimulation of dendritic cells (DCs), and it may also play a pivotal role in promoting the survival of DCs. |
| 725 | 17786327 | In this study, the feasibility of creating a cancer vaccine using DCs adenovirally transduced with the carcinoembryonic antigen (CEA) gene and the GM-CSF gene was examined. |
| 726 | 17786327 | Co-transduction of the GM-CSF gene into DCs inhibited apoptosis of these DCs themselves via up-regulation of Bcl-x(L) expression, leading to the extension of the lifespan of these DCs. |
| 727 | 17786327 | Furthermore, the transduction of the GM-CSF gene into DCs also suppressed the incidence of apoptosis of DCs induced by transforming growth factor-beta1 (TGFbeta-1). |
| 728 | 17786327 | Immunotherapy using these genetically modified DCs may therefore be useful with several advantages as follows: i) adenoviral toxicity to DCs can be reduced; ii) the lifespan of vaccinated DCs can be prolonged; and iii) GM-CSF may protect DCs from apoptosis induced by tumor-derived TGFbeta-1 in the regional lymph nodes. |
| 729 | 17786327 | Benefits of gene transduction of granulocyte macrophage colony-stimulating factor in cancer vaccine using genetically modified dendritic cells. |
| 730 | 17786327 | Granulocyte macrophage colony-stimulating factor (GM-CSF) is a key cytokine for the generation and stimulation of dendritic cells (DCs), and it may also play a pivotal role in promoting the survival of DCs. |
| 731 | 17786327 | In this study, the feasibility of creating a cancer vaccine using DCs adenovirally transduced with the carcinoembryonic antigen (CEA) gene and the GM-CSF gene was examined. |
| 732 | 17786327 | Co-transduction of the GM-CSF gene into DCs inhibited apoptosis of these DCs themselves via up-regulation of Bcl-x(L) expression, leading to the extension of the lifespan of these DCs. |
| 733 | 17786327 | Furthermore, the transduction of the GM-CSF gene into DCs also suppressed the incidence of apoptosis of DCs induced by transforming growth factor-beta1 (TGFbeta-1). |
| 734 | 17786327 | Immunotherapy using these genetically modified DCs may therefore be useful with several advantages as follows: i) adenoviral toxicity to DCs can be reduced; ii) the lifespan of vaccinated DCs can be prolonged; and iii) GM-CSF may protect DCs from apoptosis induced by tumor-derived TGFbeta-1 in the regional lymph nodes. |
| 735 | 17873879 | These macrophages induced, by a mechanism dependent on IL-10, retinoic acid and exogenous transforming growth factor-beta, the differentiation of Foxp3+ regulatory T cells. |
| 736 | 17881504 | In this study, we determined if the sensitivity of the currently available in vitro test to detect bovine tuberculosis could be enhanced by adding the following immunomodulators: interleukin-2 (IL-2); granulocyte-macrophage colony-stimulating factor (GM-CSF); antibodies neutralizing IL-10 and transforming growth factor beta (TGF-beta); mono-methyl-l-arginine, which blocks nitric oxide production; and l-methyl-tryptophan, which interferes with the indoleamine dioxygenase pathway. |
| 737 | 17881504 | Mono-methyl-l-arginine, l-methyl-tryptophan, or an antibody neutralizing TGF-beta had minimal impact on IFN-gamma production. |
| 738 | 17881504 | IL-2 and GM-CSF promoted IFN-gamma release whether antigen was present or not. |
| 739 | 17881504 | In this study, we determined if the sensitivity of the currently available in vitro test to detect bovine tuberculosis could be enhanced by adding the following immunomodulators: interleukin-2 (IL-2); granulocyte-macrophage colony-stimulating factor (GM-CSF); antibodies neutralizing IL-10 and transforming growth factor beta (TGF-beta); mono-methyl-l-arginine, which blocks nitric oxide production; and l-methyl-tryptophan, which interferes with the indoleamine dioxygenase pathway. |
| 740 | 17881504 | Mono-methyl-l-arginine, l-methyl-tryptophan, or an antibody neutralizing TGF-beta had minimal impact on IFN-gamma production. |
| 741 | 17881504 | IL-2 and GM-CSF promoted IFN-gamma release whether antigen was present or not. |
| 742 | 17982065 | NIMA(d)-exposed splenocytes exhibited bystander suppression of tetanus-specific delayed-type hypersensitivity responses, which was reversed with Abs to TGF-beta and IL-10. |
| 743 | 17982065 | Rejector and acceptor NIMA(d)-exposed mice had reduced T effector responses and increased Foxp3(+) T(R) cells (CD4(+)CD25(+)Foxp3(+) T(R)) in spleen and lymph nodes compared with controls. |
| 744 | 17982065 | The key features distinguishing NIMA(d)-exposed acceptors from all other mice were: 1) higher frequency of IL-10- and TGF-beta-producing cells primarily in the CD4(+)CD25(+) T cell subset within lymph nodes and allografts, 2) a suppressed delayed-type hypersensitivity response to B6D2F1 Ags, and 3) allografts enriched in LAP(+), Foxp3(+), and CD4(+) T cells, with few CD8(+) T cells. |
| 745 | 17997199 | This Th1 shift was supported by an increased T-bet/GATA3 mRNA ratio. |
| 746 | 17997199 | IL-5 production within the airways was suppressed after the pretreatment with rCTB-Bet v 1, while local allergen-specific IgA antibodies were markedly enhanced by pretreatment with the construct. |
| 747 | 17997199 | Upregulation of Foxp3, IL-10 and TGF-beta mRNA expression was detected in splenocytes after pretreatment with unconjugated allergen but not with the fusion molecule, indicating that antigen conjugation to a mucosal carrier modifies the immunomodulating properties of an antigen/allergen. |
| 748 | 18032570 | Real-time PCR analysis of the acquired RNA clearly demonstrated that primary tubercles from BCG-vaccinated guinea pigs were overwhelmed with mRNA from the anti-inflammatory cytokine, transforming growth factor (TGF)-beta, with some IFN-gamma and IL-12p40 mRNA. |
| 749 | 18032570 | The cytokine mRNA profile of secondary lesions from unimmunized animals was strikingly similar to the profile of primary lesions from BCG-vaccinated guinea pigs (i.e., a predominance of TGF-beta mRNA with some IL-12p40 and IFN-gamma mRNA), indicating that the lung lobes from which these lesions were retrieved had been naturally "vaccinated" by the time the bloodborne bacilli returned to the lung at 3 to 4 weeks after infection. |
| 750 | 18032570 | Furthermore, cytokine mRNA analysis of splenic granulomas from nonvaccinated and vaccinated animals showed close resemblance to primary granulomas recovered from the lungs of the same animal, that is, high levels of TNF-alpha mRNA in unimmunized animals, and mostly TGF-beta mRNA in BCG-vaccinated guinea pigs. |
| 751 | 18032570 | Real-time PCR analysis of the acquired RNA clearly demonstrated that primary tubercles from BCG-vaccinated guinea pigs were overwhelmed with mRNA from the anti-inflammatory cytokine, transforming growth factor (TGF)-beta, with some IFN-gamma and IL-12p40 mRNA. |
| 752 | 18032570 | The cytokine mRNA profile of secondary lesions from unimmunized animals was strikingly similar to the profile of primary lesions from BCG-vaccinated guinea pigs (i.e., a predominance of TGF-beta mRNA with some IL-12p40 and IFN-gamma mRNA), indicating that the lung lobes from which these lesions were retrieved had been naturally "vaccinated" by the time the bloodborne bacilli returned to the lung at 3 to 4 weeks after infection. |
| 753 | 18032570 | Furthermore, cytokine mRNA analysis of splenic granulomas from nonvaccinated and vaccinated animals showed close resemblance to primary granulomas recovered from the lungs of the same animal, that is, high levels of TNF-alpha mRNA in unimmunized animals, and mostly TGF-beta mRNA in BCG-vaccinated guinea pigs. |
| 754 | 18040852 | The splenocytes from protected mice and morphine low concentration-treated infected-PM, elaborated significantly (p < 0.05) enhanced levels of interleukin-12, interferon-gamma, tumor necrosis factor-alpha, granulocyte-macrophage colony-stimulating factor and nitrite in the culture medium; a high dose/concentration suppressed their elaboration. |
| 755 | 18040852 | Curiously, only morphine high dose/concentration-treated infected mice splenocytes and infected PM, produced significantly (p < 0.05) increased quantity of transforming growth factor-beta1. |
| 756 | 18180378 | Activation of extracellular signal-regulated kinase (ERK) increased TGF-beta expression while expression of a constitutively activated interferon regulatory factor-3 (IRF3) stimulated IL-10 secretion by DCs. |
| 757 | 18180378 | ERK and IRF3 suppressed the immune response and stimulated expansion of regulatory T cells. |
| 758 | 18237828 | Gene expression in fish vaccinated at 15 degrees C (the protected fish) was up-regulated with regard to the pro-inflammatory cytokines IFN-gamma, TNF-alpha, IL-6 and the anti-inflammatory cytokines IL-10 and TGF-beta, the cell receptors TcR, CD8alpha, CD4, C5aR and the teleost specific immunoglobulin IgT. |
| 759 | 18317534 | In brief, naturally occurring thymic-derived CD4+CD25+ Tregs are characterized by constitutive expression of the transcription factor FOXP3, while antigen-induced or adaptive Tregs are mainly identified by expression of immunosuppressive cytokines (interleukin-10 (IL-10) and/or transforming growth factor-beta (TGF-beta)). |
| 760 | 18329193 | Because cytokines play a key role in immunity, the expression levels of TGF-beta, IFN-gamma, IL-4 and IL-6 were measured, by RT-PCR in the spleen, the ileum and the mesenteric lymph node of the animals at the end of the experiment. |
| 761 | 18329193 | In the mesenteric lymph node, a significantly lower expression of both TGF-beta and IFN-gamma mRNA expression levels is observed in animals feed with DON when compared with control piglets. |
| 762 | 18329193 | Because cytokines play a key role in immunity, the expression levels of TGF-beta, IFN-gamma, IL-4 and IL-6 were measured, by RT-PCR in the spleen, the ileum and the mesenteric lymph node of the animals at the end of the experiment. |
| 763 | 18329193 | In the mesenteric lymph node, a significantly lower expression of both TGF-beta and IFN-gamma mRNA expression levels is observed in animals feed with DON when compared with control piglets. |
| 764 | 18363998 | This lymphocyte family consists of diverse subsets ranging from interferon-gamma (IFN-gamma)-producing T-helper 1 (Th1) cells to transforming growth factor-beta (TGF-beta)-secreting T-regulatory cells, which have opposite roles in modulating immune responses to pathogens, tumor cells, and self-antigens. |
| 765 | 18369622 | Besides the T reg cell, we have identified another immunoregulatory circuit initiated by NKT cells that produce IL-13 in response to tumor growth and this IL-13 then induces myeloid cells to make TGF-beta that inhibits cytotoxic T cell-mediated tumor immunosurveillance in several mouse tumor models. |
| 766 | 18419605 | Immunosuppression induced by immature dendritic cells is mediated by TGF-beta/IL-10 double-positive CD4+ regulatory T cells. |
| 767 | 18419605 | In this study, we investigated the in vitro T cell stimulatory capacity of iDC and mature DC (mDC) and found that both DC types induced a significant increase in the number of transforming growth factor (TGF)-beta and interleukin (IL)-10 double-positive CD4(+) T cells within 1 week of autologous DC/T cell co-cultures. |
| 768 | 18419605 | In iDC/T cell cultures, where antigen-specific T cell priming was significantly reduced as compared to mDC/T cell cultures, we demonstrated that the tolerogenic effect of iDC was mediated by soluble TGF-beta and IL-10 secreted by CD4(+)CD25(-)FOXP3(-) T cells. |
| 769 | 18419605 | In addition, the suppressive capacity of CD4(+) T cells conditioned by iDC was transferable to already primed antigen-specific CD8(+) T cell cultures. |
| 770 | 18419605 | In contrast, addition of CD4(+) T cells conditioned by mDC to primed antigen-specific CD8(+) T cells resulted in enhanced CD8(+) T cell responses, notwithstanding the presence of TGF-beta(+)/IL-10(+) T cells in the transferred fraction. |
| 771 | 18419605 | We show that iDC-conditioned CD4(+) T cells are globally immunosuppressive, while mDC induce globally immunostimulatory CD4(+) T cells. |
| 772 | 18419605 | Furthermore, TGF-beta(+)/IL-10(+) T cells are expanded by DC independent of their maturation status, but their suppressive function is dependent on immaturity of DC. |
| 773 | 18419605 | Immunosuppression induced by immature dendritic cells is mediated by TGF-beta/IL-10 double-positive CD4+ regulatory T cells. |
| 774 | 18419605 | In this study, we investigated the in vitro T cell stimulatory capacity of iDC and mature DC (mDC) and found that both DC types induced a significant increase in the number of transforming growth factor (TGF)-beta and interleukin (IL)-10 double-positive CD4(+) T cells within 1 week of autologous DC/T cell co-cultures. |
| 775 | 18419605 | In iDC/T cell cultures, where antigen-specific T cell priming was significantly reduced as compared to mDC/T cell cultures, we demonstrated that the tolerogenic effect of iDC was mediated by soluble TGF-beta and IL-10 secreted by CD4(+)CD25(-)FOXP3(-) T cells. |
| 776 | 18419605 | In addition, the suppressive capacity of CD4(+) T cells conditioned by iDC was transferable to already primed antigen-specific CD8(+) T cell cultures. |
| 777 | 18419605 | In contrast, addition of CD4(+) T cells conditioned by mDC to primed antigen-specific CD8(+) T cells resulted in enhanced CD8(+) T cell responses, notwithstanding the presence of TGF-beta(+)/IL-10(+) T cells in the transferred fraction. |
| 778 | 18419605 | We show that iDC-conditioned CD4(+) T cells are globally immunosuppressive, while mDC induce globally immunostimulatory CD4(+) T cells. |
| 779 | 18419605 | Furthermore, TGF-beta(+)/IL-10(+) T cells are expanded by DC independent of their maturation status, but their suppressive function is dependent on immaturity of DC. |
| 780 | 18419605 | Immunosuppression induced by immature dendritic cells is mediated by TGF-beta/IL-10 double-positive CD4+ regulatory T cells. |
| 781 | 18419605 | In this study, we investigated the in vitro T cell stimulatory capacity of iDC and mature DC (mDC) and found that both DC types induced a significant increase in the number of transforming growth factor (TGF)-beta and interleukin (IL)-10 double-positive CD4(+) T cells within 1 week of autologous DC/T cell co-cultures. |
| 782 | 18419605 | In iDC/T cell cultures, where antigen-specific T cell priming was significantly reduced as compared to mDC/T cell cultures, we demonstrated that the tolerogenic effect of iDC was mediated by soluble TGF-beta and IL-10 secreted by CD4(+)CD25(-)FOXP3(-) T cells. |
| 783 | 18419605 | In addition, the suppressive capacity of CD4(+) T cells conditioned by iDC was transferable to already primed antigen-specific CD8(+) T cell cultures. |
| 784 | 18419605 | In contrast, addition of CD4(+) T cells conditioned by mDC to primed antigen-specific CD8(+) T cells resulted in enhanced CD8(+) T cell responses, notwithstanding the presence of TGF-beta(+)/IL-10(+) T cells in the transferred fraction. |
| 785 | 18419605 | We show that iDC-conditioned CD4(+) T cells are globally immunosuppressive, while mDC induce globally immunostimulatory CD4(+) T cells. |
| 786 | 18419605 | Furthermore, TGF-beta(+)/IL-10(+) T cells are expanded by DC independent of their maturation status, but their suppressive function is dependent on immaturity of DC. |
| 787 | 18419605 | Immunosuppression induced by immature dendritic cells is mediated by TGF-beta/IL-10 double-positive CD4+ regulatory T cells. |
| 788 | 18419605 | In this study, we investigated the in vitro T cell stimulatory capacity of iDC and mature DC (mDC) and found that both DC types induced a significant increase in the number of transforming growth factor (TGF)-beta and interleukin (IL)-10 double-positive CD4(+) T cells within 1 week of autologous DC/T cell co-cultures. |
| 789 | 18419605 | In iDC/T cell cultures, where antigen-specific T cell priming was significantly reduced as compared to mDC/T cell cultures, we demonstrated that the tolerogenic effect of iDC was mediated by soluble TGF-beta and IL-10 secreted by CD4(+)CD25(-)FOXP3(-) T cells. |
| 790 | 18419605 | In addition, the suppressive capacity of CD4(+) T cells conditioned by iDC was transferable to already primed antigen-specific CD8(+) T cell cultures. |
| 791 | 18419605 | In contrast, addition of CD4(+) T cells conditioned by mDC to primed antigen-specific CD8(+) T cells resulted in enhanced CD8(+) T cell responses, notwithstanding the presence of TGF-beta(+)/IL-10(+) T cells in the transferred fraction. |
| 792 | 18419605 | We show that iDC-conditioned CD4(+) T cells are globally immunosuppressive, while mDC induce globally immunostimulatory CD4(+) T cells. |
| 793 | 18419605 | Furthermore, TGF-beta(+)/IL-10(+) T cells are expanded by DC independent of their maturation status, but their suppressive function is dependent on immaturity of DC. |
| 794 | 18490734 | Before or after AAC, animals received BCG, TLR4 agonist, IFN-gamma, or TLR4 antagonist i.p. |
| 795 | 18490734 | BCG decreased the expression of TLR2 or TLR4 on the heart tissue but TLR4 agonist increased the expression of TLR2 or TLR4 on the immune cells that infiltrate into the heart tissue. |
| 796 | 18490734 | This led to an increased expression ratio of IFN-gamma/TGF-beta in the heart. |
| 797 | 18493984 | IL-2 induces in vivo suppression by CD4(+)CD25(+)Foxp3(+) regulatory T cells. |
| 798 | 18493984 | At the same time, IL-2 is essential for the peripheral homeostasis of CD4(+)CD25(+)Foxp3(+ )regulatory T cells (Treg). |
| 799 | 18493984 | IL-2 treatment induces Treg expansion as well as IL-10 production and increases their suppressive potential in vitro. |
| 800 | 18493984 | The suppressive effect can be transferred onto naive animals by Treg from IL-2-treated mice and the suppression depends on the synergistic action of IL-10 and TGF-beta. |
| 801 | 18502198 | In addition, CIM significantly promotes an elevated level of IL-4 and IFN-gamma in antigen-specific CD4(+) T cells and a robust antigen-specific cytotoxic response in the animals immunized with pcD-S2 plus CIM. |
| 802 | 18502198 | Further, CIM induces pro-inflammatory cytokine expression such as the IL-12 and down-regulates anti-inflammatory cytokine expression such as IL-10 and TGF-beta, which may lead to an impairment of CD4(+)CD25(+) Treg cell-mediated suppression. |
| 803 | 18509051 | LJM19-immunized hamsters maintained a low parasite load that correlated with an overall high IFN-gamma/TGF-beta ratio and inducible NOS expression in the spleen and liver up to 5 months postinfection. |
| 804 | 18522647 | Role of IL-17, transforming growth factor-beta, and IL-6 in the development of arthritis and production of anti-outer surface protein A borreliacidal antibodies in Borrelia-vaccinated and -challenged mice. |
| 805 | 18522647 | Here, we show in Borrelia-vaccinated and -challenged mice that two cytokines known to induce the production of IL-17, IL-6 and transforming growth factor (TGF)-beta, are also involved in the development of arthritis. |
| 806 | 18522647 | These findings demonstrate a role for the combined effects of IL-17, IL-6, and TGF-beta in the adaptive immune events leading to the development of Borrelia-induced arthritis. |
| 807 | 18522647 | Role of IL-17, transforming growth factor-beta, and IL-6 in the development of arthritis and production of anti-outer surface protein A borreliacidal antibodies in Borrelia-vaccinated and -challenged mice. |
| 808 | 18522647 | Here, we show in Borrelia-vaccinated and -challenged mice that two cytokines known to induce the production of IL-17, IL-6 and transforming growth factor (TGF)-beta, are also involved in the development of arthritis. |
| 809 | 18522647 | These findings demonstrate a role for the combined effects of IL-17, IL-6, and TGF-beta in the adaptive immune events leading to the development of Borrelia-induced arthritis. |
| 810 | 18541347 | The results showed that (1) the anti-rUfl antibodies could be elicited in the mice after immunization by recombinant plasmid pCR3.1-rUfl; (2) the birth rate of the female mice immunized by pCR3.1-rUfl was significantly reduced (p<0.01); (3) anti-rUfl antibodies could bind with uroguanylin in the uteri of the non-pregnant mice immunized by pCR3.1-rUfl; (4) in the non-mated experiments, in the uteri of normal, pCR3.1- and pCR3.1-rUfl-immunized mice, expression of p53 and vascular endothelial growth factor (VEGF) was not detected, Bax was expressed, and transforming growth factor beta 1 (TGFbeta1) expression was very little; (5) in the mated experiments, p53, Bax, VEGF and TGFbeta1 were expressed in the uteri of saline- and pCR3.1-immunized mice that were pregnant. |
| 811 | 18566377 | Down-regulation of CD4+CD25+ regulatory T (Treg) cell function might be beneficial to enhance the immunogenicity of viral and tumor vaccines or to induce breakdown of immunotolerance. |
| 812 | 18566377 | In this study, we show that P17, a short synthetic peptide that inhibits TGF-beta1 and TGF-beta2 developed in our laboratory, is able to inhibit Treg activity in vitro and in vivo. |
| 813 | 18566377 | EG.7-OVA tumors, administration of P17 improved their proliferation, reduced the number of CD4+Foxp3+ T cells, and inhibited tumor growth. |
| 814 | 18572242 | Nine cytokine genes (IL-2, -4, -10, -12, -13, -18, TNFalpha, TGFbeta and IFNgamma) and Cox-2 were selected for analysis. |
| 815 | 18579694 | Differential expression of interleukin-4 (IL-4) and IL-4 delta 2 mRNA, but not transforming growth factor beta (TGF-beta), TGF-beta RII, Foxp3, gamma interferon, T-bet, or GATA-3 mRNA, in patients with fast and slow responses to antituberculosis treatment. |
| 816 | 18579694 | This study investigated interleukin-4 (IL-4), IL-4 delta 2, transforming growth factor beta (TGF-beta), TGF-beta RII, Foxp3, GATA-3, T-bet, and gamma interferon (IFN-gamma) transcription in peripheral blood samples of adult pulmonary tuberculosis patients prior to and after 1 week of therapy. |
| 817 | 18579694 | There were no significant differences in expression of TGF-beta, TGF-beta RII, Foxp3, IFN-gamma, and GATA-3 between the groups. |
| 818 | 18579694 | Differential expression of interleukin-4 (IL-4) and IL-4 delta 2 mRNA, but not transforming growth factor beta (TGF-beta), TGF-beta RII, Foxp3, gamma interferon, T-bet, or GATA-3 mRNA, in patients with fast and slow responses to antituberculosis treatment. |
| 819 | 18579694 | This study investigated interleukin-4 (IL-4), IL-4 delta 2, transforming growth factor beta (TGF-beta), TGF-beta RII, Foxp3, GATA-3, T-bet, and gamma interferon (IFN-gamma) transcription in peripheral blood samples of adult pulmonary tuberculosis patients prior to and after 1 week of therapy. |
| 820 | 18579694 | There were no significant differences in expression of TGF-beta, TGF-beta RII, Foxp3, IFN-gamma, and GATA-3 between the groups. |
| 821 | 18579694 | Differential expression of interleukin-4 (IL-4) and IL-4 delta 2 mRNA, but not transforming growth factor beta (TGF-beta), TGF-beta RII, Foxp3, gamma interferon, T-bet, or GATA-3 mRNA, in patients with fast and slow responses to antituberculosis treatment. |
| 822 | 18579694 | This study investigated interleukin-4 (IL-4), IL-4 delta 2, transforming growth factor beta (TGF-beta), TGF-beta RII, Foxp3, GATA-3, T-bet, and gamma interferon (IFN-gamma) transcription in peripheral blood samples of adult pulmonary tuberculosis patients prior to and after 1 week of therapy. |
| 823 | 18579694 | There were no significant differences in expression of TGF-beta, TGF-beta RII, Foxp3, IFN-gamma, and GATA-3 between the groups. |
| 824 | 18641317 | CD4 cells induced to express FoxP3, IL-10, and TGF-beta1 in response to TCR signaling and TGF-beta1 can reverse diabetes with clinical restoration of prediabetic serum levels of IL-10. |
| 825 | 18675506 | Vaccination with transforming growth factor-beta insensitive dendritic cells suppresses pulmonary metastases of renal carcinoma in mice. |
| 826 | 18675506 | Tumor lysate-pulsed DCs (TP-DCs) were infected with retrovirus containing gene of dominant negative TGF-beta type II receptor (TbetaRIIDN) and thus made TGF-beta insensitive. |
| 827 | 18675506 | Vaccination with transforming growth factor-beta insensitive dendritic cells suppresses pulmonary metastases of renal carcinoma in mice. |
| 828 | 18675506 | Tumor lysate-pulsed DCs (TP-DCs) were infected with retrovirus containing gene of dominant negative TGF-beta type II receptor (TbetaRIIDN) and thus made TGF-beta insensitive. |
| 829 | 18682270 | We have found that in BCG primed subjects MVA85A vaccination reduces transforming growth factor beta 1 (TGF-beta1) mRNA in peripheral blood lymphocytes and reduces TGF-beta1 protein in the serum, but increases IFN-gamma ELISPOT responses to the recall antigen SK/SD. |
| 830 | 18682270 | TGF-beta1 is essential for the generation of regulatory T cells and we see a correlation across vaccinees between CD4+CD25hiFoxP3+ cells and TGF-beta1 serum levels. |
| 831 | 18682270 | We have found that in BCG primed subjects MVA85A vaccination reduces transforming growth factor beta 1 (TGF-beta1) mRNA in peripheral blood lymphocytes and reduces TGF-beta1 protein in the serum, but increases IFN-gamma ELISPOT responses to the recall antigen SK/SD. |
| 832 | 18682270 | TGF-beta1 is essential for the generation of regulatory T cells and we see a correlation across vaccinees between CD4+CD25hiFoxP3+ cells and TGF-beta1 serum levels. |
| 833 | 18684965 | Vaccination without autoantigen protects against collagen II-induced arthritis via immune deviation and regulatory T cells. |
| 834 | 18684965 | A Salmonella vector expressing colonization factor Ag I (CFA/I), shown to behave as an anti-inflammatory vaccine, stimulates the production of CD4(+)CD25(+) T cells and regulatory cytokines. |
| 835 | 18684965 | In this work, we queried whether Salmonella-CFA/I can protect DBA/1 mice from collagen-induced arthritis. |
| 836 | 18684965 | Clinical findings were accompanied by the suppression of inflammatory cytokines TNF-alpha, IL-1beta, IL-6, and IL-27. |
| 837 | 18684965 | Vaccination evoked a multi-tier response consisting of IL-4 producing Th2 cells, an increased production of TGF-beta by CD4(+) T cells, and suppression of collagen II-specific CD4(+) T cell proliferation. |
| 838 | 18684965 | To assess the contribution of Salmonella-CFA/I-primed CD4(+) T cells, adoptive transfer studies with total CD4(+), CD4(+)CD25(-), or CD4(+)CD25(+) T cells were performed 15 days postchallenge. |
| 839 | 18684965 | Mice receiving either subset showed reduced disease incidence and low clinical scores; however, mice receiving total CD4(+) T cells showed delayed disease onset by 10 days with reduced clinical scores, reduced IL-17 and IL-27, but enhanced IL-4, IL-10, IL-13, and TGF-beta. |
| 840 | 18684965 | Inhibition of TGF-beta or IL-4 compromised protective immunity. |
| 841 | 18684965 | These data show that Salmonella-CFA/I vaccination of DBA/1 mice protects against collagen-induced arthritis by stimulating TGF-beta- and IL-4-producing regulatory CD4(+) T cells. |
| 842 | 18684965 | Vaccination without autoantigen protects against collagen II-induced arthritis via immune deviation and regulatory T cells. |
| 843 | 18684965 | A Salmonella vector expressing colonization factor Ag I (CFA/I), shown to behave as an anti-inflammatory vaccine, stimulates the production of CD4(+)CD25(+) T cells and regulatory cytokines. |
| 844 | 18684965 | In this work, we queried whether Salmonella-CFA/I can protect DBA/1 mice from collagen-induced arthritis. |
| 845 | 18684965 | Clinical findings were accompanied by the suppression of inflammatory cytokines TNF-alpha, IL-1beta, IL-6, and IL-27. |
| 846 | 18684965 | Vaccination evoked a multi-tier response consisting of IL-4 producing Th2 cells, an increased production of TGF-beta by CD4(+) T cells, and suppression of collagen II-specific CD4(+) T cell proliferation. |
| 847 | 18684965 | To assess the contribution of Salmonella-CFA/I-primed CD4(+) T cells, adoptive transfer studies with total CD4(+), CD4(+)CD25(-), or CD4(+)CD25(+) T cells were performed 15 days postchallenge. |
| 848 | 18684965 | Mice receiving either subset showed reduced disease incidence and low clinical scores; however, mice receiving total CD4(+) T cells showed delayed disease onset by 10 days with reduced clinical scores, reduced IL-17 and IL-27, but enhanced IL-4, IL-10, IL-13, and TGF-beta. |
| 849 | 18684965 | Inhibition of TGF-beta or IL-4 compromised protective immunity. |
| 850 | 18684965 | These data show that Salmonella-CFA/I vaccination of DBA/1 mice protects against collagen-induced arthritis by stimulating TGF-beta- and IL-4-producing regulatory CD4(+) T cells. |
| 851 | 18684965 | Vaccination without autoantigen protects against collagen II-induced arthritis via immune deviation and regulatory T cells. |
| 852 | 18684965 | A Salmonella vector expressing colonization factor Ag I (CFA/I), shown to behave as an anti-inflammatory vaccine, stimulates the production of CD4(+)CD25(+) T cells and regulatory cytokines. |
| 853 | 18684965 | In this work, we queried whether Salmonella-CFA/I can protect DBA/1 mice from collagen-induced arthritis. |
| 854 | 18684965 | Clinical findings were accompanied by the suppression of inflammatory cytokines TNF-alpha, IL-1beta, IL-6, and IL-27. |
| 855 | 18684965 | Vaccination evoked a multi-tier response consisting of IL-4 producing Th2 cells, an increased production of TGF-beta by CD4(+) T cells, and suppression of collagen II-specific CD4(+) T cell proliferation. |
| 856 | 18684965 | To assess the contribution of Salmonella-CFA/I-primed CD4(+) T cells, adoptive transfer studies with total CD4(+), CD4(+)CD25(-), or CD4(+)CD25(+) T cells were performed 15 days postchallenge. |
| 857 | 18684965 | Mice receiving either subset showed reduced disease incidence and low clinical scores; however, mice receiving total CD4(+) T cells showed delayed disease onset by 10 days with reduced clinical scores, reduced IL-17 and IL-27, but enhanced IL-4, IL-10, IL-13, and TGF-beta. |
| 858 | 18684965 | Inhibition of TGF-beta or IL-4 compromised protective immunity. |
| 859 | 18684965 | These data show that Salmonella-CFA/I vaccination of DBA/1 mice protects against collagen-induced arthritis by stimulating TGF-beta- and IL-4-producing regulatory CD4(+) T cells. |
| 860 | 18713984 | The reprogrammed Tregs cease to express IL-10 and TGFbeta, fail to suppress T cell responses, and gain the ability to produce IFN-gamma, IL-17, and TNF-alpha. |
| 861 | 18714045 | Because TGF-beta is known to induce regulatory T cells (Tregs), we further showed that the DC/4T1+Adv-TGF-beta-R fusion vaccine induced fewer CD4(+)CD25(+)Foxp3(+) Tregs than the DC/4T1+Adv-LacZ fusion vaccine in vitro and in vivo. |
| 862 | 18714045 | The suppressive role of splenic CD4(+)CD25(+) Tregs isolated from mice immunized with DC/4T1+Adv-LacZ was demonstrated using a CTL killing assay. |
| 863 | 18722494 | The complete coding cDNA was cloned into a pGEX 4T-2 plasmid and expressed in Escherichia coli as a glutathione-S-transferase-tagged (GST) recombinant protein. |
| 864 | 18722494 | At the same time the levels of TGF-beta and IFN-gamma were high while a very low production of IL-10 was verified. |
| 865 | 18827195 | Throughout the infection (until 120 days), we monitored outcome (CFU), molecules involved in the development of immunoregulation (Foxp3, hemoxygenase 1, idoleamine 2,3-dioxygenase, and transforming growth factor beta [TGF-beta]), and indicators of cytokine balance (tumor necrosis factor, inducible nitric oxide synthase, interleukin-4 [IL-4], and IL-4delta2; an inhibitory splice variant of IL-4 associated with improved outcome in human TB). |
| 866 | 18827195 | Oral M. vaccae had a significant effect on CFU and led to increased expression of Th1 markers and of IL-4delta2, while suppressing IL-4, Foxp3, and TGF-beta. |
| 867 | 18827195 | Throughout the infection (until 120 days), we monitored outcome (CFU), molecules involved in the development of immunoregulation (Foxp3, hemoxygenase 1, idoleamine 2,3-dioxygenase, and transforming growth factor beta [TGF-beta]), and indicators of cytokine balance (tumor necrosis factor, inducible nitric oxide synthase, interleukin-4 [IL-4], and IL-4delta2; an inhibitory splice variant of IL-4 associated with improved outcome in human TB). |
| 868 | 18827195 | Oral M. vaccae had a significant effect on CFU and led to increased expression of Th1 markers and of IL-4delta2, while suppressing IL-4, Foxp3, and TGF-beta. |
| 869 | 18981115 | Imatinib mesylate inhibits CD4+ CD25+ regulatory T cell activity and enhances active immunotherapy against BCR-ABL- tumors. |
| 870 | 18981115 | Suppressive as well as stimulating effects of this drug on CD4(+) and CD8(+) T lymphocytes or dendritic cells have been reported. |
| 871 | 18981115 | In the current study, we have investigated the influence of imatinib mesylate on CD4(+)CD25(+)FoxP3(+) regulatory T cells (Treg), a critical population of lymphocytes that contributes to peripheral tolerance. |
| 872 | 18981115 | Used at concentrations achieved clinically, imatinib impaired Treg immunosuppressive function and FoxP3 expression but not production of IL-10 and TGF-beta in vitro. |
| 873 | 18981115 | Imatinib significantly reduced the activation of the transcription factors STAT3 and STAT5 in Treg. |
| 874 | 18981115 | Analysis of Treg TCR-induced signaling cascade indicated that imatinib inhibited phosphorylation of ZAP70 and LAT. |
| 875 | 19009291 | Also, anti-inflammatory effects on LPS-stimulated monocytes (TNF-alpha is decreased) and costimulatory effects on anti-CD3 stimulated T cells, (enhanced T cell proliferation and proinflammatory cytokine production) are observed. |
| 876 | 19009291 | Both drugs inhibit IL-2-mediated generation of FOXP3 positive CTLA-4 positive CD25high CD4+ T regulatory cells from PBMCs by upto 50%. |
| 877 | 19009291 | Inhibition of T regulatory cell function was not due to changes in TGF-beta or IL-10 production but was associated with decreased T regulatory cell FOXP3 expression. |
| 878 | 19050244 | Mucosal administration of Ag conjugated to cholera toxin B subunit (CTB) can efficiently induce peripheral immunologic tolerance, so-called oral tolerance, associated with development of Foxp3(+)CD25(+)CD4(+) regulatory T (Treg) cells. |
| 879 | 19050244 | B cells from OVA/CTB-treated mice expressed more IL-10 and less CD86 than control B cells. |
| 880 | 19050244 | Adoptive transfer of these cells before parenteral immunization with OVA led to efficient suppression of proliferation and to induction of apoptotic depletion of Ag-specific CD25(-)CD4(+) effector T cells associated with the expansion of Treg cells. |
| 881 | 19050244 | However, also OVA/CTB-treated microMT(-/-) mice could suppress the immune response to parenteral immunization with OVA, which was associated with a strong increase in Foxp3(-)CD4(+) T cells expressing LAP/TGF-beta. |
| 882 | 19050244 | Our results indicate that mucosal tolerance comprises at least two separate pathways: one being B cell dependent and associated with expansion of Treg cells and Treg-mediated suppression and depletion of effector T cells, and one being B cell independent and associated with development of Foxp3(-)LAP(+)TGF-beta(+) regulatory T cells. |
| 883 | 19168736 | Again, mice vaccinated through the i.p. and i.v. routes showed high levels of NO production after challenge infection. s.c. vaccination resulted in an increased capacity of the spleen cells to produce prechallenge transforming growth factor beta (TGF-beta) levels during the in vitro antigen recall response, whereas i.p. immunization induced production of prechallenge gamma interferon, interleukin-12 (IL-12), and IL-4 levels, with a Th1 bias. |
| 884 | 19191902 | Analysis of interferon-gamma (IFN-gamma) and interleukin-4 (IL-4) levels in bronchoalveolar lavage fluid (BALF) and lung tissue revealed that the suppression was associated with a shift from a Th2 response to a Th1 response. |
| 885 | 19191902 | At the same time, rBCG induced a CD4(+) CD25(+) Foxp3(+) T-cell subtype that could suppress the proliferation of Th2 effector cells in vitro in an antigen-specific manner. |
| 886 | 19191902 | Moreover, suppression of CD4(+) CD25(+) T cells could be adoptively transferred. |
| 887 | 19191902 | The generic immune response is associated with a shift from a Th2 to a Th1 cytokine response, whereas the specific immune response against Der p2 appears to be related to the expansion of transforming growth factor-beta (TGF-beta)-producing CD4(+) CD25(+) Foxp3(+) regulatory T cells. rBCG can suppress asthmatic airway inflammation through both immune deviation and immune suppression and may be a feasible, efficient immunotherapy for asthma. |
| 888 | 19330258 | Genetic polymorphisms in vitamin D receptor, vitamin D-binding protein, Toll-like receptor 2, nitric oxide synthase 2, and interferon-gamma genes and its association with susceptibility to tuberculosis. |
| 889 | 19330258 | Many studies have focused on the candidate genes for tuberculosis susceptibility ranging from those expressed in several cells from the innate or adaptive immune system such as Toll-like receptors, cytokines (TNF-alpha, TGF-beta, IFN-gamma, IL-1b, IL-1RA, IL-12, IL-10), nitric oxide synthase and vitamin D, both nuclear receptors and their carrier, the vitamin D-binding protein (VDBP). |
| 890 | 19330258 | Thus, in this mini-review, we summarize the current state of investigation on some of the genetic determinants, such as the candidate polymorphisms of vitamin D, VDBP, Toll-like receptor, nitric oxide synthase 2 and interferon-gamma genes, to generate resistance or susceptibility to M. tuberculosis infection. |
| 891 | 19396174 | Furthermore, IL-7 modulates the expression of two ubiquitin ligases: Casitas B-lineage lymphoma b (Cbl-b), a negative regulator of T cell activation, is repressed, and SMAD-specific E3 ubiquitin protein ligase-2 (Smurf2) is enhanced, which antagonizes transforming growth factor-beta signaling. |
| 892 | 19414774 | Our previous studies demonstrate that the stromal microenvironment of the spleen, lung, and liver can program generation of CD11c(low)CD11b(high)Ia(low) DCs with regulatory function (CD11b(high)Ia(low) regulatory DCs). |
| 893 | 19414774 | In this study, we used the freshly isolated tumor cells to mimic tumor microenvironment to coculture DCs and found that the freshly isolated tumor cells could drive DCs to differentiate into regulatory DCs with a CD11c(low)CD11b(high)Ia(low) phenotype and high expression of IL-10, NO, vascular endothelial growth factor, and arginase I. |
| 894 | 19414774 | Tumor-educated CD11b(high)Ia(low) regulatory DCs inhibited CD4(+) T cell proliferation both in vitro and in vivo. 3LL lung cancer-derived TGF-beta and PGE(2) were responsible for the generation of regulatory DCs. |
| 895 | 19489682 | The association of interleukin-1beta (IL-1B) -511C > T and IL-1 receptor antagonist (IL-1RN) VNTR, transforming growth factor-beta (TGF-B1) +28C > T and interferon-gamma (IFN-G) + 874T>A polymorphisms with bladder cancer (CaB) susceptibility and risk of recurrence in Bacillus Calmette-Guérin (BCG)-treated patients was analyzed in 287 controls and 213 CaB patients (73 BCG treated). |
| 896 | 19489682 | TGF-B TT and IFN-G +874 A carriers were associated with reduced (hazard ratio (HR) 0.37) and enhanced (HR 2.24) risk of recurrence after BCG immunotherapy, respectively. |
| 897 | 19489682 | The association of interleukin-1beta (IL-1B) -511C > T and IL-1 receptor antagonist (IL-1RN) VNTR, transforming growth factor-beta (TGF-B1) +28C > T and interferon-gamma (IFN-G) + 874T>A polymorphisms with bladder cancer (CaB) susceptibility and risk of recurrence in Bacillus Calmette-Guérin (BCG)-treated patients was analyzed in 287 controls and 213 CaB patients (73 BCG treated). |
| 898 | 19489682 | TGF-B TT and IFN-G +874 A carriers were associated with reduced (hazard ratio (HR) 0.37) and enhanced (HR 2.24) risk of recurrence after BCG immunotherapy, respectively. |
| 899 | 19604492 | Opposing effects of TGF-beta and IL-15 cytokines control the number of short-lived effector CD8+ T cells. |
| 900 | 19604492 | We found, after Listeria infection, plasma transforming growth factor beta (TGF-beta) titers increased concomitant with the expansion of effector CD8(+) T cells. |
| 901 | 19604492 | Blocking TGF-beta signaling did not affect effector function of CD8(+) T cells. |
| 902 | 19604492 | However, TGF-beta controlled effector cell number by lowering Bcl-2 amounts and selectively promoting the apoptosis of short-lived effector cells. |
| 903 | 19604492 | TGF-beta-mediated apoptosis of this effector subpopulation occurred during clonal expansion and contraction, whereas interleukin-15 (IL-15) promoted their survival only during contraction. |
| 904 | 19604492 | Opposing effects of TGF-beta and IL-15 cytokines control the number of short-lived effector CD8+ T cells. |
| 905 | 19604492 | We found, after Listeria infection, plasma transforming growth factor beta (TGF-beta) titers increased concomitant with the expansion of effector CD8(+) T cells. |
| 906 | 19604492 | Blocking TGF-beta signaling did not affect effector function of CD8(+) T cells. |
| 907 | 19604492 | However, TGF-beta controlled effector cell number by lowering Bcl-2 amounts and selectively promoting the apoptosis of short-lived effector cells. |
| 908 | 19604492 | TGF-beta-mediated apoptosis of this effector subpopulation occurred during clonal expansion and contraction, whereas interleukin-15 (IL-15) promoted their survival only during contraction. |
| 909 | 19604492 | Opposing effects of TGF-beta and IL-15 cytokines control the number of short-lived effector CD8+ T cells. |
| 910 | 19604492 | We found, after Listeria infection, plasma transforming growth factor beta (TGF-beta) titers increased concomitant with the expansion of effector CD8(+) T cells. |
| 911 | 19604492 | Blocking TGF-beta signaling did not affect effector function of CD8(+) T cells. |
| 912 | 19604492 | However, TGF-beta controlled effector cell number by lowering Bcl-2 amounts and selectively promoting the apoptosis of short-lived effector cells. |
| 913 | 19604492 | TGF-beta-mediated apoptosis of this effector subpopulation occurred during clonal expansion and contraction, whereas interleukin-15 (IL-15) promoted their survival only during contraction. |
| 914 | 19604492 | Opposing effects of TGF-beta and IL-15 cytokines control the number of short-lived effector CD8+ T cells. |
| 915 | 19604492 | We found, after Listeria infection, plasma transforming growth factor beta (TGF-beta) titers increased concomitant with the expansion of effector CD8(+) T cells. |
| 916 | 19604492 | Blocking TGF-beta signaling did not affect effector function of CD8(+) T cells. |
| 917 | 19604492 | However, TGF-beta controlled effector cell number by lowering Bcl-2 amounts and selectively promoting the apoptosis of short-lived effector cells. |
| 918 | 19604492 | TGF-beta-mediated apoptosis of this effector subpopulation occurred during clonal expansion and contraction, whereas interleukin-15 (IL-15) promoted their survival only during contraction. |
| 919 | 19604492 | Opposing effects of TGF-beta and IL-15 cytokines control the number of short-lived effector CD8+ T cells. |
| 920 | 19604492 | We found, after Listeria infection, plasma transforming growth factor beta (TGF-beta) titers increased concomitant with the expansion of effector CD8(+) T cells. |
| 921 | 19604492 | Blocking TGF-beta signaling did not affect effector function of CD8(+) T cells. |
| 922 | 19604492 | However, TGF-beta controlled effector cell number by lowering Bcl-2 amounts and selectively promoting the apoptosis of short-lived effector cells. |
| 923 | 19604492 | TGF-beta-mediated apoptosis of this effector subpopulation occurred during clonal expansion and contraction, whereas interleukin-15 (IL-15) promoted their survival only during contraction. |
| 924 | 19658096 | All individuals demonstrated stable IFN-gamma, IL-2 and IL-4 ex vivo ELISPOT effector responses against P. falciparum-infected RBC (iRBC) Ag, 28 and 90 days after challenge. |
| 925 | 19658096 | However, infected RBC-specific central memory responses, as measured by IFN-gamma cultured ELISPOT, were low and unstable over time, despite CD4(+) T cells being highly proliferative by CFSE dilution, and showed an inverse relationship to parasite density. |
| 926 | 19658096 | This activity could not be accounted for by the expression of IL-10, TGF-beta, FOXP3 or CTLA-4, but proliferating T cells expressed high levels of CD95, indicating a pro-apoptotic phenotype. |
| 927 | 19710454 | Systemic IgA responses following s.c. immunization were T cell independent and did not require TACI or TGFbeta, whereas mucosal IgA production was dependent on Th cells, TACI, and TGFbeta. |
| 928 | 19830696 | Blockade of TGF-beta enhances tumor vaccine efficacy mediated by CD8(+) T cells. |
| 929 | 19830696 | Though TGF-beta inhibition enhances antitumor immunity mediated by CD8(+) T cells in several tumor models, it is not always sufficient for rejection of tumors. |
| 930 | 19830696 | Though the abrogation of CD1d-restricted NKT cells, which have been reported to induce TGF-beta production by MDSC through an IL-13-IL-4R-STAT6 pathway, partially enhanced antitumor immunity regardless of vaccination, abrogation of the NKT cell-IL-13-IL-4R-STAT-6 immunoregulatory pathway did not enhance vaccine efficacy. |
| 931 | 19830696 | Taken together, these data indicated that anti-TGF-beta enhances efficacy of a prophylactic vaccine in normal individuals despite their not having the elevated TGF-beta levels found in patients with cancer and that the effect is not dependent on TGF-beta solely from CD4(+)CD25(+) T regulatory cells or the NKT cell-IL-13-IL-4R-STAT-6 immunoregulatory pathway. |
| 932 | 19830696 | Blockade of TGF-beta enhances tumor vaccine efficacy mediated by CD8(+) T cells. |
| 933 | 19830696 | Though TGF-beta inhibition enhances antitumor immunity mediated by CD8(+) T cells in several tumor models, it is not always sufficient for rejection of tumors. |
| 934 | 19830696 | Though the abrogation of CD1d-restricted NKT cells, which have been reported to induce TGF-beta production by MDSC through an IL-13-IL-4R-STAT6 pathway, partially enhanced antitumor immunity regardless of vaccination, abrogation of the NKT cell-IL-13-IL-4R-STAT-6 immunoregulatory pathway did not enhance vaccine efficacy. |
| 935 | 19830696 | Taken together, these data indicated that anti-TGF-beta enhances efficacy of a prophylactic vaccine in normal individuals despite their not having the elevated TGF-beta levels found in patients with cancer and that the effect is not dependent on TGF-beta solely from CD4(+)CD25(+) T regulatory cells or the NKT cell-IL-13-IL-4R-STAT-6 immunoregulatory pathway. |
| 936 | 19830696 | Blockade of TGF-beta enhances tumor vaccine efficacy mediated by CD8(+) T cells. |
| 937 | 19830696 | Though TGF-beta inhibition enhances antitumor immunity mediated by CD8(+) T cells in several tumor models, it is not always sufficient for rejection of tumors. |
| 938 | 19830696 | Though the abrogation of CD1d-restricted NKT cells, which have been reported to induce TGF-beta production by MDSC through an IL-13-IL-4R-STAT6 pathway, partially enhanced antitumor immunity regardless of vaccination, abrogation of the NKT cell-IL-13-IL-4R-STAT-6 immunoregulatory pathway did not enhance vaccine efficacy. |
| 939 | 19830696 | Taken together, these data indicated that anti-TGF-beta enhances efficacy of a prophylactic vaccine in normal individuals despite their not having the elevated TGF-beta levels found in patients with cancer and that the effect is not dependent on TGF-beta solely from CD4(+)CD25(+) T regulatory cells or the NKT cell-IL-13-IL-4R-STAT-6 immunoregulatory pathway. |
| 940 | 19830696 | Blockade of TGF-beta enhances tumor vaccine efficacy mediated by CD8(+) T cells. |
| 941 | 19830696 | Though TGF-beta inhibition enhances antitumor immunity mediated by CD8(+) T cells in several tumor models, it is not always sufficient for rejection of tumors. |
| 942 | 19830696 | Though the abrogation of CD1d-restricted NKT cells, which have been reported to induce TGF-beta production by MDSC through an IL-13-IL-4R-STAT6 pathway, partially enhanced antitumor immunity regardless of vaccination, abrogation of the NKT cell-IL-13-IL-4R-STAT-6 immunoregulatory pathway did not enhance vaccine efficacy. |
| 943 | 19830696 | Taken together, these data indicated that anti-TGF-beta enhances efficacy of a prophylactic vaccine in normal individuals despite their not having the elevated TGF-beta levels found in patients with cancer and that the effect is not dependent on TGF-beta solely from CD4(+)CD25(+) T regulatory cells or the NKT cell-IL-13-IL-4R-STAT-6 immunoregulatory pathway. |
| 944 | 19923459 | Soluble B and T lymphocyte attenuator possesses antitumor effects and facilitates heat shock protein 70 vaccine-triggered antitumor immunity against a murine TC-1 cervical cancer model in vivo. |
| 945 | 19923459 | B and T lymphocyte attenuator (BTLA)-herpesvirus entry mediator (HVEM) signaling coinhibitory pathway is believed to impair antitumor immune competences. |
| 946 | 19923459 | To address this issue, we constructed a eukaryotic expression plasmid (psBTLA) that expressed the extracellular domain of murine BTLA (soluble form of BTLA), which could bind HVEM, the ligand of BTLA, and block BTLA-HVEM interactions. |
| 947 | 19923459 | The data in this study showed that treatment by injection of psBTLA resulted in down-regulation of IL-10 and TGF-beta and promotion of dendritic cell function by increasing the expression of B7-1 and IL-12, but the adaptive antitumor immune responses achieved by psBTLA administration alone were limited and could not eradicate the tumor effectively. |
| 948 | 19923459 | Next, we evaluated the immunotherapeutic efficacy and mechanism of combination therapy of heat shock protein 70 (HSP70) vaccine/psBTLA by using murine TC-1 cervical cancer mice as an ectopic tumor model. |
| 949 | 19923459 | Our in vivo studies revealed that treatment with HSP70 vaccine alone did not lead to satisfactory tumor growth inhibition, whereas cotreatment with psBTLA significantly improved antitumor immunity and compensated the deficiency of HSP70 vaccine by increasing the expression of Th1 cytokines, IL-2, and IFN-gamma and decreasing transcription levels of IL-10, TGF-beta, and Foxp3 in the tumor microenvironment. |
| 950 | 19923459 | Soluble B and T lymphocyte attenuator possesses antitumor effects and facilitates heat shock protein 70 vaccine-triggered antitumor immunity against a murine TC-1 cervical cancer model in vivo. |
| 951 | 19923459 | B and T lymphocyte attenuator (BTLA)-herpesvirus entry mediator (HVEM) signaling coinhibitory pathway is believed to impair antitumor immune competences. |
| 952 | 19923459 | To address this issue, we constructed a eukaryotic expression plasmid (psBTLA) that expressed the extracellular domain of murine BTLA (soluble form of BTLA), which could bind HVEM, the ligand of BTLA, and block BTLA-HVEM interactions. |
| 953 | 19923459 | The data in this study showed that treatment by injection of psBTLA resulted in down-regulation of IL-10 and TGF-beta and promotion of dendritic cell function by increasing the expression of B7-1 and IL-12, but the adaptive antitumor immune responses achieved by psBTLA administration alone were limited and could not eradicate the tumor effectively. |
| 954 | 19923459 | Next, we evaluated the immunotherapeutic efficacy and mechanism of combination therapy of heat shock protein 70 (HSP70) vaccine/psBTLA by using murine TC-1 cervical cancer mice as an ectopic tumor model. |
| 955 | 19923459 | Our in vivo studies revealed that treatment with HSP70 vaccine alone did not lead to satisfactory tumor growth inhibition, whereas cotreatment with psBTLA significantly improved antitumor immunity and compensated the deficiency of HSP70 vaccine by increasing the expression of Th1 cytokines, IL-2, and IFN-gamma and decreasing transcription levels of IL-10, TGF-beta, and Foxp3 in the tumor microenvironment. |
| 956 | 19940990 | Real-time PCR analysis revealed that combination therapy led to an increase in IFN-gamma and tumor necrosis factor-alpha mRNA expression; however, levels of Foxp3 and transforming growth factor-beta within the remote tumor tissues were decreased. |
| 957 | 20130130 | Peripheral blood mononuclear cells (PBMCs) from healthy donor women were stimulated in vitro with HPV-16 VLPs (2.5 microg/ml) in the presence of E2 and P4 administered either alone or in combination; and lymphoproliferation, cytokine production, transcription factor expression, and steroid hormone receptor expression were analyzed. |
| 958 | 20130130 | HPV-16 VLPs significantly increased the levels of lymphoproliferation, proinflammatory cytokine (gamma interferon [IFN-gamma], interleukin-1beta [IL-1beta], IL-2, IL-6, IL-8, IL-12p70, IL-17, tumor necrosis factor alpha [TNF-alpha]) production, anti-inflammatory cytokine (IL-1ra, IL-10) production, and the expression of Eralpha and Erbeta but decreased the levels of Foxp3 expression and production of transforming growth factor beta (TGF-beta). |
| 959 | 20130130 | Exposure of PBMCs to E2 and P4 either alone or in combination significantly decreased the levels of lymphoproliferation and production of proinflammatory cytokines (IFN-gamma, IL-12p70, TNF-alpha) but increased the levels of production of IL-10 and TGF-beta and the expression of Foxp3 in response to HPV-16 VLPs. |
| 960 | 20130130 | Peripheral blood mononuclear cells (PBMCs) from healthy donor women were stimulated in vitro with HPV-16 VLPs (2.5 microg/ml) in the presence of E2 and P4 administered either alone or in combination; and lymphoproliferation, cytokine production, transcription factor expression, and steroid hormone receptor expression were analyzed. |
| 961 | 20130130 | HPV-16 VLPs significantly increased the levels of lymphoproliferation, proinflammatory cytokine (gamma interferon [IFN-gamma], interleukin-1beta [IL-1beta], IL-2, IL-6, IL-8, IL-12p70, IL-17, tumor necrosis factor alpha [TNF-alpha]) production, anti-inflammatory cytokine (IL-1ra, IL-10) production, and the expression of Eralpha and Erbeta but decreased the levels of Foxp3 expression and production of transforming growth factor beta (TGF-beta). |
| 962 | 20130130 | Exposure of PBMCs to E2 and P4 either alone or in combination significantly decreased the levels of lymphoproliferation and production of proinflammatory cytokines (IFN-gamma, IL-12p70, TNF-alpha) but increased the levels of production of IL-10 and TGF-beta and the expression of Foxp3 in response to HPV-16 VLPs. |
| 963 | 20308630 | Gene expression analysis using tumor-derived RNA demonstrated that imiquimod induced high levels of IL-10 in addition to TNF-alpha and IFN-gamma. |
| 964 | 20308630 | Elevated serum IL-10 appeared to be derived from IL-10 and dual cytokine secreting (IFN-gamma(+) and IL-10(+)) CD4(+) T cells rather than CD4(+)CD25(+)Foxp3(+) T regulatory cells, which were also induced by imiquimod treatment. |
| 965 | 20308630 | Blockade of IL-10, but not TGF-beta, enhanced the antitumor effect of imiquimod by significantly prolonging survival in treated mice. |
| 966 | 20419805 | The genotyping for TNF (-308), TGFB1 (+869, +915), IL-10 (-1082, -819, -592), IL-6 (-174), and IFNG (+874) was accomplished by the PCR-SSP technique. |
| 967 | 20447476 | The prime-boost regimen induced not only HBHA-specific IFN-gamma, but also other cytokines, such as IL-12 and TGF-beta, which may be associated with the generation of lung Th1 effector-memory lymphocytes, responsible for the enhanced protection against M. tuberculosis challenge. |
| 968 | 20466823 | Optimal TLR9 signal converts tolerogenic CD4-8- DCs into immunogenic ones capable of stimulating antitumor immunity via activating CD4+ Th1/Th17 and NK cell responses. |
| 969 | 20466823 | We have demonstrated previously that CD4-8- DCs secreting TGF-beta stimulate CD4+ Tr1 cell responses. |
| 970 | 20466823 | Here, we have assessed whether TLR4 and TLR9 signaling through LPS and CpG stimulation can convert CD4-8- DC-induced tolerance. |
| 971 | 20466823 | CpG-treated, CD4-8- DCOVA-secreting IL-6/IL-15 induced IFN-gamma/IL-17-secreting/T-bet- and ROR-gammat-expressing CD4+ Th1/Th17, whereas LPS-treated CD4-8- DCOVA stimulated IFN-gamma-secreting/T-bet-expressing CD4+ Th1 responses. |
| 972 | 20466823 | CpG-treated, CD4-8- DCOVA-stimulated CD4+ Th1/Th17 cell responses and antitumor immunity were found to be reduced by using neutralizing anti-IL-6, IL-15, and NK1.1 antibodies in wild-type C57BL/6 mice, IL-15R-/- mice for immunization, or CD4-8- (IL-6-/-) DCOVA for immunization in C57BL/6 mice. |
| 973 | 20466823 | Interestingly, in vitro-generated CD4+ Th17 cells significantly enhanced LPS-treated, CD4-8- DCOVA-induced in vivo antitumor immunity via increasing CD8+ CTL responses (P<0.05), although they did not show any direct killing activity against tumor cells in vitro. |
| 974 | 20466823 | Taken together, our data demonstrate an effect of conversion of tolerogenic DCs into immunogenic ones capable of stimulating antitumor immunity via activating CD4+ Th1/Th17 and NK cell responses by optimal CpG signaling, which may advance current understanding of the importance of TLR9 signaling in a DC-based cancer vaccine. |
| 975 | 20472030 | In vitro, soluble proteases isolated from LaAg (LaSP-Sol) directly activated IL-4, IL-10 and TGF-beta production by immune cells. |
| 976 | 20479237 | We show that protection against inhalation anthrax by an irradiated spore vaccine depends on CT-mediated induction of IL-17-producing CD4 Th17 cells. |
| 977 | 20479237 | Th17 cells induced by CT have a unique cytokine profile compared with those induced by IL-6 and TGF-beta, and their induction by CT requires cAMP-dependent secretion of IL-1beta and beta-calcitonin gene-related peptide by dendritic cells. |
| 978 | 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. |
| 979 | 20483237 | Pro-inflammatory cytokines like TNF's, IL-6 and IL-17 family have been cloned. |
| 980 | 20483237 | Among the T(H)1 type interleukins, IL-2, IL-15, IL-12alpha, IL-12beta, IL-18 have been cloned. |
| 981 | 20483237 | Among IL-10 and its family members, IL-10, IL-19/20, IL-22 and IL-26 have been discovered. |
| 982 | 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. |
| 983 | 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. |
| 984 | 20488794 | Interestingly, the VAD diet elicited high levels of mucin MUC2 by goblet cell hyperplasia and subsequently reduced gut microbiome, including segmented filamentous bacteria. |
| 985 | 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. |
| 986 | 20548030 | To focus on the consequences of Treg deficiency confined to the skin, we generated mixed CCR4(KO) FoxP3(KO) bone marrow (CCR4/FoxP3) chimeras in which skin, but not other tissues or central lymphoid organs, lack Treg. |
| 987 | 20548030 | Levels of the antiviral cytokines, type I and II IFNs and IL-12, were reduced, whereas expression of the proinflammatory cytokines, IL-6, IL-10, TGF-beta, and IL-23, was increased. |
| 988 | 20548030 | Importantly, infection of CCR4/FoxP3 chimeras by a noncutaneous route (i.p.) induced immune responses comparable to controls. |
| 989 | 20598784 | IEC supernatants showed higher levels of IL-10, IL-6 and TGF-beta. |
| 990 | 20705860 | Activation of beta-catenin in dendritic cells regulates immunity versus tolerance in the intestine. |
| 991 | 20705860 | We report here that the Wnt-beta-catenin signaling in intestinal dendritic cells regulates the balance between inflammatory versus regulatory responses in the gut. beta-catenin in intestinal dendritic cells was required for the expression of anti-inflammatory mediators such as retinoic acid-metabolizing enzymes, interleukin-10, and transforming growth factor-beta, and the stimulation of regulatory T cell induction while suppressing inflammatory effector T cells. |
| 992 | 20705860 | Furthermore, ablation of beta-catenin expression in DCs enhanced inflammatory responses and disease in a mouse model of inflammatory bowel disease. |
| 993 | 20705860 | Thus, beta-catenin signaling programs DCs to a tolerogenic state, limiting the inflammatory response. |
| 994 | 21074276 | Regulation of IgA production in cattle is not completely understood and thus we have focused in part on highly conserved factors such as transforming growth factor beta, Type I and Type 2 interferons, neuropeptides which interdigitate mucosal tissues (vasoactive intestinal peptide or VIP), and a small peptide (IgA inducing peptide or IGIP) which can serve as targets for modulation and increasing SIgA virus-specific antibodies. |
| 995 | 21074276 | In previous studies in cattle, IgA has been shown to be regulated by several cytokines including IFN-gamma, Type I interferons such as IFN-alpha and IFN-tau, transforming growth factor beta, IgA inducing peptide and other potential factors such as APRIL and BlyS which have not yet been fully evaluated in cattle. |
| 996 | 21074276 | Many of these factors, namely TGF-beta and Type I interferons block cell cycle progression which is an essential component of Ig class switching and thus these factors require additional regulatory factors such as IL-2 to drive cells through cell cycle resulting in class switch recombination. |
| 997 | 21074276 | Regulation of IgA production in cattle is not completely understood and thus we have focused in part on highly conserved factors such as transforming growth factor beta, Type I and Type 2 interferons, neuropeptides which interdigitate mucosal tissues (vasoactive intestinal peptide or VIP), and a small peptide (IgA inducing peptide or IGIP) which can serve as targets for modulation and increasing SIgA virus-specific antibodies. |
| 998 | 21074276 | In previous studies in cattle, IgA has been shown to be regulated by several cytokines including IFN-gamma, Type I interferons such as IFN-alpha and IFN-tau, transforming growth factor beta, IgA inducing peptide and other potential factors such as APRIL and BlyS which have not yet been fully evaluated in cattle. |
| 999 | 21074276 | Many of these factors, namely TGF-beta and Type I interferons block cell cycle progression which is an essential component of Ig class switching and thus these factors require additional regulatory factors such as IL-2 to drive cells through cell cycle resulting in class switch recombination. |
| 1000 | 21074276 | Regulation of IgA production in cattle is not completely understood and thus we have focused in part on highly conserved factors such as transforming growth factor beta, Type I and Type 2 interferons, neuropeptides which interdigitate mucosal tissues (vasoactive intestinal peptide or VIP), and a small peptide (IgA inducing peptide or IGIP) which can serve as targets for modulation and increasing SIgA virus-specific antibodies. |
| 1001 | 21074276 | In previous studies in cattle, IgA has been shown to be regulated by several cytokines including IFN-gamma, Type I interferons such as IFN-alpha and IFN-tau, transforming growth factor beta, IgA inducing peptide and other potential factors such as APRIL and BlyS which have not yet been fully evaluated in cattle. |
| 1002 | 21074276 | Many of these factors, namely TGF-beta and Type I interferons block cell cycle progression which is an essential component of Ig class switching and thus these factors require additional regulatory factors such as IL-2 to drive cells through cell cycle resulting in class switch recombination. |
| 1003 | 21290396 | Significant progress has also been made in the characterisation of other schistosome growth factor receptors, such as transforming growth factor beta receptor and epidermal growth factor receptor, and in our understanding of their roles in the host-parasite molecular dialogue and parasite development. |
| 1004 | 22106408 | Active immunization against the proregions of GDF9 or BMP15 alters ovulation rate and litter size in mice. |
| 1005 | 22106408 | The transforming growth factor β (TGFB) superfamily proteins bone morphogenetic protein 15 (BMP15) and growth differentiation factor 9 (GDF9), are essential for mammalian fertility. |
| 1006 | 22106408 | Recent in vitro evidence suggests that the proregions of mouse BMP15 and GDF9 interact with their mature proteins after secretion. |
| 1007 | 22106408 | Mice were immunized with either N- or C-terminus proregion peptides of BMP15 or GDF9, or a full-length GDF9 proregion protein, each conjugated to keyhole limpet hemocyanin (KLH). |
| 1008 | 22106408 | Antibody titers in sera increased throughout the study period, with no cross-reactivity observed between BMP15 and GDF9 sera and antigens. |
| 1009 | 22106408 | These findings are consistent with the hypothesis that the proregions of BMP15 and GDF9, after secretion by the oocyte, have physiologically important roles in regulating ovulation rate and litter size in mice. |
| 1010 | 23844022 | Stimulation of bone marrow-derived dendritic cells induced production of regulatory cytokines IL-10 and TGF-beta. |
| 1011 | 23844022 | Furthermore, eMOD prevented the development of airway inflammation, as demonstrated by attenuation of bronchoalveolar lavages eosinophil influx, peribronchial inflammatory infiltrate, and mucus secretion in lungs and IL-4 and IL-5 levels in lung cell cultures. |
| 1012 | 24153333 | Regulatory T cells are characterized by IL-10 and TGF-beta secretion and expression of important cell surface suppressive molecules such as cytotoxic T lymphocyte antigen-4 and programmed death-1 that directly or indirectly influence effector cells of allergic inflammation, such as mast cells, basophils and eosinophils. |
| 1013 | 24362687 | Many studies have reported genetic associations between severe RSV bronchiolitis and SNPs in genes within plausible biological pathways, such as in innate host defense genes (SPA, SPD, TLR4, and VDR), cytokine or chemokine response genes (CCR5, IFN, IL6, IL10, TGFB1), and altered Th1/Th2 immune responses (IL4, IL13). |
| 1014 | 24793154 | The increased proportion of T regs and high expression of Foxp3 and CTLA-4 on lung cancer cells and tumour infiltrating lymphocytes were observed. |
| 1015 | 24793154 | Other components of immune response inhibition and tumour promotion are: Th17 cell population, M2 macrophage polarisation, the presence of myeloid derived suppressor cells (MDSCs) and a significantly elevated concentration of cytokines: TGF-b and IL-10 in the tumour microenvironment. |
| 1016 | 24793154 | Lung cancer immunotherapy has two main directions: the first goal is to improve the cytotoxic effect (for example by inhibition of CTLA-4, stimulation of dendritic cell function, inhibition of lymphocyte apoptosis), and the second way is the production of anti-cancer vaccines using known cancer antigens: MAGE A3, MUC1, EGF and TGF-b. |
| 1017 | 24793154 | The increased proportion of T regs and high expression of Foxp3 and CTLA-4 on lung cancer cells and tumour infiltrating lymphocytes were observed. |
| 1018 | 24793154 | Other components of immune response inhibition and tumour promotion are: Th17 cell population, M2 macrophage polarisation, the presence of myeloid derived suppressor cells (MDSCs) and a significantly elevated concentration of cytokines: TGF-b and IL-10 in the tumour microenvironment. |
| 1019 | 24793154 | Lung cancer immunotherapy has two main directions: the first goal is to improve the cytotoxic effect (for example by inhibition of CTLA-4, stimulation of dendritic cell function, inhibition of lymphocyte apoptosis), and the second way is the production of anti-cancer vaccines using known cancer antigens: MAGE A3, MUC1, EGF and TGF-b. |
| 1020 | 24934404 | Association of candidate gene polymorphisms and TGF-beta/IL-10 levels with malaria in three regions of Cameroon: a case-control study. |
| 1021 | 25052849 | We found that preexisting levels of transforming growth factor beta (TGF-β) had an inverse correlation with in vivo and in vitro immunologic responses to the AE37 vaccine which were measured as delayed-type hypersensitivity (DTH) and interferon gamma (IFN-γ) production in response to the native HER-2(776-790) (or AE36) peptide, respectively. |
| 1022 | 25773885 | When phosphorylation of STAT3 was inhibited in DCs, we found that DCs did not suppress NK cells, and observed an increase in the production of lymphotoxin-alpha (LTα) and interleukin-12 (IL-12) as well as reduced release of transforming growth factor beta (TGF-β). |
| 1023 | 25870800 | It is accomplished by M2 macrophage polarization, the activity of myeloid derived suppressor cells (MDSCs) and a significantly elevated concentration of cytokines: transforming growth factor beta (TGFβ) and IL-10 in the tumor microenvironment. |
| 1024 | 25870800 | Very active suppression of immune protection is the predominant role of the programmed death 1 (PD-1)-PD-L1 pathway. |
| 1025 | 25870800 | Cytotoxic T lymphocyte antigen-4 (CTLA-4) is the molecule capable of inhibiting the activation signal. |
| 1026 | 25870800 | The second way in lung cancer immunotherapy is production of anti-cancer vaccines using recognized cancer antigens: MAGE-A3, membrane associated glycoprotein (MUC-1), and EGF. |
| 1027 | 26148331 | We observed that at d 3-4 post vaccination, 6 genes were down-regulated, namely APC, CD3G, FASLG, IL7, CD8A and TLR1. |
| 1028 | 26148331 | Meanwhile at 6-7 days post vaccination, 9 genes were significantly up-regulated, including RIPK2, TGFB1, MICB, SOCS1, IL2RA, MS4A1, PTPRC, IL2 and IL8. |
| 1029 | 26148331 | By days 12-15 the genes RIPK2, IL4, IL12B and TLR2 were overexpressed. |
| 1030 | 26391398 | Ac2PIM-responsive miR-150 and miR-143 target receptor-interacting protein kinase 2 and transforming growth factor beta-activated kinase 1 to suppress NOD2-induced immunomodulators. |
| 1031 | 26391398 | While Ac2PIM treatment of macrophages compromised their ability to induce NOD2-dependent immunomodulators like cyclooxygenase (COX)-2, suppressor of cytokine signaling (SOCS)-3, and matrix metalloproteinase (MMP)-9, no change in the NOD2-responsive NO, TNF-α, VEGF-A, and IL-12 levels was observed. |
| 1032 | 26391398 | Further, genome-wide microRNA expression profiling identified Ac2PIM-responsive miR-150 and miR-143 to target NOD2 signaling adaptors, RIP2 and TAK1, respectively. |
| 1033 | 26391398 | Interestingly, Ac2PIM was found to activate the SRC-FAK-PYK2-CREB cascade via TLR2 to recruit CBP/P300 at the promoters of miR-150 and miR-143 and epigenetically induce their expression. |
| 1034 | 26391398 | Loss-of-function studies utilizing specific miRNA inhibitors establish that Ac2PIM, via the miRNAs, abrogate NOD2-induced PI3K-PKCδ-MAPK pathway to suppress β-catenin-mediated expression of COX-2, SOCS-3, and MMP-9. |