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Gene Information
Gene symbol: STAT3
Gene name: signal transducer and activator of transcription 3 (acute-phase response factor)
HGNC ID: 11364
Synonyms: APRF
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 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. |
| 2 | 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. |
| 3 | 15356132 | IL-6 regulates in vivo dendritic cell differentiation through STAT3 activation. |
| 4 | 15356132 | We examined this effect further in knockin mice expressing mutant versions of the IL-6 signal transducer gp130, with defective signaling through either Src homology region 2 domain-containing phosphatase 2/Gab/MAPK (gp130(F759/F759)) or STAT3 (gp130(FxxQ/FxxQ)), and combined gp130 and IL-6 defects (gp130(F759/F759)/IL-6 KO mice). |
| 5 | 15356132 | Importantly, we found STAT3 activation by IL-6 was required for the suppression of LPS-induced DC maturation. |
| 6 | 15356132 | In addition, STAT3 phosphorylation in DCs was regulated by IL-6 in vivo, and STAT3 was necessary for the IL-6 suppression of bone marrow-derived DC activation/maturation. |
| 7 | 15356132 | IL-6 is thus a potent regulator of DC differentiation in vivo, and IL-6-gp130-STAT3 signaling in DCs may represent a critical target for controlling T cell-mediated immune responses in vivo. |
| 8 | 15356132 | IL-6 regulates in vivo dendritic cell differentiation through STAT3 activation. |
| 9 | 15356132 | We examined this effect further in knockin mice expressing mutant versions of the IL-6 signal transducer gp130, with defective signaling through either Src homology region 2 domain-containing phosphatase 2/Gab/MAPK (gp130(F759/F759)) or STAT3 (gp130(FxxQ/FxxQ)), and combined gp130 and IL-6 defects (gp130(F759/F759)/IL-6 KO mice). |
| 10 | 15356132 | Importantly, we found STAT3 activation by IL-6 was required for the suppression of LPS-induced DC maturation. |
| 11 | 15356132 | In addition, STAT3 phosphorylation in DCs was regulated by IL-6 in vivo, and STAT3 was necessary for the IL-6 suppression of bone marrow-derived DC activation/maturation. |
| 12 | 15356132 | IL-6 is thus a potent regulator of DC differentiation in vivo, and IL-6-gp130-STAT3 signaling in DCs may represent a critical target for controlling T cell-mediated immune responses in vivo. |
| 13 | 15356132 | IL-6 regulates in vivo dendritic cell differentiation through STAT3 activation. |
| 14 | 15356132 | We examined this effect further in knockin mice expressing mutant versions of the IL-6 signal transducer gp130, with defective signaling through either Src homology region 2 domain-containing phosphatase 2/Gab/MAPK (gp130(F759/F759)) or STAT3 (gp130(FxxQ/FxxQ)), and combined gp130 and IL-6 defects (gp130(F759/F759)/IL-6 KO mice). |
| 15 | 15356132 | Importantly, we found STAT3 activation by IL-6 was required for the suppression of LPS-induced DC maturation. |
| 16 | 15356132 | In addition, STAT3 phosphorylation in DCs was regulated by IL-6 in vivo, and STAT3 was necessary for the IL-6 suppression of bone marrow-derived DC activation/maturation. |
| 17 | 15356132 | IL-6 is thus a potent regulator of DC differentiation in vivo, and IL-6-gp130-STAT3 signaling in DCs may represent a critical target for controlling T cell-mediated immune responses in vivo. |
| 18 | 15356132 | IL-6 regulates in vivo dendritic cell differentiation through STAT3 activation. |
| 19 | 15356132 | We examined this effect further in knockin mice expressing mutant versions of the IL-6 signal transducer gp130, with defective signaling through either Src homology region 2 domain-containing phosphatase 2/Gab/MAPK (gp130(F759/F759)) or STAT3 (gp130(FxxQ/FxxQ)), and combined gp130 and IL-6 defects (gp130(F759/F759)/IL-6 KO mice). |
| 20 | 15356132 | Importantly, we found STAT3 activation by IL-6 was required for the suppression of LPS-induced DC maturation. |
| 21 | 15356132 | In addition, STAT3 phosphorylation in DCs was regulated by IL-6 in vivo, and STAT3 was necessary for the IL-6 suppression of bone marrow-derived DC activation/maturation. |
| 22 | 15356132 | IL-6 is thus a potent regulator of DC differentiation in vivo, and IL-6-gp130-STAT3 signaling in DCs may represent a critical target for controlling T cell-mediated immune responses in vivo. |
| 23 | 15356132 | IL-6 regulates in vivo dendritic cell differentiation through STAT3 activation. |
| 24 | 15356132 | We examined this effect further in knockin mice expressing mutant versions of the IL-6 signal transducer gp130, with defective signaling through either Src homology region 2 domain-containing phosphatase 2/Gab/MAPK (gp130(F759/F759)) or STAT3 (gp130(FxxQ/FxxQ)), and combined gp130 and IL-6 defects (gp130(F759/F759)/IL-6 KO mice). |
| 25 | 15356132 | Importantly, we found STAT3 activation by IL-6 was required for the suppression of LPS-induced DC maturation. |
| 26 | 15356132 | In addition, STAT3 phosphorylation in DCs was regulated by IL-6 in vivo, and STAT3 was necessary for the IL-6 suppression of bone marrow-derived DC activation/maturation. |
| 27 | 15356132 | IL-6 is thus a potent regulator of DC differentiation in vivo, and IL-6-gp130-STAT3 signaling in DCs may represent a critical target for controlling T cell-mediated immune responses in vivo. |
| 28 | 16275627 | Chlorophyllin attenuates IFN-gamma expression in lipopolysaccharide-stimulated murine splenic mononuclear cells via suppressing IL-12 production. |
| 29 | 16275627 | RT-PCR analysis showed that LPS-activated IFN-gamma expression gradually declined by CHL treatment in a dose dependent manner while mRNA production of TNF-alpha, IL-2, and FasL was not changed. |
| 30 | 16275627 | CHL also suppressed IL-12 production (p70, a heterodimer of p40 and p35) and the mRNA expression of IL-12 p40 and IL-12 receptors (both IL-12Rbeta1 and IL-12Rbeta2), which are involved in the induction of IFN-gamma expression. |
| 31 | 16275627 | Furthermore, an electrophoretic mobility shift assay showed that CHL inhibited DNA binding activity of NF-kappaB, STAT-3, and STAT-4 to their cognate DNA recognition motifs, all of which contribute to the IL-12-induced IFN-gamma transcription. |
| 32 | 16275627 | Exogenous addition of recombinant IL-12 abrogated the inhibitory effect of CHL on IFN-gamma and its mRNA expression in LPS-activated splenocytes. |
| 33 | 16275627 | Collectively, these results show that CHL inhibits IFN-gamma production by LPS-stimulated splenic mononuclear cells due to down-regulation of IL-12 production. |
| 34 | 17143781 | Of the genes tested, 21 genes (IRF-1, IFN 1-2 promoter, IFNAR-1, IRF-10, IFN-gamma, 2',5'-OAS, IAP-1, caspase 8, TRAIL-like, STAT-3, IL-6, IL-8, MIP-3 alpha, MHC-I, MHC-II, TVB, GLVR-1, OTF, IL-13R alpha, ST3GAL-VI and PGK) showed an increased expression. |
| 35 | 17143781 | The remaining seven genes (IFNAR-2, IFN-alpha, NF-kappaB subunit p65, BLRcp38, DDX1, G6PDH and UB) showed a constant expression or only slight alteration. |
| 36 | 18061513 | Several tumor-derived factors such as VEGF, IL-6, IL-10, M-CSF, and STAT-3 have been shown to be responsible for systemic and local DC defects. |
| 37 | 18209042 | IFN-gamma itself induced IL-27p28 expression and survival but did not promote relevant CCR7-driven migration or activated Th-1 cell recruitment capacity in MDDC. |
| 38 | 18209042 | Administered in association with classical maturation stimuli such as CD40 or TLR-4 stimulation, IFN-gamma up-regulated IL-27 and IL-12 production, CCR7-driven migration, and activated Th-1 cell recruitment, whereas it decreased IL-10 production and STAT3 phosphorylation. |
| 39 | 18209042 | CD38 signaling, which orchestrates migration, survival, and Th-1 polarizing ability of mature MDDC, was involved in IFN-gamma-mediated effects. |
| 40 | 18981115 | Imatinib mesylate inhibits CD4+ CD25+ regulatory T cell activity and enhances active immunotherapy against BCR-ABL- tumors. |
| 41 | 18981115 | Suppressive as well as stimulating effects of this drug on CD4(+) and CD8(+) T lymphocytes or dendritic cells have been reported. |
| 42 | 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. |
| 43 | 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. |
| 44 | 18981115 | Imatinib significantly reduced the activation of the transcription factors STAT3 and STAT5 in Treg. |
| 45 | 18981115 | Analysis of Treg TCR-induced signaling cascade indicated that imatinib inhibited phosphorylation of ZAP70 and LAT. |
| 46 | 19109391 | There was a significant increase in Stat3- and interleukin-6 (IL-6)-dependent transcription in Stat1(-/-) mice, implicating the Stat3 and IL-6 pathways in the observed ocular pathology. |
| 47 | 19109391 | Further, infected Stat1(-/-) mice showed phosphorylated Stat3 in the corneal epithelium. |
| 48 | 19109391 | There was a significant increase in Stat3- and interleukin-6 (IL-6)-dependent transcription in Stat1(-/-) mice, implicating the Stat3 and IL-6 pathways in the observed ocular pathology. |
| 49 | 19109391 | Further, infected Stat1(-/-) mice showed phosphorylated Stat3 in the corneal epithelium. |
| 50 | 20351189 | Dendritic cells and Stat3 are essential for CD137-induced CD8 T cell activation-induced cell death. |
| 51 | 20351189 | Virus-specific CD8 T cells in anti-CD137-injected mice rapidly upregulate Fas expression, and although necessary, was insufficient to induce CD8 T cell deletion. |
| 52 | 20351189 | Taken together, these data suggest that CD137 signaling in DCs can regulate CD8 T cell survival through a Stat3 and Fas-mediated pathway. |
| 53 | 20351189 | Dendritic cells and Stat3 are essential for CD137-induced CD8 T cell activation-induced cell death. |
| 54 | 20351189 | Virus-specific CD8 T cells in anti-CD137-injected mice rapidly upregulate Fas expression, and although necessary, was insufficient to induce CD8 T cell deletion. |
| 55 | 20351189 | Taken together, these data suggest that CD137 signaling in DCs can regulate CD8 T cell survival through a Stat3 and Fas-mediated pathway. |
| 56 | 20375997 | Interestingly, CT regulated the expression of the signal transducer and activator of transcription (STAT)3 gene and influenced the level and activation of both isoforms STAT3 alpha and STAT3 beta, in vitro in a B-cell line and in Peyer's patch (PP) B cells and in vivo in freshly isolated splenic B cells from CT-treated mice. |
| 57 | 20375997 | B cells pre-exposed to CT were significantly more susceptible to the activation of STAT3 by interleukin (IL)-6 and IL-10. |
| 58 | 20375997 | This exerted a stronger inhibitory effect of IL-10 on lipopolysaccharide (LPS)-stimulated B-cell proliferation and cytokine production (IL-6). |
| 59 | 20375997 | Interestingly, CT regulated the expression of the signal transducer and activator of transcription (STAT)3 gene and influenced the level and activation of both isoforms STAT3 alpha and STAT3 beta, in vitro in a B-cell line and in Peyer's patch (PP) B cells and in vivo in freshly isolated splenic B cells from CT-treated mice. |
| 60 | 20375997 | B cells pre-exposed to CT were significantly more susceptible to the activation of STAT3 by interleukin (IL)-6 and IL-10. |
| 61 | 20375997 | This exerted a stronger inhibitory effect of IL-10 on lipopolysaccharide (LPS)-stimulated B-cell proliferation and cytokine production (IL-6). |
| 62 | 20434781 | Further studies demonstrated that CS-A up-regulated STAT4 expression and thus, induced IFN-gamma production and Th1 CD4 T cell differentiation. |
| 63 | 20434781 | CS-A also up-regulated STAT3 and IL-23 expression and thus increased IL-17 producing T cells. |
| 64 | 20473939 | Besides, a favorable host environment was created by the reduced secretion of interleukin-10 and 6 and vascular endothelial growth factor (VEGF) in the tumor niche and decreased the expression of phosphorylation-signal transducer and activator of transcription 3 of TC-1 tumors. |
| 65 | 20709294 | Vaccinia induced rapid TLR2-dependent responses, leading to IL-6 production, which then initiated STAT3 signaling in dendritic and T cells. |
| 66 | 20709294 | In resistant C57BL/6 mice, the STAT1 and STAT3 pathways were rapidly activated, whereas in susceptible BALB/c mice, IL-6-dependent STAT3 activation did not occur. |
| 67 | 20709294 | Vaccinia induced rapid TLR2-dependent responses, leading to IL-6 production, which then initiated STAT3 signaling in dendritic and T cells. |
| 68 | 20709294 | In resistant C57BL/6 mice, the STAT1 and STAT3 pathways were rapidly activated, whereas in susceptible BALB/c mice, IL-6-dependent STAT3 activation did not occur. |
| 69 | 21257966 | Intrinsic IL-21 signaling is critical for CD8 T cell survival and memory formation in response to vaccinia viral infection. |
| 70 | 21257966 | CD4 T cell help plays an important role in promoting CD8 T cell immunity to pathogens. |
| 71 | 21257966 | In models of infection with vaccinia virus (VV) and Listeria monocytogenes, CD4 T cell help is critical for the survival of activated CD8 T cells during both the primary and memory recall responses. |
| 72 | 21257966 | Still unclear, however, is how CD4 T cell help promotes CD8 T cell survival. |
| 73 | 21257966 | In this study, we first showed that CD4 T cell help for the CD8 T cell response to VV infection was mediated by IL-21, a cytokine produced predominantly by activated CD4 T cells, and that direct action of IL-21 on CD8 T cells was critical for the VV-specific CD8 T cell response in vivo. |
| 74 | 21257966 | We next demonstrated that this intrinsic IL-21 signaling was essential for the survival of activated CD8 T cells and the generation of long-lived memory cells. |
| 75 | 21257966 | We further revealed that IL-21 promoted CD8 T cell survival in a mechanism dependent on activation of the STAT1 and STAT3 pathways and subsequent upregulation of the prosurvival molecules Bcl-2 and Bcl-x(L). |
| 76 | 21257966 | These results identify a critical role for intrinsic IL-21 signaling in CD8 T cell responses to an acute viral infection in vivo and may help design effective vaccine strategies. |
| 77 | 21527558 | In vaccinated mice, silencing STAT3 increased the proliferation and granzyme B levels of intratumoral CD4(+) and CD8(+) T cells. |
| 78 | 21633673 | Our results demonstrated up to an approximately fivefold induction in the infiltration of CD3(+) cells in tumor mass on STAT3 knockdown with high levels of CD4(+), CD8(+), and NKT cells. |
| 79 | 21633673 | Those DCs were activated, in an otherwise suppressive microenvironment, as evidenced by a high expression of costimulatory molecules CD86 and CD40. |
| 80 | 21784871 | Because immunosuppression continues to be a major inhibitor of cancer vaccine efficacy, we examined in this study whether therapeutically targeted delivery of a synthetic STAT-3 inhibitor to the TME, combined with an HER-2 DNA vaccine can improve immune surveillance against HER-2(+) breast cancer and prevent its recurrence. |
| 81 | 21784871 | Furthermore, we showed that treatment with these NPs resulted in priming of the immune TME, characterized by increased IFN-γ, p-STAT-1, GM-CSF, IL-2, IL-15, and IL-12b and reduced TGF-β, IL-6, and IL-10 protein expression. |
| 82 | 22169598 | In in vitro glioma cells, there was a positive correlation between the protein levels of TLR9 and both matrix metalloproteinase (MMP)-2 and MMP-9 (p<0.05), but no relationship between TLR9 levels and levels of interleukin-6, transforming growth factor-β2 or signal transducer and activator of transcription (STAT)-3 (p>0.05). |
| 83 | 22441015 | Autophagy inhibition in hypoxic cells decreases phospho-STAT3 and restores CTL-mediated tumor cell killing by a mechanism involving the ubiquitin proteasome system and SQSTM1/p62. |
| 84 | 22481968 | Immunological inhibitory cytokines, such as TGF-β, IL-10, IL-6 and VEGF, which are produced from myeloma cells, can modulate antitumor host immune response, including the abrogation of DC function, by constitutive activation of STAT3. |
| 85 | 22581824 | IL-10 directly activates and expands tumor-resident CD8(+) T cells without de novo infiltration from secondary lymphoid organs. |
| 86 | 22581824 | Here we show that treatment with the pleiotropic cytokine interleukin-10 (IL-10) induces specific activation of tumor-resident CD8(+) T cells as well as their intratumoral expansion in several mouse tumor models. |
| 87 | 22581824 | We found that inhibition of T-cell trafficking from lymphoid organs did not impair IL-10-induced tumor rejection or the activation of tumor-resident CD8(+) T cells. |
| 88 | 22581824 | Tumor-resident CD8(+) T cells expressed elevated levels of the IL-10 receptor and were directly activated by IL-10, resulting in prominent phosphorylation of STAT3 and STAT1. |
| 89 | 22581824 | Although CD4(+) T cells, regulatory T cells, NK cells, and dendritic cells have been reported as prominent targets of IL-10 in the tumor microenvironment, we found that expression of the IL-10R was required only on CD8(+) T cells to facilitate IL-10-induced tumor rejection as well as in situ expansion and proliferation of tumor-resident CD8 T cells. |
| 90 | 22581824 | Together, our findings indicate that IL-10 activates CD8(+) T-cell-mediated tumor control and suggest that IL-10 may represent a potential tumor immunotherapy in human patients with cancer. |
| 91 | 22720256 | One unique approach utilizes Salmonella for systemic delivery of inhibitory RNA, targeting the immunosuppressive molecule Stat3, and a Survivin vaccine to suppress growth of aggressive murine tumors. |
| 92 | 23100560 | Of note, synthesis of fibrinogen was dependent on the IL-1-IL-6-Stat3 cascade. |
| 93 | 23428347 | In this study, we explored the effects of a combination treatment consisting of a proteasome inhibitor, bortezomib, and an antigen specific STAT3-ablated (STAT3⁻/⁻) DC-based vaccine on the control of TC-1(P3) tumors, a p53-degraded immune resistant cancer cells. |
| 94 | 23428347 | We found that E7-antigen expressing STAT3⁻/⁻ DC (E7-DC-1STAT3⁻/⁻) vaccination enhanced generation of E7-specific CD8⁺ T cells, but was not enough to control TC-1(P3) cancer cells. |
| 95 | 23428347 | We found that apoptosis via down-regulation of STAT3 and NF-κB and up-regulation of Fas and death receptor 5 (DR5) expression in TC-1(P3) induced by bortezomib was independent of p53 status. |
| 96 | 23428347 | We also observed that TC-1(P3) cells pretreated with bortezomib had markedly enhanced anti-tumor effects on E7-specific CD8⁺ T cells through a Fas/DR5-mediated mechanism. |
| 97 | 23428347 | These results suggest that the anti-tumor effects against a p53-degraded immune resistant variant generated by antigen-expressing STAT3-ablated mature DCs may be enhanced by bortezomib via death receptor-mediated apoptosis. |
| 98 | 23428347 | In this study, we explored the effects of a combination treatment consisting of a proteasome inhibitor, bortezomib, and an antigen specific STAT3-ablated (STAT3⁻/⁻) DC-based vaccine on the control of TC-1(P3) tumors, a p53-degraded immune resistant cancer cells. |
| 99 | 23428347 | We found that E7-antigen expressing STAT3⁻/⁻ DC (E7-DC-1STAT3⁻/⁻) vaccination enhanced generation of E7-specific CD8⁺ T cells, but was not enough to control TC-1(P3) cancer cells. |
| 100 | 23428347 | We found that apoptosis via down-regulation of STAT3 and NF-κB and up-regulation of Fas and death receptor 5 (DR5) expression in TC-1(P3) induced by bortezomib was independent of p53 status. |
| 101 | 23428347 | We also observed that TC-1(P3) cells pretreated with bortezomib had markedly enhanced anti-tumor effects on E7-specific CD8⁺ T cells through a Fas/DR5-mediated mechanism. |
| 102 | 23428347 | These results suggest that the anti-tumor effects against a p53-degraded immune resistant variant generated by antigen-expressing STAT3-ablated mature DCs may be enhanced by bortezomib via death receptor-mediated apoptosis. |
| 103 | 23428347 | In this study, we explored the effects of a combination treatment consisting of a proteasome inhibitor, bortezomib, and an antigen specific STAT3-ablated (STAT3⁻/⁻) DC-based vaccine on the control of TC-1(P3) tumors, a p53-degraded immune resistant cancer cells. |
| 104 | 23428347 | We found that E7-antigen expressing STAT3⁻/⁻ DC (E7-DC-1STAT3⁻/⁻) vaccination enhanced generation of E7-specific CD8⁺ T cells, but was not enough to control TC-1(P3) cancer cells. |
| 105 | 23428347 | We found that apoptosis via down-regulation of STAT3 and NF-κB and up-regulation of Fas and death receptor 5 (DR5) expression in TC-1(P3) induced by bortezomib was independent of p53 status. |
| 106 | 23428347 | We also observed that TC-1(P3) cells pretreated with bortezomib had markedly enhanced anti-tumor effects on E7-specific CD8⁺ T cells through a Fas/DR5-mediated mechanism. |
| 107 | 23428347 | These results suggest that the anti-tumor effects against a p53-degraded immune resistant variant generated by antigen-expressing STAT3-ablated mature DCs may be enhanced by bortezomib via death receptor-mediated apoptosis. |
| 108 | 23428347 | In this study, we explored the effects of a combination treatment consisting of a proteasome inhibitor, bortezomib, and an antigen specific STAT3-ablated (STAT3⁻/⁻) DC-based vaccine on the control of TC-1(P3) tumors, a p53-degraded immune resistant cancer cells. |
| 109 | 23428347 | We found that E7-antigen expressing STAT3⁻/⁻ DC (E7-DC-1STAT3⁻/⁻) vaccination enhanced generation of E7-specific CD8⁺ T cells, but was not enough to control TC-1(P3) cancer cells. |
| 110 | 23428347 | We found that apoptosis via down-regulation of STAT3 and NF-κB and up-regulation of Fas and death receptor 5 (DR5) expression in TC-1(P3) induced by bortezomib was independent of p53 status. |
| 111 | 23428347 | We also observed that TC-1(P3) cells pretreated with bortezomib had markedly enhanced anti-tumor effects on E7-specific CD8⁺ T cells through a Fas/DR5-mediated mechanism. |
| 112 | 23428347 | These results suggest that the anti-tumor effects against a p53-degraded immune resistant variant generated by antigen-expressing STAT3-ablated mature DCs may be enhanced by bortezomib via death receptor-mediated apoptosis. |
| 113 | 23447690 | Cutting edge: STAT1 is required for IL-6-mediated Bcl6 induction for early follicular helper cell differentiation. |
| 114 | 23447690 | We found that early Bcl6(+)CXCR5(+) Tfh differentiation was severely impaired in the absence of IL-6; however, STAT3 deficiency failed to recapitulate that defect. |
| 115 | 23447690 | IL-6R signaling activates the transcription factor STAT1 specifically in CD4 T cells. |
| 116 | 23447690 | IL-6 mediated STAT3 activation is important for downregulation of IL-2Rα to limit Th1 cell differentiation in an acute viral infection. |
| 117 | 23447690 | Thus, IL-6 signaling is a major early inducer of the Tfh differentiation program unexpectedly mediated by both STAT3 and STAT1 transcription factors. |
| 118 | 23447690 | Cutting edge: STAT1 is required for IL-6-mediated Bcl6 induction for early follicular helper cell differentiation. |
| 119 | 23447690 | We found that early Bcl6(+)CXCR5(+) Tfh differentiation was severely impaired in the absence of IL-6; however, STAT3 deficiency failed to recapitulate that defect. |
| 120 | 23447690 | IL-6R signaling activates the transcription factor STAT1 specifically in CD4 T cells. |
| 121 | 23447690 | IL-6 mediated STAT3 activation is important for downregulation of IL-2Rα to limit Th1 cell differentiation in an acute viral infection. |
| 122 | 23447690 | Thus, IL-6 signaling is a major early inducer of the Tfh differentiation program unexpectedly mediated by both STAT3 and STAT1 transcription factors. |
| 123 | 23447690 | Cutting edge: STAT1 is required for IL-6-mediated Bcl6 induction for early follicular helper cell differentiation. |
| 124 | 23447690 | We found that early Bcl6(+)CXCR5(+) Tfh differentiation was severely impaired in the absence of IL-6; however, STAT3 deficiency failed to recapitulate that defect. |
| 125 | 23447690 | IL-6R signaling activates the transcription factor STAT1 specifically in CD4 T cells. |
| 126 | 23447690 | IL-6 mediated STAT3 activation is important for downregulation of IL-2Rα to limit Th1 cell differentiation in an acute viral infection. |
| 127 | 23447690 | Thus, IL-6 signaling is a major early inducer of the Tfh differentiation program unexpectedly mediated by both STAT3 and STAT1 transcription factors. |
| 128 | 23886112 | These approaches have included: (1) the use of IL-17A and IL-17F-deficient mice, (2) specific antibodies directed against IL-17, (3) an IL-17 vaccine, (4) methods to block the IL-17 receptor and (5) small-molecule inhibitors of IL-17. |
| 129 | 23886112 | This paper will review the preclinical results using various pharmacological approaches [specific IL-17 antibodies, an IL-17 receptor fusion protein, IL-12/IL-23 p40 subunit and IL-17 vaccine approaches, as well as a small molecule inhibitor (Vidofludimus)] to inhibit IL-17 in animal models of IBD. |
| 130 | 23886112 | Finally, future pharmacological approaches of interest will be discussed, such as: (1) Retinoic acid receptor-related orphan nuclear receptor gamma t (Rorγt) antagonists, (2) Retinoic acid receptor alpha (RARα) antagonists, (3) Pim-1 kinase inhibitors and (4) Dual small-molecule inhibitors of NF-κB and STAT3, like synthetic triterpenoids. |
| 131 | 23958949 | Here, we report that patients with melanoma receiving DD immediately before a dendritic cell (DC) vaccine failed to develop a tumor-antigen-specific CD4 and CD8 T-cell immune response even after repeated vaccinations. |
| 132 | 23958949 | First, DD modulated DCs toward tolerance by downregulating costimulatory receptors such as CD83 and CD25 while upregulating tolerance-associated proteins/pathways including Stat-3, β-catenin, and class II transactivator-dependent antigen presentation. |
| 133 | 24100507 | Among the seven STAT family proteins, STAT3 is constitutively activated in many diverse cancers. |
| 134 | 24100507 | STAT3 downstream proteins involved in cell proliferation and survival, such as c-Myc and Mcl-1, are downregulated by MLS-2384 in prostate cancer cells, whereas survivin is downregulated in A2058 cells. |
| 135 | 24100507 | Our findings support further development of MLS-2384 as a potential small-molecule therapeutic agent that targets JAK, Src, and STAT3 signaling in multiple human cancer cells. |
| 136 | 24100507 | Among the seven STAT family proteins, STAT3 is constitutively activated in many diverse cancers. |
| 137 | 24100507 | STAT3 downstream proteins involved in cell proliferation and survival, such as c-Myc and Mcl-1, are downregulated by MLS-2384 in prostate cancer cells, whereas survivin is downregulated in A2058 cells. |
| 138 | 24100507 | Our findings support further development of MLS-2384 as a potential small-molecule therapeutic agent that targets JAK, Src, and STAT3 signaling in multiple human cancer cells. |
| 139 | 24100507 | Among the seven STAT family proteins, STAT3 is constitutively activated in many diverse cancers. |
| 140 | 24100507 | STAT3 downstream proteins involved in cell proliferation and survival, such as c-Myc and Mcl-1, are downregulated by MLS-2384 in prostate cancer cells, whereas survivin is downregulated in A2058 cells. |
| 141 | 24100507 | Our findings support further development of MLS-2384 as a potential small-molecule therapeutic agent that targets JAK, Src, and STAT3 signaling in multiple human cancer cells. |
| 142 | 24154870 | Systemic inhibition of TLR9, but not TLR4, delayed tumor recurrence in mouse models of B16 melanoma, MB49 bladder cancer, and CT26 colon cancer after localized high-dose tumor irradiation. |
| 143 | 24154870 | The tumorigenic effects of TLR9 depended on MyD88/NF-κB-mediated upregulation of interleukin (IL)-6 expression, which in turn resulted in downstream activation of Jak/STAT3 signaling in myeloid cells. |
| 144 | 24154870 | In comparing global gene expression in wild-type, TLR9-, or STAT3-deficient myeloid cells derived from irradiated tumors, we identified a unique set of TLR9/STAT3-regulated genes involved in tumor-promoting inflammation and revascularization. |
| 145 | 24154870 | Blocking STAT3 function by two myeloid-specific genetic strategies corrected TLR9-mediated cancer recurrence after radiotherapy. |
| 146 | 24154870 | Our results suggest that combining localized tumor irradiation with myeloid cell-specific inhibition of TLR9/STAT3 signaling may help eliminate radioresistant cancers. |
| 147 | 24154870 | Systemic inhibition of TLR9, but not TLR4, delayed tumor recurrence in mouse models of B16 melanoma, MB49 bladder cancer, and CT26 colon cancer after localized high-dose tumor irradiation. |
| 148 | 24154870 | The tumorigenic effects of TLR9 depended on MyD88/NF-κB-mediated upregulation of interleukin (IL)-6 expression, which in turn resulted in downstream activation of Jak/STAT3 signaling in myeloid cells. |
| 149 | 24154870 | In comparing global gene expression in wild-type, TLR9-, or STAT3-deficient myeloid cells derived from irradiated tumors, we identified a unique set of TLR9/STAT3-regulated genes involved in tumor-promoting inflammation and revascularization. |
| 150 | 24154870 | Blocking STAT3 function by two myeloid-specific genetic strategies corrected TLR9-mediated cancer recurrence after radiotherapy. |
| 151 | 24154870 | Our results suggest that combining localized tumor irradiation with myeloid cell-specific inhibition of TLR9/STAT3 signaling may help eliminate radioresistant cancers. |
| 152 | 24154870 | Systemic inhibition of TLR9, but not TLR4, delayed tumor recurrence in mouse models of B16 melanoma, MB49 bladder cancer, and CT26 colon cancer after localized high-dose tumor irradiation. |
| 153 | 24154870 | The tumorigenic effects of TLR9 depended on MyD88/NF-κB-mediated upregulation of interleukin (IL)-6 expression, which in turn resulted in downstream activation of Jak/STAT3 signaling in myeloid cells. |
| 154 | 24154870 | In comparing global gene expression in wild-type, TLR9-, or STAT3-deficient myeloid cells derived from irradiated tumors, we identified a unique set of TLR9/STAT3-regulated genes involved in tumor-promoting inflammation and revascularization. |
| 155 | 24154870 | Blocking STAT3 function by two myeloid-specific genetic strategies corrected TLR9-mediated cancer recurrence after radiotherapy. |
| 156 | 24154870 | Our results suggest that combining localized tumor irradiation with myeloid cell-specific inhibition of TLR9/STAT3 signaling may help eliminate radioresistant cancers. |
| 157 | 24154870 | Systemic inhibition of TLR9, but not TLR4, delayed tumor recurrence in mouse models of B16 melanoma, MB49 bladder cancer, and CT26 colon cancer after localized high-dose tumor irradiation. |
| 158 | 24154870 | The tumorigenic effects of TLR9 depended on MyD88/NF-κB-mediated upregulation of interleukin (IL)-6 expression, which in turn resulted in downstream activation of Jak/STAT3 signaling in myeloid cells. |
| 159 | 24154870 | In comparing global gene expression in wild-type, TLR9-, or STAT3-deficient myeloid cells derived from irradiated tumors, we identified a unique set of TLR9/STAT3-regulated genes involved in tumor-promoting inflammation and revascularization. |
| 160 | 24154870 | Blocking STAT3 function by two myeloid-specific genetic strategies corrected TLR9-mediated cancer recurrence after radiotherapy. |
| 161 | 24154870 | Our results suggest that combining localized tumor irradiation with myeloid cell-specific inhibition of TLR9/STAT3 signaling may help eliminate radioresistant cancers. |
| 162 | 24324467 | IL-6, Prostaglandin-E2, and IL-10 were identified as factors in cultures of primary human tumors responsible for the inhibited development and activation of skin DC as well as monocyte-derived DC. |
| 163 | 24324467 | Mostly from mouse studies, the JAK2/STAT3 signaling pathway has emerged as a "master switch" of tumor-induced immune suppression. |
| 164 | 24360890 | We found a strong correlation between leptin concentration and BMI (r=0.55, p<0.0001), but no association with hemagglutination antibody inhibition (HAI), B-cell, or granzyme B responses. |
| 165 | 24360890 | We found eight SNPs in the LEP/LEPR/GHRL genes that were associated with leptin levels and four SNPs in the PTPN1/LEPR/STAT3 genes associated with peripheral blood TREC levels (p<0.05). |
| 166 | 24360890 | We also found eight SNPs in the LEP/PPARG/CRP genes associated with variations in influenza-specific HAI and B-cell responses (p<0.05). |
| 167 | 24605077 | TFH cells are characterized by their expression of master regulator, Bcl-6, and chemokine receptor, CXCR5, which are essential for the migration of T cells into the B cell follicle. |
| 168 | 24605077 | IL-6 and IL-21 cytokine-mediated STAT signaling pathways, including STAT1 and STAT3, are crucial for inducing Bcl-6 expression and TFH cell differentiation. |
| 169 | 24605077 | TFH cells express important surface molecules such as ICOS, PD-1, IL-21, BTLA, SAP and CD40L for mediating the interaction between T and B cells. |
| 170 | 24605077 | The miR-17-92 cluster induces Bcl-6 and TFH cell differentiation, whereas miR-10a negatively regulates Bcl-6 expression in T cells. |
| 171 | 24605077 | In addition, follicular regulatory T (TFR) cells are studied as thymus-derived CXCR5(+)PD-1(+)Foxp3(+) Treg cells that play a significant role in limiting the GC response. |
| 172 | 24777831 | PIAS1 and STAT-3 impair the tumoricidal potential of IFN-γ-stimulated mouse dendritic cells generated with IL-15. |
| 173 | 24777831 | We report here that the tumoricidal potential of mouse DCs generated from myeloid precursors with GM-CSF and IL-15 (IL-15 DCs) can be triggered with the Toll-like receptor (TLR) 4 ligand lipopolysaccharide to a similar extent compared with that of their counterparts, conventionally generated with IL-4 (IL-4 DCs). |
| 174 | 24777831 | In contrast, interferon (IFN)-γ induces the cytotoxic activity of IL-4 but not IL-15 DCs. |
| 175 | 24777831 | Although the IFN-γ-STAT-1 signaling pathway is overall functional in IL-15 DCs, IFN-γ fails to induce iNOS expression in these cells. iNOS expression is negatively controlled in IFN-γ-stimulated IL-15 DCs by the cooperation between the E3 SUMO ligase PIAS1 and STAT-3, and can be partially restored with PIAS1 siRNA and STAT-3 inhibitors. |
| 176 | 24777831 | PIAS1 and STAT-3 impair the tumoricidal potential of IFN-γ-stimulated mouse dendritic cells generated with IL-15. |
| 177 | 24777831 | We report here that the tumoricidal potential of mouse DCs generated from myeloid precursors with GM-CSF and IL-15 (IL-15 DCs) can be triggered with the Toll-like receptor (TLR) 4 ligand lipopolysaccharide to a similar extent compared with that of their counterparts, conventionally generated with IL-4 (IL-4 DCs). |
| 178 | 24777831 | In contrast, interferon (IFN)-γ induces the cytotoxic activity of IL-4 but not IL-15 DCs. |
| 179 | 24777831 | Although the IFN-γ-STAT-1 signaling pathway is overall functional in IL-15 DCs, IFN-γ fails to induce iNOS expression in these cells. iNOS expression is negatively controlled in IFN-γ-stimulated IL-15 DCs by the cooperation between the E3 SUMO ligase PIAS1 and STAT-3, and can be partially restored with PIAS1 siRNA and STAT-3 inhibitors. |
| 180 | 24806510 | We also assessed the impact of STAT3 deletion on phagocytosis, maturation, cytokine secretion and antigen presentation by GM-CSF derived DCs in vitro. |
| 181 | 24806510 | In contrast, STAT3 was not required for GM-CSF induced DC differentiation as both wild type and STAT3 null bone marrow cells gave rise to similar number of DCs. |
| 182 | 24806510 | STAT3 also appeared to regulate the response of GM-CSF derived DCs to CpG. |
| 183 | 24806510 | STAT3 null DCs expressed high levels of MHC-II, secreted more IL-12p70, IL-10, and TNFα were better antigen presenters in vitro. |
| 184 | 24806510 | We also assessed the impact of STAT3 deletion on phagocytosis, maturation, cytokine secretion and antigen presentation by GM-CSF derived DCs in vitro. |
| 185 | 24806510 | In contrast, STAT3 was not required for GM-CSF induced DC differentiation as both wild type and STAT3 null bone marrow cells gave rise to similar number of DCs. |
| 186 | 24806510 | STAT3 also appeared to regulate the response of GM-CSF derived DCs to CpG. |
| 187 | 24806510 | STAT3 null DCs expressed high levels of MHC-II, secreted more IL-12p70, IL-10, and TNFα were better antigen presenters in vitro. |
| 188 | 24806510 | We also assessed the impact of STAT3 deletion on phagocytosis, maturation, cytokine secretion and antigen presentation by GM-CSF derived DCs in vitro. |
| 189 | 24806510 | In contrast, STAT3 was not required for GM-CSF induced DC differentiation as both wild type and STAT3 null bone marrow cells gave rise to similar number of DCs. |
| 190 | 24806510 | STAT3 also appeared to regulate the response of GM-CSF derived DCs to CpG. |
| 191 | 24806510 | STAT3 null DCs expressed high levels of MHC-II, secreted more IL-12p70, IL-10, and TNFα were better antigen presenters in vitro. |
| 192 | 24806510 | We also assessed the impact of STAT3 deletion on phagocytosis, maturation, cytokine secretion and antigen presentation by GM-CSF derived DCs in vitro. |
| 193 | 24806510 | In contrast, STAT3 was not required for GM-CSF induced DC differentiation as both wild type and STAT3 null bone marrow cells gave rise to similar number of DCs. |
| 194 | 24806510 | STAT3 also appeared to regulate the response of GM-CSF derived DCs to CpG. |
| 195 | 24806510 | STAT3 null DCs expressed high levels of MHC-II, secreted more IL-12p70, IL-10, and TNFα were better antigen presenters in vitro. |
| 196 | 24835401 | To study this, we employed an in vitro system in which influenza hemagglutinin (HA) 1 was delivered to dendritic cells (DCs) via Dectin-1 using anti-human Dectin-1 (hDectin-1)-HA1 recombinant fusion proteins. |
| 197 | 24835401 | Nonetheless, these DCs were not able to induce a significant level of HA1-specific Th17 responses even in the presence of the Th17-promoting cytokines IL-1β and IL-6. |
| 198 | 24835401 | Thus, interruptions in STAT3 or MyD88 signaling led to substantially diminished HA1-specific Th17 induction. |
| 199 | 25367297 | CD14(+)CD16(+) inflammatory monocytes were induced after vaccination in both young and older adults. |
| 200 | 25367297 | In classical CD14(+)CD16(-) and inflammatory monocytes, production of tumor necrosis factor α and interleukin 6, as measured by intracellular staining, was strongly induced after vaccination. |
| 201 | 25367297 | In purified monocytes, we found age-associated elevation in phosphorylated signal transducer and activator of transcription-3, and decreased serine 359 phosphorylation of the negative IL-10 regulator dual-specificity phosphatase 1. |
| 202 | 25457983 | In the present study, Poly I:C (PIC, a TLR3 agonist), STAT3 siRNA and OVA antigen were co-encapsulated by poly (ethylene glycol)-b-poly (L-lysine)-b-poly (L-leucine) (PEG-PLL-PLLeu) polypeptide micelles to generate PMP/OVA/siRNA nanovaccine, which was aimed to effectively overcome DC dysfunction in vivo by deleting STAT3 gene in situ. |
| 203 | 25457983 | PMP/OVA/siRNA also elevated CD86 and CD40 expression as well as IL-12 production by TADCs more effectively than PMP/OVA did, indicating its strong potency of inducing TADC maturation and activation. |
| 204 | 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). |
| 205 | 25814664 | Here, we found that GSK-3β-dependent IDO expression in the dendritic cell (DC) plays a role in anti-tumor activity via the regulation of CD8(+) T-cell polarization and cytotoxic T lymphocyte activity. |
| 206 | 25814664 | By the inhibition of GSK-3β, attenuated IDO expression and impaired JAK1/2-Stat signaling crucial for IDO expression were observed. |
| 207 | 25814664 | Protein kinase Cδ (PKCδ) activity and the interaction between JAK1/2 and Stat3, which are important for IDO expression, were also reduced by GSK-3β inhibition. |
| 208 | 25814664 | CD8(+) T-cell proliferation mediated by OVA-pulsed DC was blocked by interferon (IFN)-γ-induced IDO expression via GSK-3β activity. |
| 209 | 25814664 | Specific cytotoxic T lymphocyte activity mediated by OVA-pulsed DC against OVA-expressing EG7 thymoma cells but not OVA-nonexpressing EL4 thymoma cells was also attenuated by the expressed IDO via IFN-γ-induced activation of GSK-3β. |
| 210 | 25814664 | Furthermore, tumor growth that was suppressed with OVA-pulsed DC vaccination was restored by IDO-expressing DC via IFN-γ-induced activation of GSK-3β in an OVA-expressing murine EG7 thymoma model. |
| 211 | 25814664 | Taken together, DC-based immune response mediated by interferon-γ-induced IDO expression via GSK-3β activity not only regulates CD8(+) T-cell proliferation and cytotoxic T lymphocyte activity but also modulates OVA-pulsed DC vaccination against EG7 thymoma. |
| 212 | 25962106 | Wogonin also promoted the secretion of calreticulin and high-mobility group protein 1 by tumor cells. |
| 213 | 25962106 | The dephosphorylation of STAT3 contributed to the decreased expression of B7H1 and MHC class I chain-related protein A, and the enhancement of calreticulin on the cell membrane. |
| 214 | 26090579 | IFN-α-Induced Downregulation of miR-221 in Dendritic Cells: Implications for HCV Pathogenesis and Treatment. |
| 215 | 26090579 | We report that IFN-α downregulates miR-221 in both DC subsets via inhibition of STAT3. |
| 216 | 26090579 | We validated proapoptotic proteins BCL2L11 and CDKN1C as miR-221 targets suggesting that IFN-α can induce DC apoptosis via miR-221 downregulation. |
| 217 | 26090579 | In addition, we validated another miR-221 target, SOCS1, which is known to be a negative regulator of JAK/STAT signaling. |
| 218 | 26090579 | Consistent with this, miR-221 overexpression in mDCs enhanced the secretion of proinflammatory cytokines IL-6 and TNF-α. |
| 219 | 26090579 | In peripheral blood mononuclear cells (PBMCs) of HIV-1/HCV co-infected individuals undergoing IFN-α-based treatment the baseline miR-221 expression was lower in non-responders compared with responders; and miR-221 expression directly correlated with DC frequency and IL-6/TNF-α secretion. |
| 220 | 26343197 | This review provides an appraisal of some of the key signaling pathways that may contribute to immune suppression in ovarian cancer, with a particular focus on the potential involvement of the c-KIT/PI3K/AKT, wnt/β-catenin, IL-6/STAT3 and AhR signaling pathways in regulation of indoleamine 2,3-dioxygenase expression in tumor-associated macrophages. |