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Gene Information
Gene symbol: TLR7
Gene name: toll-like receptor 7
HGNC ID: 15631
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 14530357 | PDCs, which express TLR7 and TLR9, responded to imidazoquinolines (imiquimod and R-848) and to CpG oligodeoxynucleotides stimulation, resulting in enhancement in expression of costimulatory molecules and induction of IFN-alpha and IL-12p70. |
| 2 | 14530357 | In contrast, MDCs, which express TLR3, TLR4, and TLR7, responded to poly(I:C), LPS, and imidazoquinolines with phenotypic maturation and high production of IL-12 p70 without producing detectable IFN-alpha. |
| 3 | 14530357 | Optimally TLR ligand-stimulated PDCs or MDCs exposed to CMV or HIV-1 Ags enhanced autologous CMV- and HIV-1-specific memory T cell responses as measured by effector cytokine production compared with TLR ligand-activated monocytes and B cells or unstimulated PDCs and MDCs. |
| 4 | 14530357 | PDCs, which express TLR7 and TLR9, responded to imidazoquinolines (imiquimod and R-848) and to CpG oligodeoxynucleotides stimulation, resulting in enhancement in expression of costimulatory molecules and induction of IFN-alpha and IL-12p70. |
| 5 | 14530357 | In contrast, MDCs, which express TLR3, TLR4, and TLR7, responded to poly(I:C), LPS, and imidazoquinolines with phenotypic maturation and high production of IL-12 p70 without producing detectable IFN-alpha. |
| 6 | 14530357 | Optimally TLR ligand-stimulated PDCs or MDCs exposed to CMV or HIV-1 Ags enhanced autologous CMV- and HIV-1-specific memory T cell responses as measured by effector cytokine production compared with TLR ligand-activated monocytes and B cells or unstimulated PDCs and MDCs. |
| 7 | 15007094 | Combined TLR and CD40 triggering induces potent CD8+ T cell expansion with variable dependence on type I IFN. |
| 8 | 15007094 | Whereas agonists for either pathway have been used as vaccine adjuvants, we show that a combination of Toll-like receptor (TLR)7 and CD40 agonists synergize to stimulate CD8+ T cell responses 10-20-fold greater than the use of either agonist alone. |
| 9 | 15007094 | Antigen-specific CD8+ T cells elicited from combination CD40/TLR7 treatment demonstrated both lytic activities and interferon (IFN)gamma production and an enhanced secondary response to antigenic challenge. |
| 10 | 15007094 | The CD8+ T cell expansion induced by CD40/TLR7 triggering was independent of CD4+ T cells, IFNgamma, and IL-12 but dependent on B7-mediated costimulation and surprisingly on type I IFN. |
| 11 | 15007094 | Combined TLR and CD40 triggering induces potent CD8+ T cell expansion with variable dependence on type I IFN. |
| 12 | 15007094 | Whereas agonists for either pathway have been used as vaccine adjuvants, we show that a combination of Toll-like receptor (TLR)7 and CD40 agonists synergize to stimulate CD8+ T cell responses 10-20-fold greater than the use of either agonist alone. |
| 13 | 15007094 | Antigen-specific CD8+ T cells elicited from combination CD40/TLR7 treatment demonstrated both lytic activities and interferon (IFN)gamma production and an enhanced secondary response to antigenic challenge. |
| 14 | 15007094 | The CD8+ T cell expansion induced by CD40/TLR7 triggering was independent of CD4+ T cells, IFNgamma, and IL-12 but dependent on B7-mediated costimulation and surprisingly on type I IFN. |
| 15 | 15550117 | Zymosan, poly(I:C) and CpG DNA, which signal through TLR2/6, 3 and 9, respectively, were found to strongly induce the production of IgG2a antibodies, whereas R-848 (TLR7) and LPS (TLR4) did so much more weakly. |
| 16 | 15550117 | In contrast, LPS, poly(I:C) and CpG DNA, but not zymosan, induced functional CD8+ T-cell responses against OVA; peptidoglycan (TLR2/?) |
| 17 | 15550117 | In addition, our results demonstrate that the ability of TLR stimuli to initiate CD8+ T-cell responses against soluble protein antigens is largely dependent on the IFN-alpha/beta signalling pathway. |
| 18 | 15832293 | They strongly activate DC and monocytes, leading to TNF-alpha and IFN-alpha secretion. |
| 19 | 15832293 | The detailed analysis of the activated cell types, the study of the cytokines released from PBMC cultured with protamine-RNA complexes and recently published results suggest that TLR-7 and TLR-8 may be involved in the recognition of protamine-stabilized RNA. |
| 20 | 16081189 | These include imidazoquinoline compounds such as Imiquimod and Resiquimod (R-848) that bind to TLR7 and 8, as well as CpG oligodeoxynucleotides (CpG ODN) that bind to TLR9. |
| 21 | 16219698 | HIV Gag protein conjugated to a Toll-like receptor 7/8 agonist improves the magnitude and quality of Th1 and CD8+ T cell responses in nonhuman primates. |
| 22 | 16219698 | NHPs immunized with HIV Gag protein and a TLR7/8 agonist or a TLR9 ligand [CpG oligodeoxynucleotides (CpG ODN)] had significantly increased Gag-specific T helper 1 and antibody responses, compared with animals immunized with HIV Gag protein alone. |
| 23 | 16219698 | HIV Gag protein conjugated to a Toll-like receptor 7/8 agonist improves the magnitude and quality of Th1 and CD8+ T cell responses in nonhuman primates. |
| 24 | 16219698 | NHPs immunized with HIV Gag protein and a TLR7/8 agonist or a TLR9 ligand [CpG oligodeoxynucleotides (CpG ODN)] had significantly increased Gag-specific T helper 1 and antibody responses, compared with animals immunized with HIV Gag protein alone. |
| 25 | 16461338 | Specifically, YF-17D activates multiple DC subsets via TLRs 2, 7, 8, and 9 to elicit the proinflammatory cytokines interleukin (IL)-12p40, IL-6, and interferon-alpha. |
| 26 | 16461338 | Furthermore, distinct TLRs appear to differentially control the Th1/Th2 balance; thus, whilst MyD88-deficient mice show a profound impairment of Th1 cytokines, TLR2-deficient mice show greatly enhanced Th1 and Tc1 responses to YF-17D. |
| 27 | 16636134 | NHP were immunized with HIV Gag protein emulsified in Montanide ISA 51, an oil-based adjuvant, with or without a TLR7/8 agonist, a TLR8 agonist, or the TLR9 ligand cytosine phosphate guanosine oligodeoxynucleotides (CpG ODN), and boosted 12 wk later with a replication-defective adenovirus-expressing HIV-Gag (rAD-Gag). |
| 28 | 16829609 | The 3' CCACCA sequence of tRNAAla(UGC) is the motif that is important in inducing Th1-like immune response, and this motif can be recognized by Toll-like receptor 3. |
| 29 | 16829609 | Moreover, the recognitions of different tRNA(Ala)(UGC) fragments by TLR3, TLR7, TLR8, and TLR9 were analyzed. |
| 30 | 16920494 | The role of TLRs during infection with Mycobacterium bovis Bacillus Calmette-Guérin (BCG) has been evaluated for TLR2 and TLR4 only. |
| 31 | 16920494 | To identify the set of TLRs involved in the recognition of BCG, we infected bone marrow-derived macrophages and bone marrow-derived dendritic cells (Flt3-ligand generated DCs) from TLR2, TLR3, TLR4, TLR7, TLR9, MyD88 knockout, TLR2/4 and TLR2/4/9 multiple knockout mice. |
| 32 | 16920494 | The degree of activation and stimulation was determined by TNFalpha, IL-6 and IL-12p40 ELISA. |
| 33 | 16920494 | Both macrophages and DCs produce markedly decreased amounts of TNFalpha and IL-6 in the absence of TLR2 whereas no significant reduction could be observed for TLR3, 4, 7, 9 single TLR-knockouts. |
| 34 | 16920494 | Similarly, up-regulation of CD86 is abolished only in TLR2/4/9-deficient DCs supporting a role of TLR9 in the recognition of M. bovis BCG by murine dendritic cells. |
| 35 | 16960116 | Treatment of human monocytes with S. gordonii but not latex beads induced a clear up-regulation of CD83, CD40, CD80, and CD54 and the down-regulation of CD14. |
| 36 | 16960116 | Furthermore, bacterial treatment stimulated an increased expression of Toll-like receptor 5 (TLR5), TLR6, and TLR7, production of the proinflammatory cytokines tumor necrosis factor alpha and interleukin 1 beta, and reduction of the phagocytic activity. |
| 37 | 16983724 | No iL-DC express TLR7 mRNA, and only CD172a+ iL-DC express TLR8. |
| 38 | 17066089 | Chronic lymphocytic leukemia (CLL) may be especially amenable to TLR agonists because it is an immunologically susceptible tumor with strong expression of several TLRs, particularly TLR-7 and TLR-9. |
| 39 | 17066089 | However, signaling pathways can be activated directly in CLL cells by TLR-7 and TLR-9 agonists, leading to the production of cytokines and costimulatory molecules in a manner that is dependent on the underlying cytogenetic abnormalities, but rendering the tumor cells more sensitive to killing by cytotoxic T cells, immunotoxins and some chemotherapeutic drugs. |
| 40 | 17066089 | Imidazoquinolines are TLR-7 agonists with strong local activity against CLL, and phase I trials of systemically administered imidazoquinolines (and also cytosine-phosphate-guanosine oligonucleotides that are TLR-9 agonists) are currently ongoing at different centers. |
| 41 | 17066089 | Chronic lymphocytic leukemia (CLL) may be especially amenable to TLR agonists because it is an immunologically susceptible tumor with strong expression of several TLRs, particularly TLR-7 and TLR-9. |
| 42 | 17066089 | However, signaling pathways can be activated directly in CLL cells by TLR-7 and TLR-9 agonists, leading to the production of cytokines and costimulatory molecules in a manner that is dependent on the underlying cytogenetic abnormalities, but rendering the tumor cells more sensitive to killing by cytotoxic T cells, immunotoxins and some chemotherapeutic drugs. |
| 43 | 17066089 | Imidazoquinolines are TLR-7 agonists with strong local activity against CLL, and phase I trials of systemically administered imidazoquinolines (and also cytosine-phosphate-guanosine oligonucleotides that are TLR-9 agonists) are currently ongoing at different centers. |
| 44 | 17066089 | Chronic lymphocytic leukemia (CLL) may be especially amenable to TLR agonists because it is an immunologically susceptible tumor with strong expression of several TLRs, particularly TLR-7 and TLR-9. |
| 45 | 17066089 | However, signaling pathways can be activated directly in CLL cells by TLR-7 and TLR-9 agonists, leading to the production of cytokines and costimulatory molecules in a manner that is dependent on the underlying cytogenetic abnormalities, but rendering the tumor cells more sensitive to killing by cytotoxic T cells, immunotoxins and some chemotherapeutic drugs. |
| 46 | 17066089 | Imidazoquinolines are TLR-7 agonists with strong local activity against CLL, and phase I trials of systemically administered imidazoquinolines (and also cytosine-phosphate-guanosine oligonucleotides that are TLR-9 agonists) are currently ongoing at different centers. |
| 47 | 17476348 | Synthetic agonists for several TLRs, including TLR3, TLR4, TLR7, TLR8, and TLR9, have been or are being developed for the treatment of cancer. |
| 48 | 17908810 | The results demonstrate that TLR3, TLR4, TLR7, and TLR9 agonists enhance immune responses against LPS-deficient outer membrane complexes. |
| 49 | 17954572 | Adjuvanting a DNA vaccine with a TLR9 ligand plus Flt3 ligand results in enhanced cellular immunity against the simian immunodeficiency virus. |
| 50 | 17954572 | Rhesus macaques were injected with Fms-like tyrosine kinase 3 (Flt3)-ligand (FL) to expand dendritic cells (DCs) and were primed with a DNA vaccine encoding immunodeficiency virus antigens mixed with ligands for TLR9 or TLR7/8. |
| 51 | 17954572 | TLR9-L (CpG DNA) mediated activation of DCs in vivo and enhanced the magnitude of antigen-specific CD8(+) interferon (IFN) gamma(+) T cells and polyfunctional CD8(+) T cells producing IFN-gamma, tumor necrosis factor alpha, and interleukin 2. |
| 52 | 18228247 | TLR7 and CD40 cooperate in IL-6 production via enhanced JNK and AP-1 activation. |
| 53 | 18228247 | To address this goal, we examined the effects of TLR stimulation on BCR and CD40-induced B cell activation. |
| 54 | 18228247 | Synergistic production of IL-6 was observed in both human and mouse primary B cells stimulated through B cell antigen receptors, CD40 and TLR7, and these two receptors also cooperated independently of BCR signals. |
| 55 | 18228247 | The enhanced IL-6 production was dependent upon the activity of c-Jun kinase (JNK) and cFos. |
| 56 | 18228247 | Dual stimulation through CD40 and TLR7 markedly enhanced JNK activity. |
| 57 | 18228247 | The increased level of active JNK in dual-stimulated cells was accompanied by an increase in the level of active AP-1 monomers cJun and cFos. |
| 58 | 18228247 | The stimulation of B cells through both CD40 and TLR7 therefore enhanced the production of cytokines through increased JNK signaling and AP-1 activity. |
| 59 | 18228247 | In addition, the dual stimulation increased cFos/AP-1 species in stimulated cells, effectively expanding the repertoire of AP-1 dimers as compared to singly stimulated B cells. |
| 60 | 18228247 | TLR7 and CD40 cooperate in IL-6 production via enhanced JNK and AP-1 activation. |
| 61 | 18228247 | To address this goal, we examined the effects of TLR stimulation on BCR and CD40-induced B cell activation. |
| 62 | 18228247 | Synergistic production of IL-6 was observed in both human and mouse primary B cells stimulated through B cell antigen receptors, CD40 and TLR7, and these two receptors also cooperated independently of BCR signals. |
| 63 | 18228247 | The enhanced IL-6 production was dependent upon the activity of c-Jun kinase (JNK) and cFos. |
| 64 | 18228247 | Dual stimulation through CD40 and TLR7 markedly enhanced JNK activity. |
| 65 | 18228247 | The increased level of active JNK in dual-stimulated cells was accompanied by an increase in the level of active AP-1 monomers cJun and cFos. |
| 66 | 18228247 | The stimulation of B cells through both CD40 and TLR7 therefore enhanced the production of cytokines through increased JNK signaling and AP-1 activity. |
| 67 | 18228247 | In addition, the dual stimulation increased cFos/AP-1 species in stimulated cells, effectively expanding the repertoire of AP-1 dimers as compared to singly stimulated B cells. |
| 68 | 18228247 | TLR7 and CD40 cooperate in IL-6 production via enhanced JNK and AP-1 activation. |
| 69 | 18228247 | To address this goal, we examined the effects of TLR stimulation on BCR and CD40-induced B cell activation. |
| 70 | 18228247 | Synergistic production of IL-6 was observed in both human and mouse primary B cells stimulated through B cell antigen receptors, CD40 and TLR7, and these two receptors also cooperated independently of BCR signals. |
| 71 | 18228247 | The enhanced IL-6 production was dependent upon the activity of c-Jun kinase (JNK) and cFos. |
| 72 | 18228247 | Dual stimulation through CD40 and TLR7 markedly enhanced JNK activity. |
| 73 | 18228247 | The increased level of active JNK in dual-stimulated cells was accompanied by an increase in the level of active AP-1 monomers cJun and cFos. |
| 74 | 18228247 | The stimulation of B cells through both CD40 and TLR7 therefore enhanced the production of cytokines through increased JNK signaling and AP-1 activity. |
| 75 | 18228247 | In addition, the dual stimulation increased cFos/AP-1 species in stimulated cells, effectively expanding the repertoire of AP-1 dimers as compared to singly stimulated B cells. |
| 76 | 18228247 | TLR7 and CD40 cooperate in IL-6 production via enhanced JNK and AP-1 activation. |
| 77 | 18228247 | To address this goal, we examined the effects of TLR stimulation on BCR and CD40-induced B cell activation. |
| 78 | 18228247 | Synergistic production of IL-6 was observed in both human and mouse primary B cells stimulated through B cell antigen receptors, CD40 and TLR7, and these two receptors also cooperated independently of BCR signals. |
| 79 | 18228247 | The enhanced IL-6 production was dependent upon the activity of c-Jun kinase (JNK) and cFos. |
| 80 | 18228247 | Dual stimulation through CD40 and TLR7 markedly enhanced JNK activity. |
| 81 | 18228247 | The increased level of active JNK in dual-stimulated cells was accompanied by an increase in the level of active AP-1 monomers cJun and cFos. |
| 82 | 18228247 | The stimulation of B cells through both CD40 and TLR7 therefore enhanced the production of cytokines through increased JNK signaling and AP-1 activity. |
| 83 | 18228247 | In addition, the dual stimulation increased cFos/AP-1 species in stimulated cells, effectively expanding the repertoire of AP-1 dimers as compared to singly stimulated B cells. |
| 84 | 18439678 | Porcine TLR8 and TLR7 are both activated by a selective TLR7 ligand, imiquimod. |
| 85 | 18439678 | We cloned and characterized porcine TLR7 and TLR8 genes from pig lymph node tissue. |
| 86 | 18439678 | Sequence analysis showed that the aa sequence identities of porcine TLR7 with human, mouse and bovine TLR7 are 85, 78 and 90%, respectively, whereas porcine TLR8 aa sequence identities with human, mouse and bovine TLR8 are 73, 69 and 79%, respectively. |
| 87 | 18439678 | Both porcine TLR7 and TLR8 proteins were expressed in cell lines and were N-glycosylated. |
| 88 | 18439678 | The stimulatory activity of TLR7 and TLR8 ligands to porcine and human TLR7 and TLR8 in transiently transfected Cos-7 and 293T cells were analyzed using a NF-kappaB reporter assay. |
| 89 | 18439678 | Two imidazoquinoline molecules, imiquimod and gardiquimod, markedly activated both porcine TLR7 and TLR8 whereas only human TLR7, but not TLR8, was activated by the ligands. |
| 90 | 18439678 | We further showed that porcine TLR7 and TLR8 are located intracellularly and are mainly within the endoplasmic reticulum. |
| 91 | 18439678 | Porcine TLR8 and TLR7 are both activated by a selective TLR7 ligand, imiquimod. |
| 92 | 18439678 | We cloned and characterized porcine TLR7 and TLR8 genes from pig lymph node tissue. |
| 93 | 18439678 | Sequence analysis showed that the aa sequence identities of porcine TLR7 with human, mouse and bovine TLR7 are 85, 78 and 90%, respectively, whereas porcine TLR8 aa sequence identities with human, mouse and bovine TLR8 are 73, 69 and 79%, respectively. |
| 94 | 18439678 | Both porcine TLR7 and TLR8 proteins were expressed in cell lines and were N-glycosylated. |
| 95 | 18439678 | The stimulatory activity of TLR7 and TLR8 ligands to porcine and human TLR7 and TLR8 in transiently transfected Cos-7 and 293T cells were analyzed using a NF-kappaB reporter assay. |
| 96 | 18439678 | Two imidazoquinoline molecules, imiquimod and gardiquimod, markedly activated both porcine TLR7 and TLR8 whereas only human TLR7, but not TLR8, was activated by the ligands. |
| 97 | 18439678 | We further showed that porcine TLR7 and TLR8 are located intracellularly and are mainly within the endoplasmic reticulum. |
| 98 | 18439678 | Porcine TLR8 and TLR7 are both activated by a selective TLR7 ligand, imiquimod. |
| 99 | 18439678 | We cloned and characterized porcine TLR7 and TLR8 genes from pig lymph node tissue. |
| 100 | 18439678 | Sequence analysis showed that the aa sequence identities of porcine TLR7 with human, mouse and bovine TLR7 are 85, 78 and 90%, respectively, whereas porcine TLR8 aa sequence identities with human, mouse and bovine TLR8 are 73, 69 and 79%, respectively. |
| 101 | 18439678 | Both porcine TLR7 and TLR8 proteins were expressed in cell lines and were N-glycosylated. |
| 102 | 18439678 | The stimulatory activity of TLR7 and TLR8 ligands to porcine and human TLR7 and TLR8 in transiently transfected Cos-7 and 293T cells were analyzed using a NF-kappaB reporter assay. |
| 103 | 18439678 | Two imidazoquinoline molecules, imiquimod and gardiquimod, markedly activated both porcine TLR7 and TLR8 whereas only human TLR7, but not TLR8, was activated by the ligands. |
| 104 | 18439678 | We further showed that porcine TLR7 and TLR8 are located intracellularly and are mainly within the endoplasmic reticulum. |
| 105 | 18439678 | Porcine TLR8 and TLR7 are both activated by a selective TLR7 ligand, imiquimod. |
| 106 | 18439678 | We cloned and characterized porcine TLR7 and TLR8 genes from pig lymph node tissue. |
| 107 | 18439678 | Sequence analysis showed that the aa sequence identities of porcine TLR7 with human, mouse and bovine TLR7 are 85, 78 and 90%, respectively, whereas porcine TLR8 aa sequence identities with human, mouse and bovine TLR8 are 73, 69 and 79%, respectively. |
| 108 | 18439678 | Both porcine TLR7 and TLR8 proteins were expressed in cell lines and were N-glycosylated. |
| 109 | 18439678 | The stimulatory activity of TLR7 and TLR8 ligands to porcine and human TLR7 and TLR8 in transiently transfected Cos-7 and 293T cells were analyzed using a NF-kappaB reporter assay. |
| 110 | 18439678 | Two imidazoquinoline molecules, imiquimod and gardiquimod, markedly activated both porcine TLR7 and TLR8 whereas only human TLR7, but not TLR8, was activated by the ligands. |
| 111 | 18439678 | We further showed that porcine TLR7 and TLR8 are located intracellularly and are mainly within the endoplasmic reticulum. |
| 112 | 18439678 | Porcine TLR8 and TLR7 are both activated by a selective TLR7 ligand, imiquimod. |
| 113 | 18439678 | We cloned and characterized porcine TLR7 and TLR8 genes from pig lymph node tissue. |
| 114 | 18439678 | Sequence analysis showed that the aa sequence identities of porcine TLR7 with human, mouse and bovine TLR7 are 85, 78 and 90%, respectively, whereas porcine TLR8 aa sequence identities with human, mouse and bovine TLR8 are 73, 69 and 79%, respectively. |
| 115 | 18439678 | Both porcine TLR7 and TLR8 proteins were expressed in cell lines and were N-glycosylated. |
| 116 | 18439678 | The stimulatory activity of TLR7 and TLR8 ligands to porcine and human TLR7 and TLR8 in transiently transfected Cos-7 and 293T cells were analyzed using a NF-kappaB reporter assay. |
| 117 | 18439678 | Two imidazoquinoline molecules, imiquimod and gardiquimod, markedly activated both porcine TLR7 and TLR8 whereas only human TLR7, but not TLR8, was activated by the ligands. |
| 118 | 18439678 | We further showed that porcine TLR7 and TLR8 are located intracellularly and are mainly within the endoplasmic reticulum. |
| 119 | 18439678 | Porcine TLR8 and TLR7 are both activated by a selective TLR7 ligand, imiquimod. |
| 120 | 18439678 | We cloned and characterized porcine TLR7 and TLR8 genes from pig lymph node tissue. |
| 121 | 18439678 | Sequence analysis showed that the aa sequence identities of porcine TLR7 with human, mouse and bovine TLR7 are 85, 78 and 90%, respectively, whereas porcine TLR8 aa sequence identities with human, mouse and bovine TLR8 are 73, 69 and 79%, respectively. |
| 122 | 18439678 | Both porcine TLR7 and TLR8 proteins were expressed in cell lines and were N-glycosylated. |
| 123 | 18439678 | The stimulatory activity of TLR7 and TLR8 ligands to porcine and human TLR7 and TLR8 in transiently transfected Cos-7 and 293T cells were analyzed using a NF-kappaB reporter assay. |
| 124 | 18439678 | Two imidazoquinoline molecules, imiquimod and gardiquimod, markedly activated both porcine TLR7 and TLR8 whereas only human TLR7, but not TLR8, was activated by the ligands. |
| 125 | 18439678 | We further showed that porcine TLR7 and TLR8 are located intracellularly and are mainly within the endoplasmic reticulum. |
| 126 | 18439678 | Porcine TLR8 and TLR7 are both activated by a selective TLR7 ligand, imiquimod. |
| 127 | 18439678 | We cloned and characterized porcine TLR7 and TLR8 genes from pig lymph node tissue. |
| 128 | 18439678 | Sequence analysis showed that the aa sequence identities of porcine TLR7 with human, mouse and bovine TLR7 are 85, 78 and 90%, respectively, whereas porcine TLR8 aa sequence identities with human, mouse and bovine TLR8 are 73, 69 and 79%, respectively. |
| 129 | 18439678 | Both porcine TLR7 and TLR8 proteins were expressed in cell lines and were N-glycosylated. |
| 130 | 18439678 | The stimulatory activity of TLR7 and TLR8 ligands to porcine and human TLR7 and TLR8 in transiently transfected Cos-7 and 293T cells were analyzed using a NF-kappaB reporter assay. |
| 131 | 18439678 | Two imidazoquinoline molecules, imiquimod and gardiquimod, markedly activated both porcine TLR7 and TLR8 whereas only human TLR7, but not TLR8, was activated by the ligands. |
| 132 | 18439678 | We further showed that porcine TLR7 and TLR8 are located intracellularly and are mainly within the endoplasmic reticulum. |
| 133 | 18474642 | In the present study, we determined whether imiquimod and its related compound R848, which are TLR7 and/or TLR8 agonists, represent potential vaccine adjuvants when delivered topically, subcutaneously, or intramuscularly. |
| 134 | 18490712 | Here we show that treatment of murine fetal thymic organ cultures (FTOCs) with TLR3 or TLR7 ligands induced rapid expression of IFN-alpha and -beta mRNA, hallmarks of acute and chronic viral infections. |
| 135 | 18490712 | Down-regulation of IL-7R alpha-chain expression, together with an increased expression of suppressor of cytokine signaling-1 and a concomitant decreased expression of the transcriptional regulator growth factor independence 1 were observed in TLR ligands or IFN-treated FTOCs. |
| 136 | 18490712 | Because TLR ligands are widely used as vaccine adjuvants, their immunomodulatory actions mediated mainly by IFN-alpha suggested by our results should be taken in consideration. |
| 137 | 18566444 | Immunization of malignant melanoma patients with full-length NY-ESO-1 protein using TLR7 agonist imiquimod as vaccine adjuvant. |
| 138 | 18566444 | In this study, we evaluated the safety and feasibility of topical imiquimod, a TLR7 agonist, in a series of vaccinations against the cancer/testis Ag NY-ESO-1 in patients with malignant melanoma. |
| 139 | 18566444 | Immunization of malignant melanoma patients with full-length NY-ESO-1 protein using TLR7 agonist imiquimod as vaccine adjuvant. |
| 140 | 18566444 | In this study, we evaluated the safety and feasibility of topical imiquimod, a TLR7 agonist, in a series of vaccinations against the cancer/testis Ag NY-ESO-1 in patients with malignant melanoma. |
| 141 | 18698004 | However, in vitro and in vivo stimulation by Toll-like receptor-7, or -9 or viruses licenses pDCs to cross-present soluble or particulate Ags by a transporter associated with antigen processing-dependent mechanism. |
| 142 | 18789542 | CD14+ cells are required for IL-12 response in bovine blood mononuclear cells activated with Toll-like receptor (TLR) 7 and TLR8 ligands. |
| 143 | 18789542 | Single-stranded viral RNA (ssRNA) was recently identified as the natural ligand for TLR7 and TLR8. ssRNA sequences from viruses, as well as their synthetic analogues stimulate innate immune responses in immune cells from humans and mice, but their immunostimulatory activity has not been investigated in ruminants. |
| 144 | 18789542 | In vitro incubation of bovine peripheral blood mononuclear cells (PBMCs) with ORN-induced production of IL-12, IFN-gamma and TNF-alpha. |
| 145 | 18789542 | Depletion of CD14+ cells from PBMC abrogated the IL-12 response and consequently the IFN-gamma response, suggesting that CD14+ cells are required for PBMC immune activation with ORN. |
| 146 | 18789542 | Consistent with these findings, the putative receptors for ORN (TLR7 and TLR8) were expressed at higher levels in the CD14+ fraction than the CD14- PBMC fraction. |
| 147 | 18789542 | CD14+ cells are required for IL-12 response in bovine blood mononuclear cells activated with Toll-like receptor (TLR) 7 and TLR8 ligands. |
| 148 | 18789542 | Single-stranded viral RNA (ssRNA) was recently identified as the natural ligand for TLR7 and TLR8. ssRNA sequences from viruses, as well as their synthetic analogues stimulate innate immune responses in immune cells from humans and mice, but their immunostimulatory activity has not been investigated in ruminants. |
| 149 | 18789542 | In vitro incubation of bovine peripheral blood mononuclear cells (PBMCs) with ORN-induced production of IL-12, IFN-gamma and TNF-alpha. |
| 150 | 18789542 | Depletion of CD14+ cells from PBMC abrogated the IL-12 response and consequently the IFN-gamma response, suggesting that CD14+ cells are required for PBMC immune activation with ORN. |
| 151 | 18789542 | Consistent with these findings, the putative receptors for ORN (TLR7 and TLR8) were expressed at higher levels in the CD14+ fraction than the CD14- PBMC fraction. |
| 152 | 18989354 | To further enhance the efficacy of DNA-EP, we have evaluated the toll-like receptor7 (TLR7) agonist-2, 9, substituted 8-hydroxyadenosine derivative or SM360320--as an adjuvant to vaccines against HER2/neu and CEA in BALB-neuT and CEA transgenic mice (CEA.Tg), respectively. |
| 153 | 18989354 | SM360320 induced in vivo secretion of interferon alpha (IFNalpha) and exerted a significant antitumor effect in CEA.Tg mice challenged with a syngenic tumor cell line expressing CEA and an additive effect with a CEA vaccine. |
| 154 | 18989354 | These data demonstrate that SM360320 exerts significant antitumor effects and can act in association with DNA-EP for CEA-positive colon cancer and HER2-positive mammary carcinoma. |
| 155 | 18995910 | Here we cloned and characterized bovine TLR8 (bTLR8) and found that it is highly responsive to two TLR7 ligands, imiquimod and gardiquimod, in transfected cell lines. |
| 156 | 19096763 | The established role of TLRs in human disease therapy is based on TLR7 and TLR4 agonists, respectively for the novel treatment of some types of skin cancer and for the anti-hepatitis B virus vaccine. |
| 157 | 19330719 | Intracellular TLRs, represented by TLRs 3, 7, 8 and 9, are specialized for the recognition of different types of microbe-derived nucleic acids. |
| 158 | 19428918 | Agonists for TLR7, TLR8, and TLR9 have been shown to enhance vaccine immunogenicity. |
| 159 | 19449004 | We observed expression of TLR7 and TLR8 in primary human AML cells and AML cell lines. |
| 160 | 19525489 | Innate immune stimulants may have applications as vaccine adjuvants as well as in the treatment of cancer and some viral diseases, and clinical studies have been performed using agonists of Toll-like receptors (TLRs) 7, 8, and 9. |
| 161 | 19577301 | However, there were no major changes in the expression levels of transcripts for cell surface proteins (MHC I, MHC II 2 beta-chain, TCR-beta, TLR-7, DCAR, CD44, and CD58) and cytokines (IL-2, IFN-gamma, RANTES, MIP-1beta-like and MCP-1 like chemokines). |
| 162 | 19578865 | We investigated the effect of different toll like receptor (TLR) agonists including LPS (TLR4 agonist), polyinosinic acid-polycytidylic acid (PIC, TLR3 agonist), CpG oligonucleotide (TLR9 agonist), and imiquimod (TLR7 agonist) on human monocyte-derived dendritic cells (mdDCs) loading of human papillomavirus (HPV) type 11 E7 epitope. |
| 163 | 19578865 | This was characterized by an enhanced expression of CD40, CD80, CD86, CD83 and HLA-DR, and a high level of IL-12 production. |
| 164 | 19776194 | Upregulation of a tumor necrosis factor alpha-inducing factor homolog in challenged chickens compared to naïve chickens was observed, regardless of the incidence of necrotic enteritis. |
| 165 | 19776194 | In addition, the members of the TLR2 subfamily were found to be most strongly involved in the host response to C. perfringens challenge, although the expression of TLR4 and TLR7 was also upregulated in spleen tissues. |
| 166 | 19776194 | While the combination of TLR1.2, TLR2.1, and TLR15 appeared to play a major role in the splenic response, the expression of TLR2.2 and TLR1.1 was positively correlated to the expression of adaptor molecules MyD88, TRAF6, TRIF, and receptor interacting protein 1 in the ileal tissues, demonstrating a dynamic spatial and temporal innate host response to C. perfringens. |
| 167 | 19786561 | Our data demonstrate that combining ML0276 with either a Toll-like receptor 4 (TLR4) (EM005), TLR7 (imiquimod), or TLR9 (CpG DNA) agonist during immunization induces Th1 responses that limit local inflammation upon experimental M. leprae infection. |
| 168 | 19801508 | CD40- or TLR7-stimulated B cell APCs induced similar CD8(+) T cell responses, but costimulation through the BCR and TLR7 produced a more effective Bvac as measured by T cell stimulation and the protection of mice from an infectious pathogen. |
| 169 | 20042593 | Cell type-specific recognition of human metapneumoviruses (HMPVs) by retinoic acid-inducible gene I (RIG-I) and TLR7 and viral interference of RIG-I ligand recognition by HMPV-B1 phosphoprotein. |
| 170 | 20042593 | In this study, we investigated the abilities of two prototype strains of HMPV (A1 [NL1 0] and B1 [NL199]) to activate RIG-I and induce type I IFNs. |
| 171 | 20042593 | Despite the abilities of both HMPV-A1 and HMPV-B1 to infect and replicate in cell lines and primary cells, only the HMPV-A1 strain triggered RIG-I to induce IFNA/B gene transcription. |
| 172 | 20042593 | The failure of the HMPV-B1 strain to elicit type I IFN production was dependent on the B1 phosphoprotein, which specifically prevented RIG-I-mediated sensing of HMPV viral 5' triphosphate RNA. |
| 173 | 20051250 | Co-stimulation with TLR7/8 and TLR9 agonists induce down-regulation of innate immune responses in sheep blood mononuclear and B cells. |
| 174 | 20051250 | Sheep PBMC stimulated with either CpG (TLR9 agonist) or RNA oligoribonucleotides ([ORNs], TLR7/8 agonist) exhibited significant IL-12 production, but only CpG induced IFNalpha, IgM and proliferative responses. |
| 175 | 20051250 | In contrast, poly(I:C) (TLR3 agonist) and LPS (TLR4 agonist) did not induce any of these responses. |
| 176 | 20051250 | Sheep B cells constitutively expressed TLR7, TLR8 and TLR9 mRNA transcripts, suggesting a possible role of TLR cross-talk in the down-regulatory mechanisms. |
| 177 | 20051250 | Co-stimulation with TLR7/8 and TLR9 agonists induce down-regulation of innate immune responses in sheep blood mononuclear and B cells. |
| 178 | 20051250 | Sheep PBMC stimulated with either CpG (TLR9 agonist) or RNA oligoribonucleotides ([ORNs], TLR7/8 agonist) exhibited significant IL-12 production, but only CpG induced IFNalpha, IgM and proliferative responses. |
| 179 | 20051250 | In contrast, poly(I:C) (TLR3 agonist) and LPS (TLR4 agonist) did not induce any of these responses. |
| 180 | 20051250 | Sheep B cells constitutively expressed TLR7, TLR8 and TLR9 mRNA transcripts, suggesting a possible role of TLR cross-talk in the down-regulatory mechanisms. |
| 181 | 20051250 | Co-stimulation with TLR7/8 and TLR9 agonists induce down-regulation of innate immune responses in sheep blood mononuclear and B cells. |
| 182 | 20051250 | Sheep PBMC stimulated with either CpG (TLR9 agonist) or RNA oligoribonucleotides ([ORNs], TLR7/8 agonist) exhibited significant IL-12 production, but only CpG induced IFNalpha, IgM and proliferative responses. |
| 183 | 20051250 | In contrast, poly(I:C) (TLR3 agonist) and LPS (TLR4 agonist) did not induce any of these responses. |
| 184 | 20051250 | Sheep B cells constitutively expressed TLR7, TLR8 and TLR9 mRNA transcripts, suggesting a possible role of TLR cross-talk in the down-regulatory mechanisms. |
| 185 | 20071494 | In cultured cells infected with TROVAC-AIV H5, there was an early increase in the expression of type I interferons (IFN), Toll-like receptors 3 and 7 (TLR3 and TLR7, respectively), TRIF, and MyD88, which was followed by a decrease in the expression of these genes at later time points. |
| 186 | 20071494 | There also was an increase in the expression of interleukin-1beta (IL-1beta), IL-8, and beta-defensin genes at early time points postinfection. |
| 187 | 20071494 | In chickens immunized with TROVAC-AIV H5, there was higher expression of IFN-gamma and IL-10 at day 5 postvaccination in spleen of vaccinated birds than in that of control birds. |
| 188 | 20100933 | We used multicolor flow cytometry and intracellular cytokine staining of myeloid DCs (mDCs) and plasmacytoid DCs (pDCs) and found substantial decreases in older compared with young individuals in TNF-alpha, IL-6, and/or IL-12 (p40) production in mDCs and in TNF-alpha and IFN-alpha production in pDCs in response to TLR1/2, TLR2/6, TLR3, TLR5, and TLR8 engagement in mDCs and TLR7 and TLR9 in pDCs. |
| 189 | 20121698 | The following firm conclusions can be drawn: multiple TLRs activate innate immunity upon RSV infection; TLR4 can influence TLR2 expression, suggesting that optimal induction of multiple signaling pathways is required to elicit protective, rather than deleterious innate immune responses following infection; in mice, TLR4, TLR2/-6, and TLR7 have immune-stimulating properties, while TLR3 activation occurs later and appears to downregulate immune responses; in humans, polymorphism studies have demonstrated an important role for TLR4-signaling; and activation of TLR-signaling leads to antiviral cytokine production, such as TNF-a and IFNs. |
| 190 | 20424013 | Although Toll-like receptor 7 acted as the adjuvant receptor for the immunogenicity of both live virus and WV vaccines, the requirement for type I IFN production by pDCs for the immunogenicity of the vaccines was restricted to WV. |
| 191 | 20451253 | Production of monocyte chemoattractant protein-1 (MCP-1/CCL2), macrophage inflammatory protein-1 (MIP-1/CCL3) and regulated on activation, normal T cell expressed and secreted (RANTES/CCL5), were determined in cell culture supernatants by ELISA or cytokine cytometric bead array. |
| 192 | 20451253 | Pharmacological inhibitors of p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), nuclear factor-kappaB (NF-kB) and phosphatidylinositol 3-kinase (PI3K), were used to investigate the role of signaling pathways. |
| 193 | 20451253 | TLR agonists induced significantly elevated MCP-1, RANTES, and MIP-1. |
| 194 | 20451253 | Production of RANTES and MIP-1 was particularly prominent after stimulation of DCs with TLR3 (Poly(I:C)), and TLR7/8 (R848) or TLR9 (CpG ODN) agonists, respectively. |
| 195 | 20451253 | A positive role was identified for NF-kB, PI3K and ERK, whereas JNK had a negative regulatory effect on chemokine production in DCs. |
| 196 | 20451253 | Positive and negative regulatory roles for the p38 MAPK pathway were observed. |
| 197 | 20463102 | Peripheral blood mononuclear cells (PBMCs) and cord blood pDCs were stimulated with resiquimod, and alpha interferon (IFN-alpha) production and the pDC phenotype were assessed. |
| 198 | 20463102 | RV infection did not induce pDC maturation until the age of 6 months, and it reduced TLR7-dependent resiquimod-induced IFN-alpha production similarly in both groups. |
| 199 | 20463102 | RV is a weak inducer of IFN-alpha production until the age of 6 months and inhibits IFN-alpha responses triggered by the TLR7 pathway. |
| 200 | 20463102 | Peripheral blood mononuclear cells (PBMCs) and cord blood pDCs were stimulated with resiquimod, and alpha interferon (IFN-alpha) production and the pDC phenotype were assessed. |
| 201 | 20463102 | RV infection did not induce pDC maturation until the age of 6 months, and it reduced TLR7-dependent resiquimod-induced IFN-alpha production similarly in both groups. |
| 202 | 20463102 | RV is a weak inducer of IFN-alpha production until the age of 6 months and inhibits IFN-alpha responses triggered by the TLR7 pathway. |
| 203 | 20625151 | Phosphorothioate 2' deoxyribose oligomers as microbicides that inhibit human immunodeficiency virus type 1 (HIV-1) infection and block Toll-like receptor 7 (TLR7) and TLR9 triggering by HIV-1. |
| 204 | 20709105 | Expression of selected gene groups was tested via qPCR at 7 different time-points: cytokines (IL-2, IFN-γ, IL-4, IL-6, and IL-10), type I interferons (IFN-α4, IFN-α11, IFN-α12, and IFN-β), toll-like receptors (TLR2, TLR3, TLR7, and TLR9), iNOS and CCR7. |
| 205 | 20709105 | Intranasally administered DBF and the mixture of virus+DBF induced an elevated expression of IFN-γ, IL-6 and IL-10 cytokines, type I interferons, iNOS, and pDC markers in NALT. |
| 206 | 20875795 | Immunological basis of M13 phage vaccine: Regulation under MyD88 and TLR9 signaling. |
| 207 | 20875795 | These responses were almost comparable, but slightly weaker, in TLR2-, TLR4- and TLR7-deficient mice relative to wild-type mice, suggesting that this enhancing effect is not due to plausible LPS contamination. |
| 208 | 20937315 | The adjuvant effects of the TLR7 agonist, imiquimod, and the TLR9 agonist, ODN1826, were tested with rAAV expressing the melanoma antigen, Trp2. |
| 209 | 20937315 | TLR7 and TLR9 agonists can be used to enhance the immune response to rAAV immunogens, but antagonism can be observed when combined. |
| 210 | 20937315 | The adjuvant effects of the TLR7 agonist, imiquimod, and the TLR9 agonist, ODN1826, were tested with rAAV expressing the melanoma antigen, Trp2. |
| 211 | 20937315 | TLR7 and TLR9 agonists can be used to enhance the immune response to rAAV immunogens, but antagonism can be observed when combined. |
| 212 | 20943980 | In order to elucidate the exact role of Toll-like receptor (TLR) or RIG-I-like receptor (RLR) signaling on immunogenicity and protective efficacy against influenza A virus infection (A/PR/8/34 [PR8]; H1N1), we adapted several innate signal-deficient mice (e.g., TRIF(-/-), MyD88(-/-), MyD88(-/-) TRIF(-/-), TLR3(-/-) TLR7(-/-), and IPS-1(-/-)). |
| 213 | 20943980 | In this study, we found that MyD88 signaling was required for recruitment of CD11b(+) granulocytes, production of early inflammatory cytokines, optimal proliferation of CD4 T cells, and production of Th1 cytokines by T cells. |
| 214 | 20943980 | We found that MyD88(-/-) and MyD88(-/-) TRIF(-/-) mice were more susceptible to primary influenza virus infection than the B6 mice but were fully protected against homologous (H1N1) and heterosubtypic (H5N2) secondary infection when primed with a nonlethal dose of PR8 virus. |
| 215 | 21173782 | Using Toll-like receptor (TLR) and MyD88 gene knock-out (GKO) mice the effect of TLRs and MyD88 on virus replication, interferon (IFN)-β production, natural killer (NK) cell and CD8T cell responses were assessed following ectromelia virus (ECTV) and recombinant vaccinia virus (rVV) infection. |
| 216 | 21173782 | Results showed that TLR2(-/-), TLR4(-/-)and TLR7(-/-) mice survived ECTV infection whereas MyD88(-/-) and TLR9(-/-)mice, in contrast, were highly susceptible. |
| 217 | 21173782 | Next, following infection with rVV, MyD88(-/-) mice elicited reduced serum IFN-β, NK cell and CD8T cell responses compared with wild-type mice, whereas TLR9(-/-) mice showed elevated CD8T cell responses. |
| 218 | 21173782 | Interestingly, even though rVV co-expressing interleukin (IL)-2 enhanced NK cell activation in MyD88(-/-) mice, this was not associated with an antiviral effect, as observed in normal mice. |
| 219 | 21173782 | Surprisingly, co-infection with rVV IL-2/rVV IL-12, but not rVV IL-2/rVV IFN-β, restored the attenuated phenotype of rVV IL-2 in MyD88(-/-) mice indicating that the IL-2/IL-12 combination promotes antiviral responses. |
| 220 | 21248035 | Antigen-specific T-cell responses to a recombinant fowlpox virus are dependent on MyD88 and interleukin-18 and independent of Toll-like receptor 7 (TLR7)- and TLR9-mediated innate immune recognition. |
| 221 | 21248035 | We show that Toll-like receptor 7 (TLR7) and TLR9 are important for type I interferon secretion by dendritic cells, while TLR9 is solely required for proinflammatory cytokine secretion. |
| 222 | 21248035 | Despite this functional role for TLR7 and TLR9 in vitro, only the adapter protein myeloid differentiation primary response gene 88 (MyD88) was shown to be essential for the formation of adaptive immunity to FWPV(OVA) in vivo. |
| 223 | 21248035 | We demonstrate that this is not by means of mediating T-cell-dependent interleukin-1 (IL-1) signaling, but rather, we suggest that MyD88 functions to support T-cell-specific IL-18 receptor signaling, which in turn is essential for the formation of adaptive immunity to FWPV-encoded OVA. |
| 224 | 21248035 | Antigen-specific T-cell responses to a recombinant fowlpox virus are dependent on MyD88 and interleukin-18 and independent of Toll-like receptor 7 (TLR7)- and TLR9-mediated innate immune recognition. |
| 225 | 21248035 | We show that Toll-like receptor 7 (TLR7) and TLR9 are important for type I interferon secretion by dendritic cells, while TLR9 is solely required for proinflammatory cytokine secretion. |
| 226 | 21248035 | Despite this functional role for TLR7 and TLR9 in vitro, only the adapter protein myeloid differentiation primary response gene 88 (MyD88) was shown to be essential for the formation of adaptive immunity to FWPV(OVA) in vivo. |
| 227 | 21248035 | We demonstrate that this is not by means of mediating T-cell-dependent interleukin-1 (IL-1) signaling, but rather, we suggest that MyD88 functions to support T-cell-specific IL-18 receptor signaling, which in turn is essential for the formation of adaptive immunity to FWPV-encoded OVA. |
| 228 | 21248035 | Antigen-specific T-cell responses to a recombinant fowlpox virus are dependent on MyD88 and interleukin-18 and independent of Toll-like receptor 7 (TLR7)- and TLR9-mediated innate immune recognition. |
| 229 | 21248035 | We show that Toll-like receptor 7 (TLR7) and TLR9 are important for type I interferon secretion by dendritic cells, while TLR9 is solely required for proinflammatory cytokine secretion. |
| 230 | 21248035 | Despite this functional role for TLR7 and TLR9 in vitro, only the adapter protein myeloid differentiation primary response gene 88 (MyD88) was shown to be essential for the formation of adaptive immunity to FWPV(OVA) in vivo. |
| 231 | 21248035 | We demonstrate that this is not by means of mediating T-cell-dependent interleukin-1 (IL-1) signaling, but rather, we suggest that MyD88 functions to support T-cell-specific IL-18 receptor signaling, which in turn is essential for the formation of adaptive immunity to FWPV-encoded OVA. |
| 232 | 21350488 | Here we demonstrate that immunization of mice with synthetic nanoparticles containing antigens plus ligands that signal through TLR4 and TLR7 induces synergistic increases in antigen-specific, neutralizing antibodies compared to immunization with nanoparticles containing antigens plus a single TLR ligand. |
| 233 | 21487111 | TLR7 and TLR8 are intracellular sensors activated by single-stranded RNA species generated during viral infections. |
| 234 | 21487111 | Various synthetic small molecules can also activate TLR7 or TLR8 or both through an unknown mechanism. |
| 235 | 21487111 | Notably, direct interaction between small molecules and TLR7 or TLR8 has never been shown. |
| 236 | 21487111 | All fluorescent compounds induced the production of IFN-α, TNF-α, and IL-6 and the up-regulation of CD80 and CD86 by pDCs showing they retained TLR7-stimulating activity. |
| 237 | 21487111 | TLR7 and TLR8 are intracellular sensors activated by single-stranded RNA species generated during viral infections. |
| 238 | 21487111 | Various synthetic small molecules can also activate TLR7 or TLR8 or both through an unknown mechanism. |
| 239 | 21487111 | Notably, direct interaction between small molecules and TLR7 or TLR8 has never been shown. |
| 240 | 21487111 | All fluorescent compounds induced the production of IFN-α, TNF-α, and IL-6 and the up-regulation of CD80 and CD86 by pDCs showing they retained TLR7-stimulating activity. |
| 241 | 21487111 | TLR7 and TLR8 are intracellular sensors activated by single-stranded RNA species generated during viral infections. |
| 242 | 21487111 | Various synthetic small molecules can also activate TLR7 or TLR8 or both through an unknown mechanism. |
| 243 | 21487111 | Notably, direct interaction between small molecules and TLR7 or TLR8 has never been shown. |
| 244 | 21487111 | All fluorescent compounds induced the production of IFN-α, TNF-α, and IL-6 and the up-regulation of CD80 and CD86 by pDCs showing they retained TLR7-stimulating activity. |
| 245 | 21487111 | TLR7 and TLR8 are intracellular sensors activated by single-stranded RNA species generated during viral infections. |
| 246 | 21487111 | Various synthetic small molecules can also activate TLR7 or TLR8 or both through an unknown mechanism. |
| 247 | 21487111 | Notably, direct interaction between small molecules and TLR7 or TLR8 has never been shown. |
| 248 | 21487111 | All fluorescent compounds induced the production of IFN-α, TNF-α, and IL-6 and the up-regulation of CD80 and CD86 by pDCs showing they retained TLR7-stimulating activity. |
| 249 | 21515797 | SIV infections of SMs are characterized by an absence of chronic immune activation, in association with significantly reduced IFN-α production by plasmacytoid dendritic cells (pDCs) following exposure to SIV or other defined TLR7 or TLR9 ligands. |
| 250 | 21533209 | Most of the TLR agonists induced TNFα, IL-1β, IL-6, and IL-10 in cord blood. |
| 251 | 21533209 | The greatest TNFα responses were observed for TLR4, -5, and -8 agonists, the highest being the thiazoloquinoline CLO75 (TLR7/8) that also uniquely induced cord blood IFNγ production. |
| 252 | 21533209 | TLR8 agonists also induced the greatest production of the Th1-polarizing cytokines TNFα and IFNγ throughout the first year of life, although the relative responses to the single TLR8 agonist and the combined TLR7/8 agonist changed with age. |
| 253 | 21533209 | In contrast, IL-1β, IL-6, and IL-10 responses to most agonists were robust at birth and remained stable through 12 months of age. |
| 254 | 21533209 | Most of the TLR agonists induced TNFα, IL-1β, IL-6, and IL-10 in cord blood. |
| 255 | 21533209 | The greatest TNFα responses were observed for TLR4, -5, and -8 agonists, the highest being the thiazoloquinoline CLO75 (TLR7/8) that also uniquely induced cord blood IFNγ production. |
| 256 | 21533209 | TLR8 agonists also induced the greatest production of the Th1-polarizing cytokines TNFα and IFNγ throughout the first year of life, although the relative responses to the single TLR8 agonist and the combined TLR7/8 agonist changed with age. |
| 257 | 21533209 | In contrast, IL-1β, IL-6, and IL-10 responses to most agonists were robust at birth and remained stable through 12 months of age. |
| 258 | 21557981 | Results showed that the plasmid with 64 copies of the CpG motif (64CpG-plasmid) significantly enhanced the mRNA expressions of interferon-gamma (IFN-γ), TLR3 and TLR7 in chicken splenocytes compared to plasmids with lesser copies of the CpG motif in vitro. |
| 259 | 21557981 | Chickens inoculated with the H5N2 avian influenza inactivated vaccines (V52) coadministrated with the 64CpG-plasmid (V52-64CpG) showed significant increments of hemagglutination inhibition (HI) titers, peripheral blood mononuclear cell (PBMC) proliferation, and mRNA expressions of IFN-α, IFN-γ, TLR3, TLR7 and TLR21 in splenocytes as compared to those of chickens inoculated with V52 alone, V52 adjuvanted with aluminum gel (V52-gel), or with V52-gel plus vector. |
| 260 | 21557981 | Results showed that the plasmid with 64 copies of the CpG motif (64CpG-plasmid) significantly enhanced the mRNA expressions of interferon-gamma (IFN-γ), TLR3 and TLR7 in chicken splenocytes compared to plasmids with lesser copies of the CpG motif in vitro. |
| 261 | 21557981 | Chickens inoculated with the H5N2 avian influenza inactivated vaccines (V52) coadministrated with the 64CpG-plasmid (V52-64CpG) showed significant increments of hemagglutination inhibition (HI) titers, peripheral blood mononuclear cell (PBMC) proliferation, and mRNA expressions of IFN-α, IFN-γ, TLR3, TLR7 and TLR21 in splenocytes as compared to those of chickens inoculated with V52 alone, V52 adjuvanted with aluminum gel (V52-gel), or with V52-gel plus vector. |
| 262 | 21641953 | They are also well suited to function as vaccine adjuvants. 3M imidazoquinoline (IRM) molecules were the first synthetic small molecules identified as TLR agonists and can affect their biological activities through TLR7, TLR8, or both. |
| 263 | 21742006 | To determine what type of adjuvant can better enhance the immunogenicity of a Chlamydia vaccine, we formulated the recombinant major outer membrane protein (Ct-rMOMP) with several ligands for Toll-like receptors (TLR) and the nucleotide-binding oligomerization domain (NOD) including Pam(2)CSK(4) (TLR2/TLR6), Poly (I:C) (TLR3), monophosphoryl lipid A (TLR4), flagellin (TLR5), imiquimod R837 (TLR7), imidazoquinoline R848 (TRL7/8), CpG-1826 (TLR9), M-Tri-(DAP) (NOD1/NOD2) and muramyldipeptide (NOD2). |
| 264 | 21742006 | As determined by the IgG2a/IgG1 ratio in the sera, mice immunized with Ct-rMOMP+Pam(2)CSK(4) showed a strong Th2 biased humoral immune response. |
| 265 | 21742006 | In addition, based on changes in body weight, weight of the lungs and number of IFU recovered from the lungs, the mice immunized with Ct-rMOMP+Pam(2)CSK(4), were better protected against the i.n. challenge than any group of mice immunized with Ct-rMOMP and the other adjuvants. |
| 266 | 21742006 | In conclusion, Pam(2)CSK(4) should be evaluated as a candidate adjuvant for a C. trachomatis vaccine. |
| 267 | 21748646 | Viral single-stranded (ss) RNA is the natural ligand for TLR7 and TLR8. |
| 268 | 21748646 | Synthetic ssRNA has been shown to act as a ligand for TLR7 and TLR8. |
| 269 | 21748646 | Viral single-stranded (ss) RNA is the natural ligand for TLR7 and TLR8. |
| 270 | 21748646 | Synthetic ssRNA has been shown to act as a ligand for TLR7 and TLR8. |
| 271 | 21839740 | Gene expression for T-helper-1 (Th1) polarizing cytokines (TNF-α, IL-1β, IL-12) and chemokines (CXCL1, CCL2) was upregulated following ex vivo stimulation of guinea pig splenocytes and whole blood with TLR-4 or TLR-7/8 agonists. |
| 272 | 21844166 | TLR7/9 versus TLR3/MDA5 signaling during virus infections and diabetes. |
| 273 | 21844166 | In this article, we discuss TLR7/9 versus TLR3/MDA5 signaling in antiviral responses and diabetes. pDCs are thought to have a critical role in antiviral defense because of their ability to rapidly secrete large amounts of IFN-I through TLR7/9 signaling. |
| 274 | 21844166 | A recent study demonstrates that although pDCs are a source of IFN-I in vivo, their overall contribution to viral containment is limited and time-dependent, such that additional cellular sources of IFN-I are required to fully control viral infections. dsRNA sensors, such as TLR3 and MDA5, provide another important trigger for antiviral IFN-I responses, which can be exploited to enhance immune responses to vaccines. |
| 275 | 21844166 | However, recent data demonstrate that IFN-I production via TLR3 and MDA5 is critical to counter diabetes caused by a virus with preferential tropism for pancreatic β-cells. |
| 276 | 21844166 | TLR7/9 versus TLR3/MDA5 signaling during virus infections and diabetes. |
| 277 | 21844166 | In this article, we discuss TLR7/9 versus TLR3/MDA5 signaling in antiviral responses and diabetes. pDCs are thought to have a critical role in antiviral defense because of their ability to rapidly secrete large amounts of IFN-I through TLR7/9 signaling. |
| 278 | 21844166 | A recent study demonstrates that although pDCs are a source of IFN-I in vivo, their overall contribution to viral containment is limited and time-dependent, such that additional cellular sources of IFN-I are required to fully control viral infections. dsRNA sensors, such as TLR3 and MDA5, provide another important trigger for antiviral IFN-I responses, which can be exploited to enhance immune responses to vaccines. |
| 279 | 21844166 | However, recent data demonstrate that IFN-I production via TLR3 and MDA5 is critical to counter diabetes caused by a virus with preferential tropism for pancreatic β-cells. |
| 280 | 21869824 | Wild-type and CEA transgenic (Tg) mice were immunized with rAAV-expressing CEA, the TLR9 agonist, oligodinucleotide (ODN)1826 and the TLR7 agonist, imiquimod. |
| 281 | 21921206 | Using a total of 28 baboons, different vaccination strategies were used including recombinant Sm-p80 protein formulated in Toll-like receptor 7 and Toll-like receptor 9 agonists, and DNA priming followed by boosting with protein plus adjuvants. |
| 282 | 21921206 | Production and expression of several cytokines (interleukin 2 [IL-2], interferon γ, IL-12α, IL-1β, IL-6, and IL-22) were up-regulated in vaccinated animals. |
| 283 | 21947541 | TLR7 and TLR8 genetic variation may cause functional alterations that result in impaired responses to measles. |
| 284 | 21947541 | In a population of 12-month-old Australian infants, receptor protein expression was examined to assess the functionality of TLR7 and TLR8 polymorphisms, and the effects of these polymorphisms on cellular and antibody responses after the first measles vaccine dose were investigated. |
| 285 | 21947541 | None of the TLR7 or TLR8 polymorphisms studied were associated with measles-specific cytokine levels or with measles IgG levels. |
| 286 | 21947541 | In conclusion, we report gender-specific associations with TLR7 and TLR8 polymorphisms and TNF-α cellular responses to its ligand. |
| 287 | 21947541 | However, we found no evidence of any functional effects of TLR7 or TLR8 polymorphisms on receptor expression, measles-specific cellular responses or measles vaccine antibody responses. |
| 288 | 21947541 | TLR7 and TLR8 genetic variation may cause functional alterations that result in impaired responses to measles. |
| 289 | 21947541 | In a population of 12-month-old Australian infants, receptor protein expression was examined to assess the functionality of TLR7 and TLR8 polymorphisms, and the effects of these polymorphisms on cellular and antibody responses after the first measles vaccine dose were investigated. |
| 290 | 21947541 | None of the TLR7 or TLR8 polymorphisms studied were associated with measles-specific cytokine levels or with measles IgG levels. |
| 291 | 21947541 | In conclusion, we report gender-specific associations with TLR7 and TLR8 polymorphisms and TNF-α cellular responses to its ligand. |
| 292 | 21947541 | However, we found no evidence of any functional effects of TLR7 or TLR8 polymorphisms on receptor expression, measles-specific cellular responses or measles vaccine antibody responses. |
| 293 | 21947541 | TLR7 and TLR8 genetic variation may cause functional alterations that result in impaired responses to measles. |
| 294 | 21947541 | In a population of 12-month-old Australian infants, receptor protein expression was examined to assess the functionality of TLR7 and TLR8 polymorphisms, and the effects of these polymorphisms on cellular and antibody responses after the first measles vaccine dose were investigated. |
| 295 | 21947541 | None of the TLR7 or TLR8 polymorphisms studied were associated with measles-specific cytokine levels or with measles IgG levels. |
| 296 | 21947541 | In conclusion, we report gender-specific associations with TLR7 and TLR8 polymorphisms and TNF-α cellular responses to its ligand. |
| 297 | 21947541 | However, we found no evidence of any functional effects of TLR7 or TLR8 polymorphisms on receptor expression, measles-specific cellular responses or measles vaccine antibody responses. |
| 298 | 21947541 | TLR7 and TLR8 genetic variation may cause functional alterations that result in impaired responses to measles. |
| 299 | 21947541 | In a population of 12-month-old Australian infants, receptor protein expression was examined to assess the functionality of TLR7 and TLR8 polymorphisms, and the effects of these polymorphisms on cellular and antibody responses after the first measles vaccine dose were investigated. |
| 300 | 21947541 | None of the TLR7 or TLR8 polymorphisms studied were associated with measles-specific cytokine levels or with measles IgG levels. |
| 301 | 21947541 | In conclusion, we report gender-specific associations with TLR7 and TLR8 polymorphisms and TNF-α cellular responses to its ligand. |
| 302 | 21947541 | However, we found no evidence of any functional effects of TLR7 or TLR8 polymorphisms on receptor expression, measles-specific cellular responses or measles vaccine antibody responses. |
| 303 | 21947541 | TLR7 and TLR8 genetic variation may cause functional alterations that result in impaired responses to measles. |
| 304 | 21947541 | In a population of 12-month-old Australian infants, receptor protein expression was examined to assess the functionality of TLR7 and TLR8 polymorphisms, and the effects of these polymorphisms on cellular and antibody responses after the first measles vaccine dose were investigated. |
| 305 | 21947541 | None of the TLR7 or TLR8 polymorphisms studied were associated with measles-specific cytokine levels or with measles IgG levels. |
| 306 | 21947541 | In conclusion, we report gender-specific associations with TLR7 and TLR8 polymorphisms and TNF-α cellular responses to its ligand. |
| 307 | 21947541 | However, we found no evidence of any functional effects of TLR7 or TLR8 polymorphisms on receptor expression, measles-specific cellular responses or measles vaccine antibody responses. |
| 308 | 22190381 | Interestingly, TLR-7 agonist decoration increased significantly the interleukin-8-related immune stimulatory capacity of polymeric chitosan and chitosan-based NP in human THP-1 macrophages when compared with controls. |
| 309 | 22239408 | We describe the syntheses and evaluation of TLR7 and TLR8 modulatory activities of dimeric constructs of imidazoquinoline linked at the C2, C4, C8, and N(1)-aryl positions. |
| 310 | 22239408 | Dimers linked at C2 position showed antagonistic activities at TLR7 and TLR8; the C2 dimer with a propylene spacer was maximally antagonistic at both TLR7 and TLR8. |
| 311 | 22239408 | We describe the syntheses and evaluation of TLR7 and TLR8 modulatory activities of dimeric constructs of imidazoquinoline linked at the C2, C4, C8, and N(1)-aryl positions. |
| 312 | 22239408 | Dimers linked at C2 position showed antagonistic activities at TLR7 and TLR8; the C2 dimer with a propylene spacer was maximally antagonistic at both TLR7 and TLR8. |
| 313 | 22359246 | There is clear evidence for type I IFN activity in both acute and chronic HIV-1 infection in vivo, and plasmacytoid dendritic cells have been identified as one important source for these responses, through innate immune detection of viral RNA by Toll-like receptor 7. |
| 314 | 22438548 | The double-stranded RNA bluetongue virus induces type I interferon in plasmacytoid dendritic cells via a MYD88-dependent TLR7/8-independent signaling pathway. |
| 315 | 22438548 | Other inflammatory cytokines, including tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), and IL-12p40, were also induced by UV-BTV in primary pDCs. |
| 316 | 22438548 | In contrast, pathways involving the MyD88 adaptor and kinases dsRNA-activated protein kinase (PKR) and stress-activated protein kinase (SAPK)/Jun N-terminal protein kinase (JNK) were implicated. |
| 317 | 22497974 | We then examined cells with single or multiple virus infections for the expression of 10 cytokine genes and demonstrated elevated expressions for 7 (IFN-α, IFN-β, IFN-γ, TNF-α, IL-6, IL-8, and IL-17) in dual rotavirus and enterovirus or triple rotavirus, enterovirus and astrovirus-infected cells but only 3 (IFN-β, TNF-α, and IL-8) in dual rotavirus and astrovirus-infected cells. |
| 318 | 22497974 | We further observed elevated levels of TLR4, TLR5, TLR7 and TLR9 mRNAs in cells with rotavirus and enterovirus or rotavirus, enterovirus and astrovirus infections when compared to single rotavirus infections. |
| 319 | 22837197 | During infection with influenza A/PR8/34 virus, the absence of either TLR7 or MyD88 leads to reduced virus-specific antibodies in the serum and antibody-secreting cells in their secondary lymphoid organs, particularly in bone marrow. |
| 320 | 22837197 | In spite of this, the absence of TLR7/MyD88 signaling did not impair the production of protective antibodies. |
| 321 | 22837197 | During infection with influenza A/PR8/34 virus, the absence of either TLR7 or MyD88 leads to reduced virus-specific antibodies in the serum and antibody-secreting cells in their secondary lymphoid organs, particularly in bone marrow. |
| 322 | 22837197 | In spite of this, the absence of TLR7/MyD88 signaling did not impair the production of protective antibodies. |
| 323 | 22952720 | We synthesized a dendrimeric molecule bearing six units of a potent TLR7/TLR8 dual-agonistic imidazoquinoline to explore if multimerization of TLR7/8 would result in altered activity profiles. |
| 324 | 22952720 | A complete loss of TLR8-stimulatory activity with selective retention of the TLR7-agonistic activity was observed in the dendrimer. |
| 325 | 22952720 | This was reflected by a complete absence of TLR8-driven proinflammatory cytokine and interferon (IFN)-γ induction in human PBMCs, with preservation of TLR7-driven IFN-α induction. |
| 326 | 22952720 | We synthesized a dendrimeric molecule bearing six units of a potent TLR7/TLR8 dual-agonistic imidazoquinoline to explore if multimerization of TLR7/8 would result in altered activity profiles. |
| 327 | 22952720 | A complete loss of TLR8-stimulatory activity with selective retention of the TLR7-agonistic activity was observed in the dendrimer. |
| 328 | 22952720 | This was reflected by a complete absence of TLR8-driven proinflammatory cytokine and interferon (IFN)-γ induction in human PBMCs, with preservation of TLR7-driven IFN-α induction. |
| 329 | 22952720 | We synthesized a dendrimeric molecule bearing six units of a potent TLR7/TLR8 dual-agonistic imidazoquinoline to explore if multimerization of TLR7/8 would result in altered activity profiles. |
| 330 | 22952720 | A complete loss of TLR8-stimulatory activity with selective retention of the TLR7-agonistic activity was observed in the dendrimer. |
| 331 | 22952720 | This was reflected by a complete absence of TLR8-driven proinflammatory cytokine and interferon (IFN)-γ induction in human PBMCs, with preservation of TLR7-driven IFN-α induction. |
| 332 | 22953039 | Moreover, we found toll-like receptor (TLR) agonists lipopolysaccharide (TLR4), fibroblast stimulating ligand-1 (TLR2/6), and ODN2006 (TLR7/9) induced reduced cytokine responses in aged mDC. |
| 333 | 22953039 | We also found that TLR4, TLR5, and innate negative regulator, sterile alpha and TIR motif containing protein (SARM), were all expressed at lower levels in young animals. |
| 334 | 22953039 | By contrast, absent in melanoma 2 and retinoic acid-inducible gene I expression was lowest in aged animals. |
| 335 | 23050463 | In all three duck species, there was up-regulation of IFN-alpha, IFN-gamma, IL-6, CCL19, RIG-I, and MHC class I and down-regulation of MHC class II, but variable expression of IL-18 and TLR7. |
| 336 | 23100517 | Plasmacytoid dendritic cells (pDCs) play a central role in innate and adaptive immune responses to viral infections, including HIV type 1 (HIV-1). pDCs produce substantial quantities of type I IFN and proinflammatory cytokines upon stimulation via TLRs, specifically TLR7 or TLR9. |
| 337 | 23100517 | Specifically, gp120 inhibited the CpG-induced maturation of pDCs and their expression of TNF-α, IL-6, TLR9, IFN regulatory factor 7, and BAFF. |
| 338 | 23100517 | Receptor-blocking and cross-linking studies showed that these inhibitory effects of gp120 were mediated by interactions with CD4 and mannose-binding C-type lectin receptors, but not with the chemokine receptors CCR5 and CXCR4. |
| 339 | 23142133 | One is the plasmacytoid DC (pDC), which expresses nucleic acid sensing receptors TLR7 and TLR9 and secretes large amounts of type I interferons in response to TLR7/9 signaling. |
| 340 | 23142133 | This DC subset expresses lipid sensors, TLR2 and TLR4, and nucleic acid sensors, TLR3, TLR9 and TLR13 and is specialized for antigen crosspresentation. |
| 341 | 23314004 | Here we found that after infection with live influenza A virus, signaling through the interleukin 1 receptor (IL-1R) was required for productive priming of CD8(+) T cells, but signaling through the PRRs TLR7 and RIG-I was not. |
| 342 | 23314004 | DCs activated by IL-1 in trans were both required and sufficient for the generation of virus-specific CD8(+) T cell immunity. |
| 343 | 23434386 | The role of Toll-like receptors (TLR), which are involved in signal transduction of influenza virus, and the subsequent induction of IFNα were confirmed using mice lacking TLR7, MyD-88, or IFNα/β receptor. |
| 344 | 23455713 | Once there, primed T cells became dysfunctional and underwent antigen-driven, interferon-γ (IFN-γ)- and Fas ligand (FasL)-mediated apoptosis, resulting in hyporesponsiveness to subsequent vaccination. |
| 345 | 23455713 | Provision of CD40-specific antibody, Toll-like receptor 7 (TLR7) agonist and interleukin-2 (IL-2) reduced T cell apoptosis but did not prevent vaccination-site sequestration. |
| 346 | 23521528 | We have engineered a nononcogenic mutated E7-specific plasmo-retroVLP vaccine (pVLP-E7), consisting of plasmid DNA, that is able to form recombinant retrovirus-based virus-like particles (VLPs) that display E7 antigen into murine leukemia virus Gag proteins pseudotyped with vesicular stomatitis virus envelope glycoprotein (VSV-G). pVLP-E7 vaccinations were studied for their ability to generate specific immune responses and for induction of protective immunity against tumor cell challenge in preventive and therapeutic models. |
| 347 | 23521528 | Intradermic vaccinations of mice with pVLP-E7 show their efficacy to generate antigen-specific T cell responses, to prevent and protect animals from early TC-1 tumor development compared with standard DNA or VLP immunizations. |
| 348 | 23521528 | Data show that pVLP-E7 vaccination can cure mice with already established tumors only when combined with Toll-like receptor-7 (TLR7) and TLR9 agonists. |
| 349 | 23523335 | TLR3 and TLR7/8 ligands are promising adjuvant candidates for the development of novel vaccines against PRRSV. |
| 350 | 23667422 | Another interesting feature was that only neonatal BDCs produced IFN-α after TLR7 or TLR9 ligand stimulation. |
| 351 | 23667422 | These findings suggest that when stimulated via TLR7 or TLR9 porcine DCs display similar if not better response than adult porcine DCs. |
| 352 | 23667422 | Another interesting feature was that only neonatal BDCs produced IFN-α after TLR7 or TLR9 ligand stimulation. |
| 353 | 23667422 | These findings suggest that when stimulated via TLR7 or TLR9 porcine DCs display similar if not better response than adult porcine DCs. |
| 354 | 23750720 | In contrast to humans, pDC in rhesus macaques expressed the interleukin (IL)-12p40 subunit in response to TLR-7/8 as well as TLR-9 stimulation. |
| 355 | 23755218 | Whole blood samples were stimulated with a combination of TLR4 and TLR7/8 ligands. |
| 356 | 23845800 | Here, we investigated NS4B-P38G mutant infection in myeloid differentiation factor 88-deficient (MyD88(-/-)) and Toll-like receptor 7-deficient (TLR7(-/-)) mice and found they had enhanced susceptibility compared to wild-type mice. |
| 357 | 23845800 | Moreover, infection with NS4B-P38G mutant in TLR7(-/-) and MyD88(-/-) mice provided full and partial protection respectively from subsequent challenge with lethal wild-type WNV. |
| 358 | 23845800 | There were reduced T cell responses in MyD88(-/-) and interleukin-1 receptor deficient (IL-1R(-/-)) mice during secondary challenge with wild-type WNV. |
| 359 | 23845800 | Collectively, these results suggest that TLR7-dependent MyD88 signaling is required for T cell priming during NS4B-P38G mutant infection, whereas the TLR7-independent MyD88 signaling pathways are involved in memory T cell development, which may contribute to host protection during secondary challenge with wild-type WNV. |
| 360 | 23845800 | Here, we investigated NS4B-P38G mutant infection in myeloid differentiation factor 88-deficient (MyD88(-/-)) and Toll-like receptor 7-deficient (TLR7(-/-)) mice and found they had enhanced susceptibility compared to wild-type mice. |
| 361 | 23845800 | Moreover, infection with NS4B-P38G mutant in TLR7(-/-) and MyD88(-/-) mice provided full and partial protection respectively from subsequent challenge with lethal wild-type WNV. |
| 362 | 23845800 | There were reduced T cell responses in MyD88(-/-) and interleukin-1 receptor deficient (IL-1R(-/-)) mice during secondary challenge with wild-type WNV. |
| 363 | 23845800 | Collectively, these results suggest that TLR7-dependent MyD88 signaling is required for T cell priming during NS4B-P38G mutant infection, whereas the TLR7-independent MyD88 signaling pathways are involved in memory T cell development, which may contribute to host protection during secondary challenge with wild-type WNV. |
| 364 | 23845800 | Here, we investigated NS4B-P38G mutant infection in myeloid differentiation factor 88-deficient (MyD88(-/-)) and Toll-like receptor 7-deficient (TLR7(-/-)) mice and found they had enhanced susceptibility compared to wild-type mice. |
| 365 | 23845800 | Moreover, infection with NS4B-P38G mutant in TLR7(-/-) and MyD88(-/-) mice provided full and partial protection respectively from subsequent challenge with lethal wild-type WNV. |
| 366 | 23845800 | There were reduced T cell responses in MyD88(-/-) and interleukin-1 receptor deficient (IL-1R(-/-)) mice during secondary challenge with wild-type WNV. |
| 367 | 23845800 | Collectively, these results suggest that TLR7-dependent MyD88 signaling is required for T cell priming during NS4B-P38G mutant infection, whereas the TLR7-independent MyD88 signaling pathways are involved in memory T cell development, which may contribute to host protection during secondary challenge with wild-type WNV. |
| 368 | 23850441 | Activations of endosomal TLRs include TLR3, TLR7/8, and TLR9 stimulates the production of cytokines, such as type I interferons (IFNs), and therefore involves in virus-host interactions. |
| 369 | 23850441 | Our results showed that EIAVFDDV13 dramatically up-regulated the expression of TLR3 and IFNβ and less robustly up-regulated the expression of TRL9 and IFNα1, whereas EIAVFDDV3-8 induced significantly lower expression of type I IFN mRNA and protein and more strongly down-regulated the expression of TLR7 and TLR8. |
| 370 | 23850441 | Activations of endosomal TLRs include TLR3, TLR7/8, and TLR9 stimulates the production of cytokines, such as type I interferons (IFNs), and therefore involves in virus-host interactions. |
| 371 | 23850441 | Our results showed that EIAVFDDV13 dramatically up-regulated the expression of TLR3 and IFNβ and less robustly up-regulated the expression of TRL9 and IFNα1, whereas EIAVFDDV3-8 induced significantly lower expression of type I IFN mRNA and protein and more strongly down-regulated the expression of TLR7 and TLR8. |
| 372 | 23912942 | TLR7/8-triggered secretion of IL-12 and IFN-α, as well as TLR9-triggered secretion of IL-12, was hyperactivated. |
| 373 | 23935491 | Blocking TLR7- and TLR9-mediated IFN-α production by plasmacytoid dendritic cells does not diminish immune activation in early SIV infection. |
| 374 | 23935491 | We show that pDC are major but not exclusive producers of IFN-α that rapidly become unresponsive to virus stimulation following SIV infection, whereas myeloid DC gain the capacity to produce IFN-α, albeit at low levels. pDC mediate a marked but transient IFN-α response in lymph nodes during the acute phase that is blocked by administration of TLR7 and TLR9 antagonist without impacting pDC recruitment. |
| 375 | 23935491 | TLR7 and TLR9 blockade did not impact virus load or the acute IFN-α response in plasma and had minimal effect on expression of IFN-stimulated genes in both blood and lymph node. |
| 376 | 23935491 | TLR7 and TLR9 blockade did not prevent activation of memory CD4+ and CD8+ T cells in blood or lymph node but led to significant increases in proliferation of both subsets in blood following SIV infection. |
| 377 | 23935491 | Our findings reveal that virus-mediated activation of pDC through TLR7 and TLR9 contributes to substantial but transient IFN-α production following pathogenic SIV infection. |
| 378 | 23935491 | Blocking TLR7- and TLR9-mediated IFN-α production by plasmacytoid dendritic cells does not diminish immune activation in early SIV infection. |
| 379 | 23935491 | We show that pDC are major but not exclusive producers of IFN-α that rapidly become unresponsive to virus stimulation following SIV infection, whereas myeloid DC gain the capacity to produce IFN-α, albeit at low levels. pDC mediate a marked but transient IFN-α response in lymph nodes during the acute phase that is blocked by administration of TLR7 and TLR9 antagonist without impacting pDC recruitment. |
| 380 | 23935491 | TLR7 and TLR9 blockade did not impact virus load or the acute IFN-α response in plasma and had minimal effect on expression of IFN-stimulated genes in both blood and lymph node. |
| 381 | 23935491 | TLR7 and TLR9 blockade did not prevent activation of memory CD4+ and CD8+ T cells in blood or lymph node but led to significant increases in proliferation of both subsets in blood following SIV infection. |
| 382 | 23935491 | Our findings reveal that virus-mediated activation of pDC through TLR7 and TLR9 contributes to substantial but transient IFN-α production following pathogenic SIV infection. |
| 383 | 23935491 | Blocking TLR7- and TLR9-mediated IFN-α production by plasmacytoid dendritic cells does not diminish immune activation in early SIV infection. |
| 384 | 23935491 | We show that pDC are major but not exclusive producers of IFN-α that rapidly become unresponsive to virus stimulation following SIV infection, whereas myeloid DC gain the capacity to produce IFN-α, albeit at low levels. pDC mediate a marked but transient IFN-α response in lymph nodes during the acute phase that is blocked by administration of TLR7 and TLR9 antagonist without impacting pDC recruitment. |
| 385 | 23935491 | TLR7 and TLR9 blockade did not impact virus load or the acute IFN-α response in plasma and had minimal effect on expression of IFN-stimulated genes in both blood and lymph node. |
| 386 | 23935491 | TLR7 and TLR9 blockade did not prevent activation of memory CD4+ and CD8+ T cells in blood or lymph node but led to significant increases in proliferation of both subsets in blood following SIV infection. |
| 387 | 23935491 | Our findings reveal that virus-mediated activation of pDC through TLR7 and TLR9 contributes to substantial but transient IFN-α production following pathogenic SIV infection. |
| 388 | 23935491 | Blocking TLR7- and TLR9-mediated IFN-α production by plasmacytoid dendritic cells does not diminish immune activation in early SIV infection. |
| 389 | 23935491 | We show that pDC are major but not exclusive producers of IFN-α that rapidly become unresponsive to virus stimulation following SIV infection, whereas myeloid DC gain the capacity to produce IFN-α, albeit at low levels. pDC mediate a marked but transient IFN-α response in lymph nodes during the acute phase that is blocked by administration of TLR7 and TLR9 antagonist without impacting pDC recruitment. |
| 390 | 23935491 | TLR7 and TLR9 blockade did not impact virus load or the acute IFN-α response in plasma and had minimal effect on expression of IFN-stimulated genes in both blood and lymph node. |
| 391 | 23935491 | TLR7 and TLR9 blockade did not prevent activation of memory CD4+ and CD8+ T cells in blood or lymph node but led to significant increases in proliferation of both subsets in blood following SIV infection. |
| 392 | 23935491 | Our findings reveal that virus-mediated activation of pDC through TLR7 and TLR9 contributes to substantial but transient IFN-α production following pathogenic SIV infection. |
| 393 | 23935491 | Blocking TLR7- and TLR9-mediated IFN-α production by plasmacytoid dendritic cells does not diminish immune activation in early SIV infection. |
| 394 | 23935491 | We show that pDC are major but not exclusive producers of IFN-α that rapidly become unresponsive to virus stimulation following SIV infection, whereas myeloid DC gain the capacity to produce IFN-α, albeit at low levels. pDC mediate a marked but transient IFN-α response in lymph nodes during the acute phase that is blocked by administration of TLR7 and TLR9 antagonist without impacting pDC recruitment. |
| 395 | 23935491 | TLR7 and TLR9 blockade did not impact virus load or the acute IFN-α response in plasma and had minimal effect on expression of IFN-stimulated genes in both blood and lymph node. |
| 396 | 23935491 | TLR7 and TLR9 blockade did not prevent activation of memory CD4+ and CD8+ T cells in blood or lymph node but led to significant increases in proliferation of both subsets in blood following SIV infection. |
| 397 | 23935491 | Our findings reveal that virus-mediated activation of pDC through TLR7 and TLR9 contributes to substantial but transient IFN-α production following pathogenic SIV infection. |
| 398 | 23940691 | Its response to synthetic TLR ligands (R848: TLR7/8, LPS: TLR4) was on a comparable threshold to the more time consuming peripheral blood mononuclear cell (PBMC) based assay. |
| 399 | 24012797 | TLRs 3, 4, 7, 8 and 9 are all validated targets for cancer and a number of companies are developing agonists and vaccine adjuvants. |
| 400 | 24074567 | Here, we conjugated a TLR7/8 ligand to lysine residues on gp120 using NHS-PEO8-maleimide linkers and investigated if this affected Ab recognition of the CD4 binding site (CD4bs), a highly conserved target for bNAbs. |
| 401 | 24155397 | Human T-cell leukemia/lymphoma virus type 1 p30, but not p12/p8, counteracts toll-like receptor 3 (TLR3) and TLR4 signaling in human monocytes and dendritic cells. |
| 402 | 24155397 | We used a human monocytic cell line, THP-1, and dendritic cells to study the mechanism of p30 and p12/p8 requirements in these cell types. p30 inhibited the expression of interferon (IFN)-responsive genes (ISG) following stimulation by lipopolysaccharide (LPS) of Toll-like receptor 4 (TLR4) and by poly(I·C) of TLR3 but not of TLR7/8 with imiquimod. |
| 403 | 24155397 | HTLV-1 infection of monocytes inhibited TLR3- and TLR4-induced ISG expression by 50 to 90% depending on the genes, whereas the isogenic clone p30 knockout virus was less effective at inhibiting TLR3 and TRL4 signaling and displayed lower infectivity. |
| 404 | 24155397 | A chromatin immunoprecipitation assay demonstrated that p30 inhibits initiation and elongation of PU.1-dependent transcription of IFN-α1, IFN-β, and TLR4 genes upon TLR stimulation. |
| 405 | 24280723 | TLR7 and 9 agonists are highly effective mucosal adjuvants for norovirus virus-like particle vaccines. |
| 406 | 24280723 | Intranasal co-delivery of VLPs with TLR7 or TLR9 agonists produced the most robust and broad-spectrum immune responses, systemically and at distal mucosal sites inducing VLP-specific antibodies at all sites evaluated. |
| 407 | 24280723 | This study demonstrates that intranasal co-delivery of VLPs with TLR7 or TLR9 agonists provides dose-sparing advantages for induction of specific and functional antibody responses against VLPs (i.e., non-replicating antigens) in the respiratory, gastrointestinal, and reproductive tract. |
| 408 | 24280723 | TLR7 and 9 agonists are highly effective mucosal adjuvants for norovirus virus-like particle vaccines. |
| 409 | 24280723 | Intranasal co-delivery of VLPs with TLR7 or TLR9 agonists produced the most robust and broad-spectrum immune responses, systemically and at distal mucosal sites inducing VLP-specific antibodies at all sites evaluated. |
| 410 | 24280723 | This study demonstrates that intranasal co-delivery of VLPs with TLR7 or TLR9 agonists provides dose-sparing advantages for induction of specific and functional antibody responses against VLPs (i.e., non-replicating antigens) in the respiratory, gastrointestinal, and reproductive tract. |
| 411 | 24280723 | TLR7 and 9 agonists are highly effective mucosal adjuvants for norovirus virus-like particle vaccines. |
| 412 | 24280723 | Intranasal co-delivery of VLPs with TLR7 or TLR9 agonists produced the most robust and broad-spectrum immune responses, systemically and at distal mucosal sites inducing VLP-specific antibodies at all sites evaluated. |
| 413 | 24280723 | This study demonstrates that intranasal co-delivery of VLPs with TLR7 or TLR9 agonists provides dose-sparing advantages for induction of specific and functional antibody responses against VLPs (i.e., non-replicating antigens) in the respiratory, gastrointestinal, and reproductive tract. |
| 414 | 24376264 | Nanoparticle adjuvant sensing by TLR7 enhances CD8+ T cell-mediated protection from Listeria monocytogenes infection. |
| 415 | 24384074 | An in vitro model of antigen presentation showed that ligands for TLR-9, 7, 4 and 1/2 increased the ability of APCs to present antigen-85B of BCG to CD4 T cells, which correlated with an increase in MHC-II expression. |
| 416 | 24384074 | TLR-activation led to a down-regulation of MARCH1 ubiquitin ligase which prevents the degradation of MHC-II and decreased IL-10 also contributed to an increase in MHC-II. |
| 417 | 24384074 | TLR-activation induced up-regulation of MHC-II was inhibited by the blockade of IRAK, NF-kB, and MAPKs. |
| 418 | 24384074 | TLR-7 and TLR-9 ligands had the most effective adjuvant like effect on MHC-II of APCs which allowed BCG vaccine mediated activation of CD4 T cells. |
| 419 | 24390332 | Toll-like receptor 7/8 (TLR7/8) and TLR9 agonists cooperate to enhance HIV-1 envelope antibody responses in rhesus macaques. |
| 420 | 24422657 | SPLV injection enhanced serum IgA, IgM, IgG, IFN-γ, IL-1β, TNF-α and IL-10 concentrations (p < 0.05) and stimulated the relative mRNA abundance of Toll-like receptors (TLR3, TLR7 or TLR9) in different tissues (p < 0.05). |
| 421 | 24422657 | Under no challenge, increasing dietary TIDT levels enhanced serum IgG (p < 0.05), IgM (p = 0.07) and IFN-γ (p < 0.05) concentration, tended to decrease serum IL-1β, TNF-α and IL-10 concentration, and regulated relative mRNA abundance of TLR3, TLR7 or TLR9 in different tissues (p < 0.05). |
| 422 | 24422657 | Under SPLV challenge, increasing dietary TIDT levels attenuated the increase of the serum IFN-γ concentration, and the increase of the relative mRNA abundance of TLR3, TLR7 and TLR9 in the different tissues (p < 0.05). |
| 423 | 24422657 | These results suggest that an appropriate dietary threonine supplementation could improve the immune status of weaned pigs injected with SPLV by down-regulating the expression of TLR3, TLR7 and TLR9 in tissues, and thus regulating T-helper cytokine secretion. |
| 424 | 24422657 | SPLV injection enhanced serum IgA, IgM, IgG, IFN-γ, IL-1β, TNF-α and IL-10 concentrations (p < 0.05) and stimulated the relative mRNA abundance of Toll-like receptors (TLR3, TLR7 or TLR9) in different tissues (p < 0.05). |
| 425 | 24422657 | Under no challenge, increasing dietary TIDT levels enhanced serum IgG (p < 0.05), IgM (p = 0.07) and IFN-γ (p < 0.05) concentration, tended to decrease serum IL-1β, TNF-α and IL-10 concentration, and regulated relative mRNA abundance of TLR3, TLR7 or TLR9 in different tissues (p < 0.05). |
| 426 | 24422657 | Under SPLV challenge, increasing dietary TIDT levels attenuated the increase of the serum IFN-γ concentration, and the increase of the relative mRNA abundance of TLR3, TLR7 and TLR9 in the different tissues (p < 0.05). |
| 427 | 24422657 | These results suggest that an appropriate dietary threonine supplementation could improve the immune status of weaned pigs injected with SPLV by down-regulating the expression of TLR3, TLR7 and TLR9 in tissues, and thus regulating T-helper cytokine secretion. |
| 428 | 24422657 | SPLV injection enhanced serum IgA, IgM, IgG, IFN-γ, IL-1β, TNF-α and IL-10 concentrations (p < 0.05) and stimulated the relative mRNA abundance of Toll-like receptors (TLR3, TLR7 or TLR9) in different tissues (p < 0.05). |
| 429 | 24422657 | Under no challenge, increasing dietary TIDT levels enhanced serum IgG (p < 0.05), IgM (p = 0.07) and IFN-γ (p < 0.05) concentration, tended to decrease serum IL-1β, TNF-α and IL-10 concentration, and regulated relative mRNA abundance of TLR3, TLR7 or TLR9 in different tissues (p < 0.05). |
| 430 | 24422657 | Under SPLV challenge, increasing dietary TIDT levels attenuated the increase of the serum IFN-γ concentration, and the increase of the relative mRNA abundance of TLR3, TLR7 and TLR9 in the different tissues (p < 0.05). |
| 431 | 24422657 | These results suggest that an appropriate dietary threonine supplementation could improve the immune status of weaned pigs injected with SPLV by down-regulating the expression of TLR3, TLR7 and TLR9 in tissues, and thus regulating T-helper cytokine secretion. |
| 432 | 24422657 | SPLV injection enhanced serum IgA, IgM, IgG, IFN-γ, IL-1β, TNF-α and IL-10 concentrations (p < 0.05) and stimulated the relative mRNA abundance of Toll-like receptors (TLR3, TLR7 or TLR9) in different tissues (p < 0.05). |
| 433 | 24422657 | Under no challenge, increasing dietary TIDT levels enhanced serum IgG (p < 0.05), IgM (p = 0.07) and IFN-γ (p < 0.05) concentration, tended to decrease serum IL-1β, TNF-α and IL-10 concentration, and regulated relative mRNA abundance of TLR3, TLR7 or TLR9 in different tissues (p < 0.05). |
| 434 | 24422657 | Under SPLV challenge, increasing dietary TIDT levels attenuated the increase of the serum IFN-γ concentration, and the increase of the relative mRNA abundance of TLR3, TLR7 and TLR9 in the different tissues (p < 0.05). |
| 435 | 24422657 | These results suggest that an appropriate dietary threonine supplementation could improve the immune status of weaned pigs injected with SPLV by down-regulating the expression of TLR3, TLR7 and TLR9 in tissues, and thus regulating T-helper cytokine secretion. |
| 436 | 24503073 | Initiation of the transcription of selected innate immune genes such as TLR3, TLR7, MyD88, IL-1β and IFN-β, as well as recruitment of macrophages, were evident following an initial down regulation of some of the observed genes (TLR3, IL-1β, and IFN-γ) in trachea and lung. |
| 437 | 24534144 | Endosomal TLRs, TLR3, TLR7/8, and TLR9 are involved in antiviral responses by promoting the production of antiviral cytokines such as type I interferons. |
| 438 | 24534144 | The aim of the present study was to evaluate the expression of TLR3, TLR7 and TLR9 in porcine alveolar macrophages (PAM) infected with different genotype 1 PRRSV strains previously sequenced and characterized by their ability to induce TNF-α: 3262 (TNF-α inducer), 3267 (TNF-α not inducer) and an attenuated vaccine strain (strain Deventer, PorcilisPRRS, Merck) that replicates scarcely in PAM. |
| 439 | 24534144 | Thus, in PAM infected with PRRSV strain 3262 the proportion of TLR3+ cells significantly increased from 24h compared with the controls; in contrast strain 3267 resulted in a lower proportion of TLR3+ PAM. |
| 440 | 24534144 | Endosomal TLRs, TLR3, TLR7/8, and TLR9 are involved in antiviral responses by promoting the production of antiviral cytokines such as type I interferons. |
| 441 | 24534144 | The aim of the present study was to evaluate the expression of TLR3, TLR7 and TLR9 in porcine alveolar macrophages (PAM) infected with different genotype 1 PRRSV strains previously sequenced and characterized by their ability to induce TNF-α: 3262 (TNF-α inducer), 3267 (TNF-α not inducer) and an attenuated vaccine strain (strain Deventer, PorcilisPRRS, Merck) that replicates scarcely in PAM. |
| 442 | 24534144 | Thus, in PAM infected with PRRSV strain 3262 the proportion of TLR3+ cells significantly increased from 24h compared with the controls; in contrast strain 3267 resulted in a lower proportion of TLR3+ PAM. |
| 443 | 24573220 | We have investigated whether poly(I:C) Toll-like receptor 3 (TLR3) and resiquimod Toll-like receptor 7 (TLR7) agonists can serve as vaccine adjuvants and promote the efficiency of therapeutic DNA vaccination against tumors expressing the human papilloma virus 16 (HPV-16) E7 protein. |
| 444 | 24573220 | TLR3 and TLR7 agonists can be used to enhance the immune response to DNA vaccine immunogens. |
| 445 | 24573220 | We have investigated whether poly(I:C) Toll-like receptor 3 (TLR3) and resiquimod Toll-like receptor 7 (TLR7) agonists can serve as vaccine adjuvants and promote the efficiency of therapeutic DNA vaccination against tumors expressing the human papilloma virus 16 (HPV-16) E7 protein. |
| 446 | 24573220 | TLR3 and TLR7 agonists can be used to enhance the immune response to DNA vaccine immunogens. |
| 447 | 24739759 | Induction of antigen-specific immunity with a vaccine targeting NY-ESO-1 to the dendritic cell receptor DEC-205. |
| 448 | 24739759 | CDX-1401 is a vaccine composed of a human mAb specific for DEC-205 fused to the full-length tumor antigen NY-ESO-1. |
| 449 | 24739759 | This phase 1 trial assessed the safety, immunogenicity, and clinical activity of escalating doses of CDX-1401 with the Toll-like receptor (TLR) agonists resiquimod (TLR7/8) and Hiltonol (poly-ICLC, TLR3) in 45 patients with advanced malignancies refractory to available therapies. |
| 450 | 24825342 | Topical rather than intradermal application of the TLR7 ligand imiquimod leads to human dermal dendritic cell maturation and CD8+ T-cell cross-priming. |
| 451 | 24825342 | Moreover, Aldara-treated DCs showed highest levels of the costimulatory molecules CD86, CD83, CD40, and CD70. |
| 452 | 24825342 | When combined with intradermal peptide vaccination, Aldara-stimulated DCs showed enhanced cross-presentation of the melanoma antigen MART-1, which resulted in increased priming and activation of MART-1-specific CD8(+) T cells. |
| 453 | 24837764 | The Rv2034 protein indeed was highly immunogenic in HLA-DR3 transgenic mice and induced HLA-DR3 restricted IFN-γ(+)/TNF(+) and IFN-γ(+) CD4(+) T-cells, specific for an epitope encoded in peptide 31-50. |
| 454 | 24837764 | CD4(+) T-cell responses were optimally induced when using TLR9- and TLR3-ligand-adjuvants or CAF09. |
| 455 | 24837764 | Rv2034-specific antibodies were observed following immunization with either TLR2-, TLR3-, TLR4-, TLR5-, TLR7- or TLR9-ligands or CAF09. |
| 456 | 24853609 | MPL® (a TLR4 agonist) and the CpG oligodeoxynucleotide of 1018 ISS, a TLR9 agonist, show strong immunogenicity effects that make them appropriate adjuvants for allergy vaccines. |
| 457 | 24853609 | In addition, intranasal administration of AZD8848 (a TLR7 agonist) and VTX-1463 (a TLR8 agonist) as stand-alone therapeutics have revealed efficacy in the relief of the symptoms of AR patients. |
| 458 | 24996122 | All three IFN plasmids induced expression of antiviral genes (Mx, Viperin, ISG15 and IFIT5) at the muscle injection site while the control plasmid had little effect. |
| 459 | 24996122 | Injection of IFNc plasmid was found to induce expression of antiviral genes and receptors for virus RNA (RIG-I, TLR3 and TLR7) in head kidney from 1 to at least 8 weeks. |
| 460 | 25131730 | TLR7/8 agonists activate a mild immune response in rabbits through TLR8 but not TLR7. |
| 461 | 25131730 | Toll-like receptors 7 (TLR7) and 8 (TLR8) recognize viral single-stranded RNA and small molecular weight agonists to activate anti-viral immune responses. |
| 462 | 25131730 | TLR7 and TLR8 have been reported to be absent and pseudogenized, respectively, in rabbit (Oryctolagus cuniculus). |
| 463 | 25131730 | TLR7/8 agonists activate a mild immune response in rabbits through TLR8 but not TLR7. |
| 464 | 25131730 | Toll-like receptors 7 (TLR7) and 8 (TLR8) recognize viral single-stranded RNA and small molecular weight agonists to activate anti-viral immune responses. |
| 465 | 25131730 | TLR7 and TLR8 have been reported to be absent and pseudogenized, respectively, in rabbit (Oryctolagus cuniculus). |
| 466 | 25131730 | TLR7/8 agonists activate a mild immune response in rabbits through TLR8 but not TLR7. |
| 467 | 25131730 | Toll-like receptors 7 (TLR7) and 8 (TLR8) recognize viral single-stranded RNA and small molecular weight agonists to activate anti-viral immune responses. |
| 468 | 25131730 | TLR7 and TLR8 have been reported to be absent and pseudogenized, respectively, in rabbit (Oryctolagus cuniculus). |
| 469 | 25186185 | PRRS vaccine enhanced serum PRRSV-specific antibody, serum virus neutralizing (SVN) antibody and interferon-γ, interleukin (IL)-10 and IL-1β concentrations (P < 0.05). |
| 470 | 25186185 | The expression of TLR3 and TLR7 mRNA in lymph nodes were higher in TTS than in the control group after PRRS vaccine inoculation (P < 0.05). |
| 471 | 25192394 | Previous SAR investigations in several scaffolds of small molecule TLR7/8 activators pointed to the strict dependence of the selectivity for TLR7 vis-à-vis TLR8 on the electronic configurations of the heterocyclic systems, which we sought to examine quantitatively with the goal of developing "heuristics" to define structural requisites governing activity at TLR7 and/or TLR8. |
| 472 | 25192394 | Density functional theory based quantum chemical calculations on these compounds followed by linear discriminant analyses permitted the classification of inactive, TLR8-active, and TLR7/8 dual-active compounds, confirming the critical role of partial charges in determining biological activity. |
| 473 | 25192394 | Previous SAR investigations in several scaffolds of small molecule TLR7/8 activators pointed to the strict dependence of the selectivity for TLR7 vis-à-vis TLR8 on the electronic configurations of the heterocyclic systems, which we sought to examine quantitatively with the goal of developing "heuristics" to define structural requisites governing activity at TLR7 and/or TLR8. |
| 474 | 25192394 | Density functional theory based quantum chemical calculations on these compounds followed by linear discriminant analyses permitted the classification of inactive, TLR8-active, and TLR7/8 dual-active compounds, confirming the critical role of partial charges in determining biological activity. |
| 475 | 25211222 | The TIR-domain containing adaptor TRAM is required for TLR7 mediated RANTES production. |
| 476 | 25211222 | TRIF related adaptor molecule (TRAM) plays a vital role in TLR4 signaling by recruiting TRIF to TLR4, followed by endosomal trafficking of the complex and initiation of IRF3 dependent type I interferon production as well as NF-κB dependent pro-inflammatory cytokine production. |
| 477 | 25211222 | Towards understanding the molecular mechanisms that regulate TLR7 functionality, we found that TRAM(-/-) murine macrophages exhibited a transcriptional and translational impairment in TLR7 mediated RANTES, but not TNFα, production. |
| 478 | 25211222 | Suppression of TRAM expression in human macrophages also resulted in an impairment in TLR7 mediated CCL5 and IFN-β, but not TNFα, gene induction. |
| 479 | 25211222 | Additionally, TRAM-G2A dose-dependently inhibited TLR7 mediated activation of CCL5, IFNβ and IFNα reporter genes. |
| 480 | 25211222 | TLR7-mediated phosphorylation and nuclear translocation of IRF3 was impaired in TRAM(-/-) cells. |
| 481 | 25211222 | Finally, co-immunoprecipitation studies indicated that TRAM physically interacts with MyD88 upon TLR7 stimulation, but not under basal conditions. |
| 482 | 25211222 | Our results clearly demonstrate that TRAM plays a, hitherto unappreciated, role in TLR7 signaling through a novel signaling axis containing, but not limited to, MyD88, TRAM and IRF3 towards the activation of anti-viral immunity. |
| 483 | 25211222 | The TIR-domain containing adaptor TRAM is required for TLR7 mediated RANTES production. |
| 484 | 25211222 | TRIF related adaptor molecule (TRAM) plays a vital role in TLR4 signaling by recruiting TRIF to TLR4, followed by endosomal trafficking of the complex and initiation of IRF3 dependent type I interferon production as well as NF-κB dependent pro-inflammatory cytokine production. |
| 485 | 25211222 | Towards understanding the molecular mechanisms that regulate TLR7 functionality, we found that TRAM(-/-) murine macrophages exhibited a transcriptional and translational impairment in TLR7 mediated RANTES, but not TNFα, production. |
| 486 | 25211222 | Suppression of TRAM expression in human macrophages also resulted in an impairment in TLR7 mediated CCL5 and IFN-β, but not TNFα, gene induction. |
| 487 | 25211222 | Additionally, TRAM-G2A dose-dependently inhibited TLR7 mediated activation of CCL5, IFNβ and IFNα reporter genes. |
| 488 | 25211222 | TLR7-mediated phosphorylation and nuclear translocation of IRF3 was impaired in TRAM(-/-) cells. |
| 489 | 25211222 | Finally, co-immunoprecipitation studies indicated that TRAM physically interacts with MyD88 upon TLR7 stimulation, but not under basal conditions. |
| 490 | 25211222 | Our results clearly demonstrate that TRAM plays a, hitherto unappreciated, role in TLR7 signaling through a novel signaling axis containing, but not limited to, MyD88, TRAM and IRF3 towards the activation of anti-viral immunity. |
| 491 | 25211222 | The TIR-domain containing adaptor TRAM is required for TLR7 mediated RANTES production. |
| 492 | 25211222 | TRIF related adaptor molecule (TRAM) plays a vital role in TLR4 signaling by recruiting TRIF to TLR4, followed by endosomal trafficking of the complex and initiation of IRF3 dependent type I interferon production as well as NF-κB dependent pro-inflammatory cytokine production. |
| 493 | 25211222 | Towards understanding the molecular mechanisms that regulate TLR7 functionality, we found that TRAM(-/-) murine macrophages exhibited a transcriptional and translational impairment in TLR7 mediated RANTES, but not TNFα, production. |
| 494 | 25211222 | Suppression of TRAM expression in human macrophages also resulted in an impairment in TLR7 mediated CCL5 and IFN-β, but not TNFα, gene induction. |
| 495 | 25211222 | Additionally, TRAM-G2A dose-dependently inhibited TLR7 mediated activation of CCL5, IFNβ and IFNα reporter genes. |
| 496 | 25211222 | TLR7-mediated phosphorylation and nuclear translocation of IRF3 was impaired in TRAM(-/-) cells. |
| 497 | 25211222 | Finally, co-immunoprecipitation studies indicated that TRAM physically interacts with MyD88 upon TLR7 stimulation, but not under basal conditions. |
| 498 | 25211222 | Our results clearly demonstrate that TRAM plays a, hitherto unappreciated, role in TLR7 signaling through a novel signaling axis containing, but not limited to, MyD88, TRAM and IRF3 towards the activation of anti-viral immunity. |
| 499 | 25211222 | The TIR-domain containing adaptor TRAM is required for TLR7 mediated RANTES production. |
| 500 | 25211222 | TRIF related adaptor molecule (TRAM) plays a vital role in TLR4 signaling by recruiting TRIF to TLR4, followed by endosomal trafficking of the complex and initiation of IRF3 dependent type I interferon production as well as NF-κB dependent pro-inflammatory cytokine production. |
| 501 | 25211222 | Towards understanding the molecular mechanisms that regulate TLR7 functionality, we found that TRAM(-/-) murine macrophages exhibited a transcriptional and translational impairment in TLR7 mediated RANTES, but not TNFα, production. |
| 502 | 25211222 | Suppression of TRAM expression in human macrophages also resulted in an impairment in TLR7 mediated CCL5 and IFN-β, but not TNFα, gene induction. |
| 503 | 25211222 | Additionally, TRAM-G2A dose-dependently inhibited TLR7 mediated activation of CCL5, IFNβ and IFNα reporter genes. |
| 504 | 25211222 | TLR7-mediated phosphorylation and nuclear translocation of IRF3 was impaired in TRAM(-/-) cells. |
| 505 | 25211222 | Finally, co-immunoprecipitation studies indicated that TRAM physically interacts with MyD88 upon TLR7 stimulation, but not under basal conditions. |
| 506 | 25211222 | Our results clearly demonstrate that TRAM plays a, hitherto unappreciated, role in TLR7 signaling through a novel signaling axis containing, but not limited to, MyD88, TRAM and IRF3 towards the activation of anti-viral immunity. |
| 507 | 25211222 | The TIR-domain containing adaptor TRAM is required for TLR7 mediated RANTES production. |
| 508 | 25211222 | TRIF related adaptor molecule (TRAM) plays a vital role in TLR4 signaling by recruiting TRIF to TLR4, followed by endosomal trafficking of the complex and initiation of IRF3 dependent type I interferon production as well as NF-κB dependent pro-inflammatory cytokine production. |
| 509 | 25211222 | Towards understanding the molecular mechanisms that regulate TLR7 functionality, we found that TRAM(-/-) murine macrophages exhibited a transcriptional and translational impairment in TLR7 mediated RANTES, but not TNFα, production. |
| 510 | 25211222 | Suppression of TRAM expression in human macrophages also resulted in an impairment in TLR7 mediated CCL5 and IFN-β, but not TNFα, gene induction. |
| 511 | 25211222 | Additionally, TRAM-G2A dose-dependently inhibited TLR7 mediated activation of CCL5, IFNβ and IFNα reporter genes. |
| 512 | 25211222 | TLR7-mediated phosphorylation and nuclear translocation of IRF3 was impaired in TRAM(-/-) cells. |
| 513 | 25211222 | Finally, co-immunoprecipitation studies indicated that TRAM physically interacts with MyD88 upon TLR7 stimulation, but not under basal conditions. |
| 514 | 25211222 | Our results clearly demonstrate that TRAM plays a, hitherto unappreciated, role in TLR7 signaling through a novel signaling axis containing, but not limited to, MyD88, TRAM and IRF3 towards the activation of anti-viral immunity. |
| 515 | 25211222 | The TIR-domain containing adaptor TRAM is required for TLR7 mediated RANTES production. |
| 516 | 25211222 | TRIF related adaptor molecule (TRAM) plays a vital role in TLR4 signaling by recruiting TRIF to TLR4, followed by endosomal trafficking of the complex and initiation of IRF3 dependent type I interferon production as well as NF-κB dependent pro-inflammatory cytokine production. |
| 517 | 25211222 | Towards understanding the molecular mechanisms that regulate TLR7 functionality, we found that TRAM(-/-) murine macrophages exhibited a transcriptional and translational impairment in TLR7 mediated RANTES, but not TNFα, production. |
| 518 | 25211222 | Suppression of TRAM expression in human macrophages also resulted in an impairment in TLR7 mediated CCL5 and IFN-β, but not TNFα, gene induction. |
| 519 | 25211222 | Additionally, TRAM-G2A dose-dependently inhibited TLR7 mediated activation of CCL5, IFNβ and IFNα reporter genes. |
| 520 | 25211222 | TLR7-mediated phosphorylation and nuclear translocation of IRF3 was impaired in TRAM(-/-) cells. |
| 521 | 25211222 | Finally, co-immunoprecipitation studies indicated that TRAM physically interacts with MyD88 upon TLR7 stimulation, but not under basal conditions. |
| 522 | 25211222 | Our results clearly demonstrate that TRAM plays a, hitherto unappreciated, role in TLR7 signaling through a novel signaling axis containing, but not limited to, MyD88, TRAM and IRF3 towards the activation of anti-viral immunity. |
| 523 | 25211222 | The TIR-domain containing adaptor TRAM is required for TLR7 mediated RANTES production. |
| 524 | 25211222 | TRIF related adaptor molecule (TRAM) plays a vital role in TLR4 signaling by recruiting TRIF to TLR4, followed by endosomal trafficking of the complex and initiation of IRF3 dependent type I interferon production as well as NF-κB dependent pro-inflammatory cytokine production. |
| 525 | 25211222 | Towards understanding the molecular mechanisms that regulate TLR7 functionality, we found that TRAM(-/-) murine macrophages exhibited a transcriptional and translational impairment in TLR7 mediated RANTES, but not TNFα, production. |
| 526 | 25211222 | Suppression of TRAM expression in human macrophages also resulted in an impairment in TLR7 mediated CCL5 and IFN-β, but not TNFα, gene induction. |
| 527 | 25211222 | Additionally, TRAM-G2A dose-dependently inhibited TLR7 mediated activation of CCL5, IFNβ and IFNα reporter genes. |
| 528 | 25211222 | TLR7-mediated phosphorylation and nuclear translocation of IRF3 was impaired in TRAM(-/-) cells. |
| 529 | 25211222 | Finally, co-immunoprecipitation studies indicated that TRAM physically interacts with MyD88 upon TLR7 stimulation, but not under basal conditions. |
| 530 | 25211222 | Our results clearly demonstrate that TRAM plays a, hitherto unappreciated, role in TLR7 signaling through a novel signaling axis containing, but not limited to, MyD88, TRAM and IRF3 towards the activation of anti-viral immunity. |
| 531 | 25214510 | Here, we demonstrate in 2 patients that treatment with interleukin 7, JC polyomavirus (JCV) capsid protein VP1, and a Toll-like receptor 7 agonist used as adjuvant, was well tolerated, and showed a very favorable safety profile and unexpected efficacy that warrant further investigation. |
| 532 | 25229618 | A humanized TLR7/TLR8 transgenic mouse line was engineered for studies using TLR7/8 ligands as vaccine adjuvants. |
| 533 | 25229618 | Illness may be caused by constitutive activation of human TLR7 or TLR8 in the bacterial artificial chromosome positive mice as increased TLR7 and TLR8 expression or activation has previously been implicated in autoimmune disease. |
| 534 | 25229618 | A humanized TLR7/TLR8 transgenic mouse line was engineered for studies using TLR7/8 ligands as vaccine adjuvants. |
| 535 | 25229618 | Illness may be caused by constitutive activation of human TLR7 or TLR8 in the bacterial artificial chromosome positive mice as increased TLR7 and TLR8 expression or activation has previously been implicated in autoimmune disease. |
| 536 | 25248345 | The concentrations of human TNF-α, IL-1β/IL-1F2, IL-6, and IL-10 were measured by a high sensitivity enzyme-linked immunosorbent assay. |
| 537 | 25248345 | The soluble forms of TLR-2, TLR-4, and TLR-7 were determined in serum samples by ELISA as well. |
| 538 | 25343487 | A mouse immunogenicity study was conducted using a stable oil-in-water emulsion (SE) of CS/D in combination with the Toll-Like Receptor 4 (TLR4) agonist Glucopyranosyl Lipid A (GLA/SE), or one of two TLR7/8 agonists: R848 (un-conjugated) or 3M-051 (covalently conjugated). |
| 539 | 25343487 | Our data indicated that the cGMP-grade, soluble CS/D antigen combined with the TLR4-containing adjuvant GLA/SE warrants further evaluation for protective responses in humans. |
| 540 | 25369126 | We examined the replication of PPRV in peripheral blood mononuclear cells (PBMC) of Indian domestic goats and water buffalo and demonstrated that the levels of TLR3 and TLR7 and downstream signalling molecules correlation with susceptibility vs resistance. |
| 541 | 25369126 | Upon stimulation of PBMC with synthetic TLR3 and TLR7 agonists or PPRV, the levels of proinflammatory cytokines were found to be significantly higher while immunosuppressive interleukin (IL) 10 levels were lower in PPRV resistant Kanni and Salem Black breeds and water buffalo at transcriptional level, correlating with reduced viralloads in infected PBMC. |
| 542 | 25369126 | We examined the replication of PPRV in peripheral blood mononuclear cells (PBMC) of Indian domestic goats and water buffalo and demonstrated that the levels of TLR3 and TLR7 and downstream signalling molecules correlation with susceptibility vs resistance. |
| 543 | 25369126 | Upon stimulation of PBMC with synthetic TLR3 and TLR7 agonists or PPRV, the levels of proinflammatory cytokines were found to be significantly higher while immunosuppressive interleukin (IL) 10 levels were lower in PPRV resistant Kanni and Salem Black breeds and water buffalo at transcriptional level, correlating with reduced viralloads in infected PBMC. |
| 544 | 25500018 | Lipopolysaccharide (LPS) and resiquimod (R-848) are TLR agonists that are recognized by TLR4 and TLR7, respectively. |
| 545 | 25500018 | LPS and R-848 synergistically up-regulated the transcripts of interferon-β (IFN-β), IFN-γ, IL-4 and IL-1β as compared to the individual response (P<0.05). |
| 546 | 25536171 | B cell TLR1/2, TLR4, TLR7 and TLR9 interact in induction of class switch DNA recombination: modulation by BCR and CD40, and relevance to T-independent antibody responses. |
| 547 | 25536171 | Here, we have addressed cross-regulation between two different TLRs or between a TLR and CD40 in CSR induction by using a B cell stimulation system involving lipopolysaccharides (LPS). |
| 548 | 25536171 | Consistent with the requirement for dual TLR and BCR engagement in CSR induction, LPS, which engages TLR4 through its lipid A moiety, triggered cytosolic Ca2+ flux in B cells through its BCR-engaging polysaccharidic moiety. |
| 549 | 25536171 | In the presence of BCR crosslinking, LPS synergized with a TLR1/2 ligand (Pam3CSK4) in CSR induction, but much less efficiently with a TLR7 (R-848) or TLR9 (CpG) ligand. |
| 550 | 25536171 | In the absence of BCR crosslinking, R-848 and CpG, which per se induced marginal CSR, virtually abrogated CSR to IgG1, IgG2a, IgG2b, IgG3 and/or IgA, as induced by LPS or CD154 (CD40 ligand) plus IL-4, IFN-γ or TGF-β, and reduced secretion of class-switched Igs, without affecting B cell proliferation or IgM expression. |
| 551 | 25536171 | The CSR inhibition by TLR9 was associated with the reduction in AID expression and/or IgH germline IH-S-CH transcription, and required co-stimulation of B cells by CpG with LPS or CD154. |
| 552 | 25536171 | Unexpectedly, B cells also failed to undergo CSR or plasma cell differentiation when co-stimulated by LPS and CD154. |
| 553 | 25536171 | Overall, by addressing the interaction of TLR1/2, TLR4, TLR7 and TLR9 in the induction of CSR and modulation of TLR-dependent CSR by BCR and CD40, our study suggests the complexity of how different stimuli cross-regulate an important B cell differentiation process and an important role of TLRs in inducing effective T-independent antibody responses to microbial pathogens, allergens and vaccines. |
| 554 | 25536171 | B cell TLR1/2, TLR4, TLR7 and TLR9 interact in induction of class switch DNA recombination: modulation by BCR and CD40, and relevance to T-independent antibody responses. |
| 555 | 25536171 | Here, we have addressed cross-regulation between two different TLRs or between a TLR and CD40 in CSR induction by using a B cell stimulation system involving lipopolysaccharides (LPS). |
| 556 | 25536171 | Consistent with the requirement for dual TLR and BCR engagement in CSR induction, LPS, which engages TLR4 through its lipid A moiety, triggered cytosolic Ca2+ flux in B cells through its BCR-engaging polysaccharidic moiety. |
| 557 | 25536171 | In the presence of BCR crosslinking, LPS synergized with a TLR1/2 ligand (Pam3CSK4) in CSR induction, but much less efficiently with a TLR7 (R-848) or TLR9 (CpG) ligand. |
| 558 | 25536171 | In the absence of BCR crosslinking, R-848 and CpG, which per se induced marginal CSR, virtually abrogated CSR to IgG1, IgG2a, IgG2b, IgG3 and/or IgA, as induced by LPS or CD154 (CD40 ligand) plus IL-4, IFN-γ or TGF-β, and reduced secretion of class-switched Igs, without affecting B cell proliferation or IgM expression. |
| 559 | 25536171 | The CSR inhibition by TLR9 was associated with the reduction in AID expression and/or IgH germline IH-S-CH transcription, and required co-stimulation of B cells by CpG with LPS or CD154. |
| 560 | 25536171 | Unexpectedly, B cells also failed to undergo CSR or plasma cell differentiation when co-stimulated by LPS and CD154. |
| 561 | 25536171 | Overall, by addressing the interaction of TLR1/2, TLR4, TLR7 and TLR9 in the induction of CSR and modulation of TLR-dependent CSR by BCR and CD40, our study suggests the complexity of how different stimuli cross-regulate an important B cell differentiation process and an important role of TLRs in inducing effective T-independent antibody responses to microbial pathogens, allergens and vaccines. |
| 562 | 25536171 | B cell TLR1/2, TLR4, TLR7 and TLR9 interact in induction of class switch DNA recombination: modulation by BCR and CD40, and relevance to T-independent antibody responses. |
| 563 | 25536171 | Here, we have addressed cross-regulation between two different TLRs or between a TLR and CD40 in CSR induction by using a B cell stimulation system involving lipopolysaccharides (LPS). |
| 564 | 25536171 | Consistent with the requirement for dual TLR and BCR engagement in CSR induction, LPS, which engages TLR4 through its lipid A moiety, triggered cytosolic Ca2+ flux in B cells through its BCR-engaging polysaccharidic moiety. |
| 565 | 25536171 | In the presence of BCR crosslinking, LPS synergized with a TLR1/2 ligand (Pam3CSK4) in CSR induction, but much less efficiently with a TLR7 (R-848) or TLR9 (CpG) ligand. |
| 566 | 25536171 | In the absence of BCR crosslinking, R-848 and CpG, which per se induced marginal CSR, virtually abrogated CSR to IgG1, IgG2a, IgG2b, IgG3 and/or IgA, as induced by LPS or CD154 (CD40 ligand) plus IL-4, IFN-γ or TGF-β, and reduced secretion of class-switched Igs, without affecting B cell proliferation or IgM expression. |
| 567 | 25536171 | The CSR inhibition by TLR9 was associated with the reduction in AID expression and/or IgH germline IH-S-CH transcription, and required co-stimulation of B cells by CpG with LPS or CD154. |
| 568 | 25536171 | Unexpectedly, B cells also failed to undergo CSR or plasma cell differentiation when co-stimulated by LPS and CD154. |
| 569 | 25536171 | Overall, by addressing the interaction of TLR1/2, TLR4, TLR7 and TLR9 in the induction of CSR and modulation of TLR-dependent CSR by BCR and CD40, our study suggests the complexity of how different stimuli cross-regulate an important B cell differentiation process and an important role of TLRs in inducing effective T-independent antibody responses to microbial pathogens, allergens and vaccines. |
| 570 | 25548274 | Thus, LREL-induced increases in the expression levels of several cell surface marker proteins, production of inflammatory cytokines IL-12p40 and TNF-α, and activation and nuclear translocation of transcription factors, as was observed in the WT DCs, were completely abrogated in DCs derived from the TLR4(-/-) mice but not in DCs derived from the TLR2(-/-), TLR7(-/-), and TLR9(-/-) mice. |
| 571 | 25568203 | Synthetic Toll-like receptor 4 (TLR4) and TLR7 ligands as influenza virus vaccine adjuvants induce rapid, sustained, and broadly protective responses. |
| 572 | 25633712 | Patients with TLR7 SNP rs179008 had a greater likelihood of developing NY-ESO-1-specific CD8⁺ responses. |
| 573 | 25698055 | In vitro evaluation of the piperidinyl-substituted oxoadenines 3a-g in human TLR7- or TLR8-transfected HEK293 cells and in human PBMCs indicated that TLR7/8 selectivity/potency and cytokine induction can be modulated by varying the length of the alkyl linker. |
| 574 | 25737587 | We also showed that the RLR pathway was dampened by the activities of interleukin-1 receptor-associated kinases 1 and 4 (IRAK1 and IRAK4), which are downstream effectors of the TLR7 pathway, suggesting that both kinases play opposing roles downstream of specific PRRs. |
| 575 | 25775582 | Immunomodulatory nucleic acids act by agonizing or antagonizing endosomal toll-like receptors (TLR3, TLR7/8, and TLR9), proteins involved in innate immune signaling. |
| 576 | 25805409 | The results showed that the mRNA and protein levels of TLR2, TLR4 and TLR7 were upregulated in response to CSFV infection, but TLR3 remained unchanged, and was downregulated after infection with the C strain and the Shimen virus, respectively. |
| 577 | 25805409 | The Shimen strain infection resulted in a significant activation of IFN regulatory factor IRF7 and suppression of IRF3. |
| 578 | 25990580 | A conjugate of octamer-binding transcription factor 4 and toll-like receptor 7 agonist prevents the growth and metastasis of testis embryonic carcinoma. |
| 579 | 26054788 | Despite this limitation, increased IFN-1, TLR-7 and IgM gene expression was detected by qRT-PCR in kidney of vaccinated fish when a 10 μg dose of the oral pIRF1A-G vaccine was administered. |
| 580 | 26054788 | In contrast, significant Mx-1, Vig-1, Vig-2, TLR-3 and TLR-8 gene expression was only detected when higher doses of pIRF1A-G (50 and 100 μg) were orally administered. |
| 581 | 26054788 | The pIRF1A-G vaccine also induced the expression of several markers of the adaptive immune response (CD4, CD8, IgM and IgT) in kidney and spleen of immunized fish in a dose-dependent manner. |
| 582 | 26182986 | We isolated RNA from peripheral blood mononuclear cells and, with PCR, detected transcripts for TLRs 2, 3, 4, 5, 6, 7, 8, 9, 10 and 13. |
| 583 | 26182986 | Stimulation of the mononuclear cells with agonists to these TLRs increased the expression of downstream TLR signaling products (IL1α, IL6, IL12A and IFNβ). |
| 584 | 26188153 | In this study, we explored the underlying mechanisms concerning the interaction between Coa-ASC16 and the immune system and we found that the whole inflammatory response elicited by Coa-ASC16 (leukocyte recruitment and IL-1β, IL-6 and IL-12 production) was dependent on the MyD88 protein. |
| 585 | 26188153 | TLR2, TLR4, TLR7 and NLRP3-inflammasome signaling were not required for induction of this inflammatory response. |
| 586 | 26188153 | In addition, Coa-ASC16 revealed an intrinsic adjuvant activity which was affected by MyD88 and IL-6 absence. |
| 587 | 26297760 | Macrophages, but not pDC or mDC, had suppressed capacity to induce IFN-γ release from CD4 T cells in acute infection, even after stimulation with virus-encoded TLR7/8 ligand. |
| 588 | 26297760 | TLR7/8-stimulated pDC, mDC and macrophages all produced IL-12 in T cell cocultures, which was suppressed in chronic infection. |
| 589 | 26395101 | In response to microbial pattern molecules, these DCs upgrade the maturation stage sufficient to improve cross-presentation of exogenous Ag, and upregulation of MHC and costimulators, allowing CD4/CD8 T cells to proliferate and liberating cytokines/chemokines that support lymphocyte attraction and survival. |
| 590 | 26395101 | Mouse CD8α(+) DCs express TLR7 and TLR9 in addition to the TLR2 family (TLR1, 2, and 6) and TLR3, whereas human CD141(+) DCs exclusively express the TLR2 family and TLR3. |
| 591 | 26395101 | In contrast, TLR2 and TLR3 are similarly expressed in both human and mouse Ag-presenting DCs. |
| 592 | 26395101 | Bacillus Calmette-Guerin peptidoglycan and polyinosinic-polycytidylic acid are representative agonists for TLR2 and TLR3, respectively, although they additionally stimulate cytoplasmic sensors: their functional specificities may not be limited to the relevant TLRs. |
| 593 | 26395101 | We herein summarize the history and perspectives of TLR2 and TLR3 agonists in vaccine-adjuvant immunotherapy for cancer. |