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Gene Information
Gene symbol: TLR2
Gene name: toll-like receptor 2
HGNC ID: 11848
Synonyms: TIL4, CD282
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 10452971 | Transfection of TLR2 into cell lines conferred responsiveness to lipoproteins, lipopeptides, and sonicated B. burgdorferi, as measured by nuclear translocation of NF-kappaB and cytokine production. |
| 2 | 10452971 | Futhermore, TLR2-dependent signaling by lipoproteins was facilitated by CD14. |
| 3 | 10452971 | Transfection of TLR2 into cell lines conferred responsiveness to lipoproteins, lipopeptides, and sonicated B. burgdorferi, as measured by nuclear translocation of NF-kappaB and cytokine production. |
| 4 | 10452971 | Futhermore, TLR2-dependent signaling by lipoproteins was facilitated by CD14. |
| 5 | 11163461 | The signal transduction cascade for this response is becoming defined and includes CD14, Toll-like receptor 2, NFkB, and cytokine production. |
| 6 | 11441107 | Cooperation of Toll-like receptor 2 and 6 for cellular activation by soluble tuberculosis factor and Borrelia burgdorferi outer surface protein A lipoprotein: role of Toll-interacting protein and IL-1 receptor signaling molecules in Toll-like receptor 2 signaling. |
| 7 | 11441107 | Toll-like receptor 2 (TLR2) and TLR4 play important roles in innate immune responses to various microbial agents. |
| 8 | 11441107 | We have previously shown that human dermal endothelial cells (HMEC) express TLR4, but very little TLR2, and respond to LPS, but not to Mycobacterium tuberculosis 19-kDa lipoprotein, unless transfected with TLR2. |
| 9 | 11441107 | We further characterized the signaling pathway in response to STF, OspA-L, and PSM in TLR2-transfected HMEC. |
| 10 | 11441107 | The TLR2 signaling pathway for NF-kappaB trans-activation shares the IL-1R signaling molecules. |
| 11 | 11441107 | Dominant negative constructs of TLR2 or TLR6 inhibit the responses of STF and OspA-L as well as PSM in TLR2-transfected HMEC, supporting the concept of functional cooperation between TLR2 and TLR6 for all these TLR2 ligands. |
| 12 | 11441107 | Moreover, we show that Toll-interacting protein (Tollip) coimmunoprecipitates with TLR2 and TLR4 using HEK 293 cells, and overexpression of Tollip inhibits NF-kappaB activation in response to TLR2 and TLR4 signaling. |
| 13 | 11441107 | Collectively, these findings suggest that there is functional interaction between TLR2 and TLR6 in the cellular response to STF and OspA-L in addition to S. epidermidis (PSM) Ags, and that engagement of TLR2 triggers a signaling cascade, which shares the IL-1R signaling molecules, similar to the TLR4-LPS signaling cascade. |
| 14 | 11441107 | Our data also suggest that Tollip may be an important constituent of both the TLR2 and TLR4 signaling pathways. |
| 15 | 11441107 | Cooperation of Toll-like receptor 2 and 6 for cellular activation by soluble tuberculosis factor and Borrelia burgdorferi outer surface protein A lipoprotein: role of Toll-interacting protein and IL-1 receptor signaling molecules in Toll-like receptor 2 signaling. |
| 16 | 11441107 | Toll-like receptor 2 (TLR2) and TLR4 play important roles in innate immune responses to various microbial agents. |
| 17 | 11441107 | We have previously shown that human dermal endothelial cells (HMEC) express TLR4, but very little TLR2, and respond to LPS, but not to Mycobacterium tuberculosis 19-kDa lipoprotein, unless transfected with TLR2. |
| 18 | 11441107 | We further characterized the signaling pathway in response to STF, OspA-L, and PSM in TLR2-transfected HMEC. |
| 19 | 11441107 | The TLR2 signaling pathway for NF-kappaB trans-activation shares the IL-1R signaling molecules. |
| 20 | 11441107 | Dominant negative constructs of TLR2 or TLR6 inhibit the responses of STF and OspA-L as well as PSM in TLR2-transfected HMEC, supporting the concept of functional cooperation between TLR2 and TLR6 for all these TLR2 ligands. |
| 21 | 11441107 | Moreover, we show that Toll-interacting protein (Tollip) coimmunoprecipitates with TLR2 and TLR4 using HEK 293 cells, and overexpression of Tollip inhibits NF-kappaB activation in response to TLR2 and TLR4 signaling. |
| 22 | 11441107 | Collectively, these findings suggest that there is functional interaction between TLR2 and TLR6 in the cellular response to STF and OspA-L in addition to S. epidermidis (PSM) Ags, and that engagement of TLR2 triggers a signaling cascade, which shares the IL-1R signaling molecules, similar to the TLR4-LPS signaling cascade. |
| 23 | 11441107 | Our data also suggest that Tollip may be an important constituent of both the TLR2 and TLR4 signaling pathways. |
| 24 | 11441107 | Cooperation of Toll-like receptor 2 and 6 for cellular activation by soluble tuberculosis factor and Borrelia burgdorferi outer surface protein A lipoprotein: role of Toll-interacting protein and IL-1 receptor signaling molecules in Toll-like receptor 2 signaling. |
| 25 | 11441107 | Toll-like receptor 2 (TLR2) and TLR4 play important roles in innate immune responses to various microbial agents. |
| 26 | 11441107 | We have previously shown that human dermal endothelial cells (HMEC) express TLR4, but very little TLR2, and respond to LPS, but not to Mycobacterium tuberculosis 19-kDa lipoprotein, unless transfected with TLR2. |
| 27 | 11441107 | We further characterized the signaling pathway in response to STF, OspA-L, and PSM in TLR2-transfected HMEC. |
| 28 | 11441107 | The TLR2 signaling pathway for NF-kappaB trans-activation shares the IL-1R signaling molecules. |
| 29 | 11441107 | Dominant negative constructs of TLR2 or TLR6 inhibit the responses of STF and OspA-L as well as PSM in TLR2-transfected HMEC, supporting the concept of functional cooperation between TLR2 and TLR6 for all these TLR2 ligands. |
| 30 | 11441107 | Moreover, we show that Toll-interacting protein (Tollip) coimmunoprecipitates with TLR2 and TLR4 using HEK 293 cells, and overexpression of Tollip inhibits NF-kappaB activation in response to TLR2 and TLR4 signaling. |
| 31 | 11441107 | Collectively, these findings suggest that there is functional interaction between TLR2 and TLR6 in the cellular response to STF and OspA-L in addition to S. epidermidis (PSM) Ags, and that engagement of TLR2 triggers a signaling cascade, which shares the IL-1R signaling molecules, similar to the TLR4-LPS signaling cascade. |
| 32 | 11441107 | Our data also suggest that Tollip may be an important constituent of both the TLR2 and TLR4 signaling pathways. |
| 33 | 11441107 | Cooperation of Toll-like receptor 2 and 6 for cellular activation by soluble tuberculosis factor and Borrelia burgdorferi outer surface protein A lipoprotein: role of Toll-interacting protein and IL-1 receptor signaling molecules in Toll-like receptor 2 signaling. |
| 34 | 11441107 | Toll-like receptor 2 (TLR2) and TLR4 play important roles in innate immune responses to various microbial agents. |
| 35 | 11441107 | We have previously shown that human dermal endothelial cells (HMEC) express TLR4, but very little TLR2, and respond to LPS, but not to Mycobacterium tuberculosis 19-kDa lipoprotein, unless transfected with TLR2. |
| 36 | 11441107 | We further characterized the signaling pathway in response to STF, OspA-L, and PSM in TLR2-transfected HMEC. |
| 37 | 11441107 | The TLR2 signaling pathway for NF-kappaB trans-activation shares the IL-1R signaling molecules. |
| 38 | 11441107 | Dominant negative constructs of TLR2 or TLR6 inhibit the responses of STF and OspA-L as well as PSM in TLR2-transfected HMEC, supporting the concept of functional cooperation between TLR2 and TLR6 for all these TLR2 ligands. |
| 39 | 11441107 | Moreover, we show that Toll-interacting protein (Tollip) coimmunoprecipitates with TLR2 and TLR4 using HEK 293 cells, and overexpression of Tollip inhibits NF-kappaB activation in response to TLR2 and TLR4 signaling. |
| 40 | 11441107 | Collectively, these findings suggest that there is functional interaction between TLR2 and TLR6 in the cellular response to STF and OspA-L in addition to S. epidermidis (PSM) Ags, and that engagement of TLR2 triggers a signaling cascade, which shares the IL-1R signaling molecules, similar to the TLR4-LPS signaling cascade. |
| 41 | 11441107 | Our data also suggest that Tollip may be an important constituent of both the TLR2 and TLR4 signaling pathways. |
| 42 | 11441107 | Cooperation of Toll-like receptor 2 and 6 for cellular activation by soluble tuberculosis factor and Borrelia burgdorferi outer surface protein A lipoprotein: role of Toll-interacting protein and IL-1 receptor signaling molecules in Toll-like receptor 2 signaling. |
| 43 | 11441107 | Toll-like receptor 2 (TLR2) and TLR4 play important roles in innate immune responses to various microbial agents. |
| 44 | 11441107 | We have previously shown that human dermal endothelial cells (HMEC) express TLR4, but very little TLR2, and respond to LPS, but not to Mycobacterium tuberculosis 19-kDa lipoprotein, unless transfected with TLR2. |
| 45 | 11441107 | We further characterized the signaling pathway in response to STF, OspA-L, and PSM in TLR2-transfected HMEC. |
| 46 | 11441107 | The TLR2 signaling pathway for NF-kappaB trans-activation shares the IL-1R signaling molecules. |
| 47 | 11441107 | Dominant negative constructs of TLR2 or TLR6 inhibit the responses of STF and OspA-L as well as PSM in TLR2-transfected HMEC, supporting the concept of functional cooperation between TLR2 and TLR6 for all these TLR2 ligands. |
| 48 | 11441107 | Moreover, we show that Toll-interacting protein (Tollip) coimmunoprecipitates with TLR2 and TLR4 using HEK 293 cells, and overexpression of Tollip inhibits NF-kappaB activation in response to TLR2 and TLR4 signaling. |
| 49 | 11441107 | Collectively, these findings suggest that there is functional interaction between TLR2 and TLR6 in the cellular response to STF and OspA-L in addition to S. epidermidis (PSM) Ags, and that engagement of TLR2 triggers a signaling cascade, which shares the IL-1R signaling molecules, similar to the TLR4-LPS signaling cascade. |
| 50 | 11441107 | Our data also suggest that Tollip may be an important constituent of both the TLR2 and TLR4 signaling pathways. |
| 51 | 11441107 | Cooperation of Toll-like receptor 2 and 6 for cellular activation by soluble tuberculosis factor and Borrelia burgdorferi outer surface protein A lipoprotein: role of Toll-interacting protein and IL-1 receptor signaling molecules in Toll-like receptor 2 signaling. |
| 52 | 11441107 | Toll-like receptor 2 (TLR2) and TLR4 play important roles in innate immune responses to various microbial agents. |
| 53 | 11441107 | We have previously shown that human dermal endothelial cells (HMEC) express TLR4, but very little TLR2, and respond to LPS, but not to Mycobacterium tuberculosis 19-kDa lipoprotein, unless transfected with TLR2. |
| 54 | 11441107 | We further characterized the signaling pathway in response to STF, OspA-L, and PSM in TLR2-transfected HMEC. |
| 55 | 11441107 | The TLR2 signaling pathway for NF-kappaB trans-activation shares the IL-1R signaling molecules. |
| 56 | 11441107 | Dominant negative constructs of TLR2 or TLR6 inhibit the responses of STF and OspA-L as well as PSM in TLR2-transfected HMEC, supporting the concept of functional cooperation between TLR2 and TLR6 for all these TLR2 ligands. |
| 57 | 11441107 | Moreover, we show that Toll-interacting protein (Tollip) coimmunoprecipitates with TLR2 and TLR4 using HEK 293 cells, and overexpression of Tollip inhibits NF-kappaB activation in response to TLR2 and TLR4 signaling. |
| 58 | 11441107 | Collectively, these findings suggest that there is functional interaction between TLR2 and TLR6 in the cellular response to STF and OspA-L in addition to S. epidermidis (PSM) Ags, and that engagement of TLR2 triggers a signaling cascade, which shares the IL-1R signaling molecules, similar to the TLR4-LPS signaling cascade. |
| 59 | 11441107 | Our data also suggest that Tollip may be an important constituent of both the TLR2 and TLR4 signaling pathways. |
| 60 | 11441107 | Cooperation of Toll-like receptor 2 and 6 for cellular activation by soluble tuberculosis factor and Borrelia burgdorferi outer surface protein A lipoprotein: role of Toll-interacting protein and IL-1 receptor signaling molecules in Toll-like receptor 2 signaling. |
| 61 | 11441107 | Toll-like receptor 2 (TLR2) and TLR4 play important roles in innate immune responses to various microbial agents. |
| 62 | 11441107 | We have previously shown that human dermal endothelial cells (HMEC) express TLR4, but very little TLR2, and respond to LPS, but not to Mycobacterium tuberculosis 19-kDa lipoprotein, unless transfected with TLR2. |
| 63 | 11441107 | We further characterized the signaling pathway in response to STF, OspA-L, and PSM in TLR2-transfected HMEC. |
| 64 | 11441107 | The TLR2 signaling pathway for NF-kappaB trans-activation shares the IL-1R signaling molecules. |
| 65 | 11441107 | Dominant negative constructs of TLR2 or TLR6 inhibit the responses of STF and OspA-L as well as PSM in TLR2-transfected HMEC, supporting the concept of functional cooperation between TLR2 and TLR6 for all these TLR2 ligands. |
| 66 | 11441107 | Moreover, we show that Toll-interacting protein (Tollip) coimmunoprecipitates with TLR2 and TLR4 using HEK 293 cells, and overexpression of Tollip inhibits NF-kappaB activation in response to TLR2 and TLR4 signaling. |
| 67 | 11441107 | Collectively, these findings suggest that there is functional interaction between TLR2 and TLR6 in the cellular response to STF and OspA-L in addition to S. epidermidis (PSM) Ags, and that engagement of TLR2 triggers a signaling cascade, which shares the IL-1R signaling molecules, similar to the TLR4-LPS signaling cascade. |
| 68 | 11441107 | Our data also suggest that Tollip may be an important constituent of both the TLR2 and TLR4 signaling pathways. |
| 69 | 11441107 | Cooperation of Toll-like receptor 2 and 6 for cellular activation by soluble tuberculosis factor and Borrelia burgdorferi outer surface protein A lipoprotein: role of Toll-interacting protein and IL-1 receptor signaling molecules in Toll-like receptor 2 signaling. |
| 70 | 11441107 | Toll-like receptor 2 (TLR2) and TLR4 play important roles in innate immune responses to various microbial agents. |
| 71 | 11441107 | We have previously shown that human dermal endothelial cells (HMEC) express TLR4, but very little TLR2, and respond to LPS, but not to Mycobacterium tuberculosis 19-kDa lipoprotein, unless transfected with TLR2. |
| 72 | 11441107 | We further characterized the signaling pathway in response to STF, OspA-L, and PSM in TLR2-transfected HMEC. |
| 73 | 11441107 | The TLR2 signaling pathway for NF-kappaB trans-activation shares the IL-1R signaling molecules. |
| 74 | 11441107 | Dominant negative constructs of TLR2 or TLR6 inhibit the responses of STF and OspA-L as well as PSM in TLR2-transfected HMEC, supporting the concept of functional cooperation between TLR2 and TLR6 for all these TLR2 ligands. |
| 75 | 11441107 | Moreover, we show that Toll-interacting protein (Tollip) coimmunoprecipitates with TLR2 and TLR4 using HEK 293 cells, and overexpression of Tollip inhibits NF-kappaB activation in response to TLR2 and TLR4 signaling. |
| 76 | 11441107 | Collectively, these findings suggest that there is functional interaction between TLR2 and TLR6 in the cellular response to STF and OspA-L in addition to S. epidermidis (PSM) Ags, and that engagement of TLR2 triggers a signaling cascade, which shares the IL-1R signaling molecules, similar to the TLR4-LPS signaling cascade. |
| 77 | 11441107 | Our data also suggest that Tollip may be an important constituent of both the TLR2 and TLR4 signaling pathways. |
| 78 | 11441107 | Cooperation of Toll-like receptor 2 and 6 for cellular activation by soluble tuberculosis factor and Borrelia burgdorferi outer surface protein A lipoprotein: role of Toll-interacting protein and IL-1 receptor signaling molecules in Toll-like receptor 2 signaling. |
| 79 | 11441107 | Toll-like receptor 2 (TLR2) and TLR4 play important roles in innate immune responses to various microbial agents. |
| 80 | 11441107 | We have previously shown that human dermal endothelial cells (HMEC) express TLR4, but very little TLR2, and respond to LPS, but not to Mycobacterium tuberculosis 19-kDa lipoprotein, unless transfected with TLR2. |
| 81 | 11441107 | We further characterized the signaling pathway in response to STF, OspA-L, and PSM in TLR2-transfected HMEC. |
| 82 | 11441107 | The TLR2 signaling pathway for NF-kappaB trans-activation shares the IL-1R signaling molecules. |
| 83 | 11441107 | Dominant negative constructs of TLR2 or TLR6 inhibit the responses of STF and OspA-L as well as PSM in TLR2-transfected HMEC, supporting the concept of functional cooperation between TLR2 and TLR6 for all these TLR2 ligands. |
| 84 | 11441107 | Moreover, we show that Toll-interacting protein (Tollip) coimmunoprecipitates with TLR2 and TLR4 using HEK 293 cells, and overexpression of Tollip inhibits NF-kappaB activation in response to TLR2 and TLR4 signaling. |
| 85 | 11441107 | Collectively, these findings suggest that there is functional interaction between TLR2 and TLR6 in the cellular response to STF and OspA-L in addition to S. epidermidis (PSM) Ags, and that engagement of TLR2 triggers a signaling cascade, which shares the IL-1R signaling molecules, similar to the TLR4-LPS signaling cascade. |
| 86 | 11441107 | Our data also suggest that Tollip may be an important constituent of both the TLR2 and TLR4 signaling pathways. |
| 87 | 11823477 | This ability is dependent on MyD88 and Toll-like receptor (TLR)2 expression, as demonstrated by a lack of a response by B cells from MyD88 or TLR2 knockout mice to the porins. |
| 88 | 11823477 | Using previously described TLR2-dependent reporter constructs, these results were confirmed and were shown to be due to induction of NF-kappaB nuclear translocation. |
| 89 | 11823477 | This ability is dependent on MyD88 and Toll-like receptor (TLR)2 expression, as demonstrated by a lack of a response by B cells from MyD88 or TLR2 knockout mice to the porins. |
| 90 | 11823477 | Using previously described TLR2-dependent reporter constructs, these results were confirmed and were shown to be due to induction of NF-kappaB nuclear translocation. |
| 91 | 12091878 | Hyporesponsiveness to vaccination with Borrelia burgdorferi OspA in humans and in TLR1- and TLR2-deficient mice. |
| 92 | 12091878 | The macrophages of low responders produced less tumor necrosis factor-alpha and interleukin-6 after OspA stimulation and had lower cell-surface expression of Toll-like receptor (TLR) 1 as compared to normal cells, but normal expression of TLR2. |
| 93 | 12091878 | After OspA immunization, mice genetically deficient in either TLR2 (TLR2(-/-)) or TLR1 (TLR1(-/-)) produced low titers of antibodies against OspA. |
| 94 | 12091878 | Notably, macrophages from TLR2(-/-) mice were unresponsive to OspA and PGN, whereas those from TLR1(-/-) mice responded normally to PGN but not to OspA. |
| 95 | 12091878 | These data indicate that TLR1 and TLR2 are required for lipoprotein recognition and that defects in the TLR1/2 signaling pathway may account for human hyporesponsiveness to OspA vaccination. |
| 96 | 12091878 | Hyporesponsiveness to vaccination with Borrelia burgdorferi OspA in humans and in TLR1- and TLR2-deficient mice. |
| 97 | 12091878 | The macrophages of low responders produced less tumor necrosis factor-alpha and interleukin-6 after OspA stimulation and had lower cell-surface expression of Toll-like receptor (TLR) 1 as compared to normal cells, but normal expression of TLR2. |
| 98 | 12091878 | After OspA immunization, mice genetically deficient in either TLR2 (TLR2(-/-)) or TLR1 (TLR1(-/-)) produced low titers of antibodies against OspA. |
| 99 | 12091878 | Notably, macrophages from TLR2(-/-) mice were unresponsive to OspA and PGN, whereas those from TLR1(-/-) mice responded normally to PGN but not to OspA. |
| 100 | 12091878 | These data indicate that TLR1 and TLR2 are required for lipoprotein recognition and that defects in the TLR1/2 signaling pathway may account for human hyporesponsiveness to OspA vaccination. |
| 101 | 12091878 | Hyporesponsiveness to vaccination with Borrelia burgdorferi OspA in humans and in TLR1- and TLR2-deficient mice. |
| 102 | 12091878 | The macrophages of low responders produced less tumor necrosis factor-alpha and interleukin-6 after OspA stimulation and had lower cell-surface expression of Toll-like receptor (TLR) 1 as compared to normal cells, but normal expression of TLR2. |
| 103 | 12091878 | After OspA immunization, mice genetically deficient in either TLR2 (TLR2(-/-)) or TLR1 (TLR1(-/-)) produced low titers of antibodies against OspA. |
| 104 | 12091878 | Notably, macrophages from TLR2(-/-) mice were unresponsive to OspA and PGN, whereas those from TLR1(-/-) mice responded normally to PGN but not to OspA. |
| 105 | 12091878 | These data indicate that TLR1 and TLR2 are required for lipoprotein recognition and that defects in the TLR1/2 signaling pathway may account for human hyporesponsiveness to OspA vaccination. |
| 106 | 12091878 | Hyporesponsiveness to vaccination with Borrelia burgdorferi OspA in humans and in TLR1- and TLR2-deficient mice. |
| 107 | 12091878 | The macrophages of low responders produced less tumor necrosis factor-alpha and interleukin-6 after OspA stimulation and had lower cell-surface expression of Toll-like receptor (TLR) 1 as compared to normal cells, but normal expression of TLR2. |
| 108 | 12091878 | After OspA immunization, mice genetically deficient in either TLR2 (TLR2(-/-)) or TLR1 (TLR1(-/-)) produced low titers of antibodies against OspA. |
| 109 | 12091878 | Notably, macrophages from TLR2(-/-) mice were unresponsive to OspA and PGN, whereas those from TLR1(-/-) mice responded normally to PGN but not to OspA. |
| 110 | 12091878 | These data indicate that TLR1 and TLR2 are required for lipoprotein recognition and that defects in the TLR1/2 signaling pathway may account for human hyporesponsiveness to OspA vaccination. |
| 111 | 12091878 | Hyporesponsiveness to vaccination with Borrelia burgdorferi OspA in humans and in TLR1- and TLR2-deficient mice. |
| 112 | 12091878 | The macrophages of low responders produced less tumor necrosis factor-alpha and interleukin-6 after OspA stimulation and had lower cell-surface expression of Toll-like receptor (TLR) 1 as compared to normal cells, but normal expression of TLR2. |
| 113 | 12091878 | After OspA immunization, mice genetically deficient in either TLR2 (TLR2(-/-)) or TLR1 (TLR1(-/-)) produced low titers of antibodies against OspA. |
| 114 | 12091878 | Notably, macrophages from TLR2(-/-) mice were unresponsive to OspA and PGN, whereas those from TLR1(-/-) mice responded normally to PGN but not to OspA. |
| 115 | 12091878 | These data indicate that TLR1 and TLR2 are required for lipoprotein recognition and that defects in the TLR1/2 signaling pathway may account for human hyporesponsiveness to OspA vaccination. |
| 116 | 12163593 | The ability to activate cells via TLR2 by wild-type MV H protein is abolished by mutation of a single amino acid, asparagine at position 481 to tyrosine, as is found in attenuated strains, which is important for interaction with CD46, the receptor for these strains. |
| 117 | 12163593 | TLR2 activation by MV wild-type H protein stimulates induction of proinflammatory cytokines such as interleukin-6 (IL-6) in human monocytic cells and surface expression of CD150, the receptor for all MV strains. |
| 118 | 12163593 | Confirming the specificity of this interaction, wild-type H protein did not induce IL-6 release in macrophages from TLR2-/- mice. |
| 119 | 12163593 | The ability to activate cells via TLR2 by wild-type MV H protein is abolished by mutation of a single amino acid, asparagine at position 481 to tyrosine, as is found in attenuated strains, which is important for interaction with CD46, the receptor for these strains. |
| 120 | 12163593 | TLR2 activation by MV wild-type H protein stimulates induction of proinflammatory cytokines such as interleukin-6 (IL-6) in human monocytic cells and surface expression of CD150, the receptor for all MV strains. |
| 121 | 12163593 | Confirming the specificity of this interaction, wild-type H protein did not induce IL-6 release in macrophages from TLR2-/- mice. |
| 122 | 12163593 | The ability to activate cells via TLR2 by wild-type MV H protein is abolished by mutation of a single amino acid, asparagine at position 481 to tyrosine, as is found in attenuated strains, which is important for interaction with CD46, the receptor for these strains. |
| 123 | 12163593 | TLR2 activation by MV wild-type H protein stimulates induction of proinflammatory cytokines such as interleukin-6 (IL-6) in human monocytic cells and surface expression of CD150, the receptor for all MV strains. |
| 124 | 12163593 | Confirming the specificity of this interaction, wild-type H protein did not induce IL-6 release in macrophages from TLR2-/- mice. |
| 125 | 12270544 | Cell activation by synthetic lipopeptides of the hepatitis C virus (HCV)--core protein is mediated by toll like receptors (TLRs) 2 and 4. |
| 126 | 12270544 | The cause of enhanced immunogenicity of lipopeptides is largely unknown but members of the novel family of Toll like receptors (TLR) such as TLR2 and TLR4 have been shown to mediate activation of cells in response to bacterial lipopolysaccharide (LPS) and other lipidated bacterial or viral components. |
| 127 | 12270544 | We studied TLR-mediated activation by 14 synthetic lipopeptides corresponding to T cell epitopes on hepatitis C virus (HCV) core in human embryonic kidney cells (HEK293) transiently over-expressing TLR2 and in Ba/F3 mouse bone marrow cells stably transfected with TLR4 and the adaptor molecule MD-2. |
| 128 | 12270544 | Nine of the 14 lipopeptides also stimulated luciferase activity in the TLR4/MD-2 double-transfected Ba/F3 cells but not Ba/F3 control cells. |
| 129 | 12270544 | Overall, there was a close statistical correlation between TLR2 and TLR4/MD-2-mediated cell activation by the lipopeptides. |
| 130 | 12270544 | In contrast, the corresponding free peptides had no stimulatory effect on TLR2 nor on TLR4/MD-2 transfected cells. |
| 131 | 12270544 | Thus, lipopeptides but not their corresponding free peptides can activate cells via TLRs 2 and 4. |
| 132 | 12270544 | Cell activation by synthetic lipopeptides of the hepatitis C virus (HCV)--core protein is mediated by toll like receptors (TLRs) 2 and 4. |
| 133 | 12270544 | The cause of enhanced immunogenicity of lipopeptides is largely unknown but members of the novel family of Toll like receptors (TLR) such as TLR2 and TLR4 have been shown to mediate activation of cells in response to bacterial lipopolysaccharide (LPS) and other lipidated bacterial or viral components. |
| 134 | 12270544 | We studied TLR-mediated activation by 14 synthetic lipopeptides corresponding to T cell epitopes on hepatitis C virus (HCV) core in human embryonic kidney cells (HEK293) transiently over-expressing TLR2 and in Ba/F3 mouse bone marrow cells stably transfected with TLR4 and the adaptor molecule MD-2. |
| 135 | 12270544 | Nine of the 14 lipopeptides also stimulated luciferase activity in the TLR4/MD-2 double-transfected Ba/F3 cells but not Ba/F3 control cells. |
| 136 | 12270544 | Overall, there was a close statistical correlation between TLR2 and TLR4/MD-2-mediated cell activation by the lipopeptides. |
| 137 | 12270544 | In contrast, the corresponding free peptides had no stimulatory effect on TLR2 nor on TLR4/MD-2 transfected cells. |
| 138 | 12270544 | Thus, lipopeptides but not their corresponding free peptides can activate cells via TLRs 2 and 4. |
| 139 | 12270544 | Cell activation by synthetic lipopeptides of the hepatitis C virus (HCV)--core protein is mediated by toll like receptors (TLRs) 2 and 4. |
| 140 | 12270544 | The cause of enhanced immunogenicity of lipopeptides is largely unknown but members of the novel family of Toll like receptors (TLR) such as TLR2 and TLR4 have been shown to mediate activation of cells in response to bacterial lipopolysaccharide (LPS) and other lipidated bacterial or viral components. |
| 141 | 12270544 | We studied TLR-mediated activation by 14 synthetic lipopeptides corresponding to T cell epitopes on hepatitis C virus (HCV) core in human embryonic kidney cells (HEK293) transiently over-expressing TLR2 and in Ba/F3 mouse bone marrow cells stably transfected with TLR4 and the adaptor molecule MD-2. |
| 142 | 12270544 | Nine of the 14 lipopeptides also stimulated luciferase activity in the TLR4/MD-2 double-transfected Ba/F3 cells but not Ba/F3 control cells. |
| 143 | 12270544 | Overall, there was a close statistical correlation between TLR2 and TLR4/MD-2-mediated cell activation by the lipopeptides. |
| 144 | 12270544 | In contrast, the corresponding free peptides had no stimulatory effect on TLR2 nor on TLR4/MD-2 transfected cells. |
| 145 | 12270544 | Thus, lipopeptides but not their corresponding free peptides can activate cells via TLRs 2 and 4. |
| 146 | 12270544 | Cell activation by synthetic lipopeptides of the hepatitis C virus (HCV)--core protein is mediated by toll like receptors (TLRs) 2 and 4. |
| 147 | 12270544 | The cause of enhanced immunogenicity of lipopeptides is largely unknown but members of the novel family of Toll like receptors (TLR) such as TLR2 and TLR4 have been shown to mediate activation of cells in response to bacterial lipopolysaccharide (LPS) and other lipidated bacterial or viral components. |
| 148 | 12270544 | We studied TLR-mediated activation by 14 synthetic lipopeptides corresponding to T cell epitopes on hepatitis C virus (HCV) core in human embryonic kidney cells (HEK293) transiently over-expressing TLR2 and in Ba/F3 mouse bone marrow cells stably transfected with TLR4 and the adaptor molecule MD-2. |
| 149 | 12270544 | Nine of the 14 lipopeptides also stimulated luciferase activity in the TLR4/MD-2 double-transfected Ba/F3 cells but not Ba/F3 control cells. |
| 150 | 12270544 | Overall, there was a close statistical correlation between TLR2 and TLR4/MD-2-mediated cell activation by the lipopeptides. |
| 151 | 12270544 | In contrast, the corresponding free peptides had no stimulatory effect on TLR2 nor on TLR4/MD-2 transfected cells. |
| 152 | 12270544 | Thus, lipopeptides but not their corresponding free peptides can activate cells via TLRs 2 and 4. |
| 153 | 12270544 | Cell activation by synthetic lipopeptides of the hepatitis C virus (HCV)--core protein is mediated by toll like receptors (TLRs) 2 and 4. |
| 154 | 12270544 | The cause of enhanced immunogenicity of lipopeptides is largely unknown but members of the novel family of Toll like receptors (TLR) such as TLR2 and TLR4 have been shown to mediate activation of cells in response to bacterial lipopolysaccharide (LPS) and other lipidated bacterial or viral components. |
| 155 | 12270544 | We studied TLR-mediated activation by 14 synthetic lipopeptides corresponding to T cell epitopes on hepatitis C virus (HCV) core in human embryonic kidney cells (HEK293) transiently over-expressing TLR2 and in Ba/F3 mouse bone marrow cells stably transfected with TLR4 and the adaptor molecule MD-2. |
| 156 | 12270544 | Nine of the 14 lipopeptides also stimulated luciferase activity in the TLR4/MD-2 double-transfected Ba/F3 cells but not Ba/F3 control cells. |
| 157 | 12270544 | Overall, there was a close statistical correlation between TLR2 and TLR4/MD-2-mediated cell activation by the lipopeptides. |
| 158 | 12270544 | In contrast, the corresponding free peptides had no stimulatory effect on TLR2 nor on TLR4/MD-2 transfected cells. |
| 159 | 12270544 | Thus, lipopeptides but not their corresponding free peptides can activate cells via TLRs 2 and 4. |
| 160 | 12270544 | Cell activation by synthetic lipopeptides of the hepatitis C virus (HCV)--core protein is mediated by toll like receptors (TLRs) 2 and 4. |
| 161 | 12270544 | The cause of enhanced immunogenicity of lipopeptides is largely unknown but members of the novel family of Toll like receptors (TLR) such as TLR2 and TLR4 have been shown to mediate activation of cells in response to bacterial lipopolysaccharide (LPS) and other lipidated bacterial or viral components. |
| 162 | 12270544 | We studied TLR-mediated activation by 14 synthetic lipopeptides corresponding to T cell epitopes on hepatitis C virus (HCV) core in human embryonic kidney cells (HEK293) transiently over-expressing TLR2 and in Ba/F3 mouse bone marrow cells stably transfected with TLR4 and the adaptor molecule MD-2. |
| 163 | 12270544 | Nine of the 14 lipopeptides also stimulated luciferase activity in the TLR4/MD-2 double-transfected Ba/F3 cells but not Ba/F3 control cells. |
| 164 | 12270544 | Overall, there was a close statistical correlation between TLR2 and TLR4/MD-2-mediated cell activation by the lipopeptides. |
| 165 | 12270544 | In contrast, the corresponding free peptides had no stimulatory effect on TLR2 nor on TLR4/MD-2 transfected cells. |
| 166 | 12270544 | Thus, lipopeptides but not their corresponding free peptides can activate cells via TLRs 2 and 4. |
| 167 | 12540559 | We here report that BALB/c interleukin-4 knockout (IL-4(-/-)) mice are weakly overcolonized compared to the wt strain but that the IL-12(-/-) knockout results in a strong overcolonization (500%). |
| 168 | 12540559 | The IL-4(-/-) mutation caused a 50% reduction and the IL-12(-/-) knockout caused a 95% reduction compared to the wt colonization rate. |
| 169 | 12540559 | For C57BL/6J mice we further analyzed the IL-18(-/-) and Toll-like receptor 2 knockout mutations, which showed reductions to 66 and 57%, respectively, whereas mice with the IL-10(-/-) phenotype were hardly infected at all (5%). |
| 170 | 12540559 | In contrast, the tumor necrosis factor receptor knockout (p55(-/-) and p55/75(-/-)) mice showed an overcolonization compared to the C57BL/6J wt strain. |
| 171 | 12540559 | With exception of the low-level infected C57BL/6J IL-10(-/-) and IL-12(-/-) knockout mice, all knockout mutants were accessible to a prophylactic vaccination and their vaccination behavior was comparable to that of the wt strains. |
| 172 | 12686724 | Among those signaling pathways, activation of NF-kappaB leads to up-regulation of IL-1beta, IL-8 and TNF-alpha, mucin MUC2 and Toll-like receptor 2 (TLR2), whereas activation of p38 MAP kinase mediates not only up-regulation of inflammatory mediators and mucin MUC5AC but also down-regulation of TLR2. |
| 173 | 12686724 | Interestingly, NTHi-induced activation of the PI3K-Akt pathway, however, leads to inhibition of p38 mitogen-activated protein (MAP) kinase. |
| 174 | 12686724 | Moreover, the TGF-beta-Smad signaling pathway cooperates with NF-kappaB to mediate up-regulation of mucin MUC2. |
| 175 | 12686724 | Finally, glucocorticoids synergistically enhance NTHi-induced TLR2 expression via specific up-regulation of the MAP kinase phosphatase-1 that, in turn, leads to inactivation of p38 MAP kinase, the negative regulator for TLR2 expression. |
| 176 | 12686724 | Among those signaling pathways, activation of NF-kappaB leads to up-regulation of IL-1beta, IL-8 and TNF-alpha, mucin MUC2 and Toll-like receptor 2 (TLR2), whereas activation of p38 MAP kinase mediates not only up-regulation of inflammatory mediators and mucin MUC5AC but also down-regulation of TLR2. |
| 177 | 12686724 | Interestingly, NTHi-induced activation of the PI3K-Akt pathway, however, leads to inhibition of p38 mitogen-activated protein (MAP) kinase. |
| 178 | 12686724 | Moreover, the TGF-beta-Smad signaling pathway cooperates with NF-kappaB to mediate up-regulation of mucin MUC2. |
| 179 | 12686724 | Finally, glucocorticoids synergistically enhance NTHi-induced TLR2 expression via specific up-regulation of the MAP kinase phosphatase-1 that, in turn, leads to inactivation of p38 MAP kinase, the negative regulator for TLR2 expression. |
| 180 | 12763684 | Cells expressing Toll-like receptor (TLR), TLR2 in association with TLR1, TLR6 or some other unknown co-receptor can respond upon interaction with a large variety of microbial ligands. |
| 181 | 12803883 | Prostaglandins, interleukin-(IL-)10, and transforming growth factor-beta are other players of in vivo endotoxin tolerance. |
| 182 | 12803883 | Cross-tolerance between LPS, TLR2 specific ligands, IL-1 and TNF has been regularly reported. |
| 183 | 12804162 | TLR2 may form heterodimers with TLR6 to identify diacylated lipoproteins, while TLR2 works in concert with TLR1 to recognize triacylated lipoproteins such as OspA. |
| 184 | 12804162 | We will discuss the role of TLR1/2 in the development of responses to OspA in TLR1-and TLR2-deficient mice, and in selected individuals that received the OspA vaccine. |
| 185 | 12804162 | Moreover, TLR1- and TLR2-deficient mice did not develop significant levels of OspA antibodies following vaccination with OspA, providing a correlation with human hyporesponsiveness to OspA. |
| 186 | 12804162 | TLR2 may form heterodimers with TLR6 to identify diacylated lipoproteins, while TLR2 works in concert with TLR1 to recognize triacylated lipoproteins such as OspA. |
| 187 | 12804162 | We will discuss the role of TLR1/2 in the development of responses to OspA in TLR1-and TLR2-deficient mice, and in selected individuals that received the OspA vaccine. |
| 188 | 12804162 | Moreover, TLR1- and TLR2-deficient mice did not develop significant levels of OspA antibodies following vaccination with OspA, providing a correlation with human hyporesponsiveness to OspA. |
| 189 | 12804162 | TLR2 may form heterodimers with TLR6 to identify diacylated lipoproteins, while TLR2 works in concert with TLR1 to recognize triacylated lipoproteins such as OspA. |
| 190 | 12804162 | We will discuss the role of TLR1/2 in the development of responses to OspA in TLR1-and TLR2-deficient mice, and in selected individuals that received the OspA vaccine. |
| 191 | 12804162 | Moreover, TLR1- and TLR2-deficient mice did not develop significant levels of OspA antibodies following vaccination with OspA, providing a correlation with human hyporesponsiveness to OspA. |
| 192 | 12816980 | Cutting edge: link between innate and adaptive immunity: Toll-like receptor 2 internalizes antigen for presentation to CD4+ T cells and could be an efficient vaccine target. |
| 193 | 12816980 | We have studied whether targeting of TLR2 results in loading of MHC class II molecules and enhancement of CD4(+) T cell responses. |
| 194 | 12816980 | To dissociate MHC class II presentation from APC maturation, we have used an antagonistic, mouse anti-human TLR2 mAb (TL2.1) as ligand and measured proliferation of a mouse Ckappa-specific human CD4(+) T cell clone. |
| 195 | 12816980 | Cutting edge: link between innate and adaptive immunity: Toll-like receptor 2 internalizes antigen for presentation to CD4+ T cells and could be an efficient vaccine target. |
| 196 | 12816980 | We have studied whether targeting of TLR2 results in loading of MHC class II molecules and enhancement of CD4(+) T cell responses. |
| 197 | 12816980 | To dissociate MHC class II presentation from APC maturation, we have used an antagonistic, mouse anti-human TLR2 mAb (TL2.1) as ligand and measured proliferation of a mouse Ckappa-specific human CD4(+) T cell clone. |
| 198 | 12816980 | Cutting edge: link between innate and adaptive immunity: Toll-like receptor 2 internalizes antigen for presentation to CD4+ T cells and could be an efficient vaccine target. |
| 199 | 12816980 | We have studied whether targeting of TLR2 results in loading of MHC class II molecules and enhancement of CD4(+) T cell responses. |
| 200 | 12816980 | To dissociate MHC class II presentation from APC maturation, we have used an antagonistic, mouse anti-human TLR2 mAb (TL2.1) as ligand and measured proliferation of a mouse Ckappa-specific human CD4(+) T cell clone. |
| 201 | 12874015 | DCs generated from peripheral blood using granulocyte macrophage colony-stimulating factor and interleukin (IL)-4 showed immunophenotypes consistent with immature DCs (iDCs). |
| 202 | 12874015 | Furthermore, OK-DCs showed significantly higher production of IL-12 and IFN-gamma compared with DCs with other stimulations. |
| 203 | 12874015 | Furthermore, OK-432 does not activate nuclear factor kappaB through Toll-like receptor 2 or Toll-like receptor 4 in the indicator cell system; however, it induces IL-12 production through the beta(2) integrin system on DCs. |
| 204 | 12874236 | Heat-killed Brucella abortus induces TNF and IL-12p40 by distinct MyD88-dependent pathways: TNF, unlike IL-12p40 secretion, is Toll-like receptor 2 dependent. |
| 205 | 12874236 | Our results show that HKBA-mediated induction of IL-12p40 and TNF is dependent on the adapter molecule MyD88. |
| 206 | 12874236 | To identify the TLR involved in HKBA recognition, we examined HKBA responses in TLR2- and TLR4-deficient animals. |
| 207 | 12874236 | TNF responses to HKBA were TLR4 independent; however, the response in TLR2-deficient mice was significantly delayed and reduced, although not completely abolished. |
| 208 | 12874236 | Studies using Chinese hamster ovary/CD14 reporter cell lines stably transfected with either human TLR2 or human TLR4 confirmed the results seen with knockout mice, namely TLR2, but not TLR4, can mediate cellular activation by HKBA. |
| 209 | 12874236 | In addition, human embryonic kidney 293 cells, which do not respond to HKBA, were made responsive by transfecting TLR2, but not TLR4 or TLR9. |
| 210 | 12874236 | Taken together, our data demonstrate that MyD88-dependent pathways are crucial for activation by HKBA and that TLR2 plays a role in TNF, but not IL-12p40 pathways activated by this microbial product. |
| 211 | 12874236 | Heat-killed Brucella abortus induces TNF and IL-12p40 by distinct MyD88-dependent pathways: TNF, unlike IL-12p40 secretion, is Toll-like receptor 2 dependent. |
| 212 | 12874236 | Our results show that HKBA-mediated induction of IL-12p40 and TNF is dependent on the adapter molecule MyD88. |
| 213 | 12874236 | To identify the TLR involved in HKBA recognition, we examined HKBA responses in TLR2- and TLR4-deficient animals. |
| 214 | 12874236 | TNF responses to HKBA were TLR4 independent; however, the response in TLR2-deficient mice was significantly delayed and reduced, although not completely abolished. |
| 215 | 12874236 | Studies using Chinese hamster ovary/CD14 reporter cell lines stably transfected with either human TLR2 or human TLR4 confirmed the results seen with knockout mice, namely TLR2, but not TLR4, can mediate cellular activation by HKBA. |
| 216 | 12874236 | In addition, human embryonic kidney 293 cells, which do not respond to HKBA, were made responsive by transfecting TLR2, but not TLR4 or TLR9. |
| 217 | 12874236 | Taken together, our data demonstrate that MyD88-dependent pathways are crucial for activation by HKBA and that TLR2 plays a role in TNF, but not IL-12p40 pathways activated by this microbial product. |
| 218 | 12874236 | Heat-killed Brucella abortus induces TNF and IL-12p40 by distinct MyD88-dependent pathways: TNF, unlike IL-12p40 secretion, is Toll-like receptor 2 dependent. |
| 219 | 12874236 | Our results show that HKBA-mediated induction of IL-12p40 and TNF is dependent on the adapter molecule MyD88. |
| 220 | 12874236 | To identify the TLR involved in HKBA recognition, we examined HKBA responses in TLR2- and TLR4-deficient animals. |
| 221 | 12874236 | TNF responses to HKBA were TLR4 independent; however, the response in TLR2-deficient mice was significantly delayed and reduced, although not completely abolished. |
| 222 | 12874236 | Studies using Chinese hamster ovary/CD14 reporter cell lines stably transfected with either human TLR2 or human TLR4 confirmed the results seen with knockout mice, namely TLR2, but not TLR4, can mediate cellular activation by HKBA. |
| 223 | 12874236 | In addition, human embryonic kidney 293 cells, which do not respond to HKBA, were made responsive by transfecting TLR2, but not TLR4 or TLR9. |
| 224 | 12874236 | Taken together, our data demonstrate that MyD88-dependent pathways are crucial for activation by HKBA and that TLR2 plays a role in TNF, but not IL-12p40 pathways activated by this microbial product. |
| 225 | 12874236 | Heat-killed Brucella abortus induces TNF and IL-12p40 by distinct MyD88-dependent pathways: TNF, unlike IL-12p40 secretion, is Toll-like receptor 2 dependent. |
| 226 | 12874236 | Our results show that HKBA-mediated induction of IL-12p40 and TNF is dependent on the adapter molecule MyD88. |
| 227 | 12874236 | To identify the TLR involved in HKBA recognition, we examined HKBA responses in TLR2- and TLR4-deficient animals. |
| 228 | 12874236 | TNF responses to HKBA were TLR4 independent; however, the response in TLR2-deficient mice was significantly delayed and reduced, although not completely abolished. |
| 229 | 12874236 | Studies using Chinese hamster ovary/CD14 reporter cell lines stably transfected with either human TLR2 or human TLR4 confirmed the results seen with knockout mice, namely TLR2, but not TLR4, can mediate cellular activation by HKBA. |
| 230 | 12874236 | In addition, human embryonic kidney 293 cells, which do not respond to HKBA, were made responsive by transfecting TLR2, but not TLR4 or TLR9. |
| 231 | 12874236 | Taken together, our data demonstrate that MyD88-dependent pathways are crucial for activation by HKBA and that TLR2 plays a role in TNF, but not IL-12p40 pathways activated by this microbial product. |
| 232 | 12874236 | Heat-killed Brucella abortus induces TNF and IL-12p40 by distinct MyD88-dependent pathways: TNF, unlike IL-12p40 secretion, is Toll-like receptor 2 dependent. |
| 233 | 12874236 | Our results show that HKBA-mediated induction of IL-12p40 and TNF is dependent on the adapter molecule MyD88. |
| 234 | 12874236 | To identify the TLR involved in HKBA recognition, we examined HKBA responses in TLR2- and TLR4-deficient animals. |
| 235 | 12874236 | TNF responses to HKBA were TLR4 independent; however, the response in TLR2-deficient mice was significantly delayed and reduced, although not completely abolished. |
| 236 | 12874236 | Studies using Chinese hamster ovary/CD14 reporter cell lines stably transfected with either human TLR2 or human TLR4 confirmed the results seen with knockout mice, namely TLR2, but not TLR4, can mediate cellular activation by HKBA. |
| 237 | 12874236 | In addition, human embryonic kidney 293 cells, which do not respond to HKBA, were made responsive by transfecting TLR2, but not TLR4 or TLR9. |
| 238 | 12874236 | Taken together, our data demonstrate that MyD88-dependent pathways are crucial for activation by HKBA and that TLR2 plays a role in TNF, but not IL-12p40 pathways activated by this microbial product. |
| 239 | 12874236 | Heat-killed Brucella abortus induces TNF and IL-12p40 by distinct MyD88-dependent pathways: TNF, unlike IL-12p40 secretion, is Toll-like receptor 2 dependent. |
| 240 | 12874236 | Our results show that HKBA-mediated induction of IL-12p40 and TNF is dependent on the adapter molecule MyD88. |
| 241 | 12874236 | To identify the TLR involved in HKBA recognition, we examined HKBA responses in TLR2- and TLR4-deficient animals. |
| 242 | 12874236 | TNF responses to HKBA were TLR4 independent; however, the response in TLR2-deficient mice was significantly delayed and reduced, although not completely abolished. |
| 243 | 12874236 | Studies using Chinese hamster ovary/CD14 reporter cell lines stably transfected with either human TLR2 or human TLR4 confirmed the results seen with knockout mice, namely TLR2, but not TLR4, can mediate cellular activation by HKBA. |
| 244 | 12874236 | In addition, human embryonic kidney 293 cells, which do not respond to HKBA, were made responsive by transfecting TLR2, but not TLR4 or TLR9. |
| 245 | 12874236 | Taken together, our data demonstrate that MyD88-dependent pathways are crucial for activation by HKBA and that TLR2 plays a role in TNF, but not IL-12p40 pathways activated by this microbial product. |
| 246 | 14500478 | Parent OM selectively up-regulated Toll-like receptor 4 (TLR4) mRNA expression and induced mo-DC maturation, as reflected by increased production of chemokines, proinflammatory cytokines, and CD83, CD80, CD86, CD40, and major histocompatibility complex (MHC) class II molecules. |
| 247 | 14500478 | In contrast, LPS-deficient OM selectively up-regulated TLR2 mRNA expression and induced moderate increases in both cytokine production and expression of CD86 and MHC class II molecules. |
| 248 | 14505917 | Co-formulation with compounds that targeted TLR-2, TLR-3, TLR-4, or TLR-9 elicited significantly diminished type 2 T cell responses that caused granulocytic inflammation and eosinophilia in the airways after challenge. |
| 249 | 14607893 | Cutting edge: different Toll-like receptor agonists instruct dendritic cells to induce distinct Th responses via differential modulation of extracellular signal-regulated kinase-mitogen-activated protein kinase and c-Fos. |
| 250 | 14607893 | Thus, Escherichia coli LPS and flagellin, which trigger TLR4 and TLR5, respectively, instruct DCs to stimulate Th1 responses via IL-12p70 production, which depends on the phosphorylation of p38 and c-Jun N-terminal kinase 1/2. |
| 251 | 14607893 | In contrast, the TLR2 agonist, Pam3cys, and the Th2 stimulus, schistosome egg Ags: 1) barely induce IL-12p70; 2) stimulate sustained duration and magnitude of extracellular signal-regulated kinase 1/2 phosphorylation, which results in stabilization of the transcription factor c-Fos, a suppressor of IL-12; and 3) yield a Th2 bias. |
| 252 | 14607893 | Thus, distinct TLR agonists differentially modulate extracellular signal-regulated kinase signaling, c-Fos activity, and cytokine responses in DCs to stimulate different Th responses. |
| 253 | 14617145 | Although the spirochetal protein OspA is capable of stimulating immune cells in a CD14- and TLR2-dependent manner, little is known about how TLR2 receptor complex ligands, such as OspA, are handled by the cell once delivered. |
| 254 | 14630697 | Moreover, cells pretreated with an inhibitor of p38 kinase (SB 208530) inhibited Gal-lectin induced TLR-2 mRNA expression by 40%. |
| 255 | 14630697 | We conclude that the Gal-lectin activates NF-kappaB and MAP kinase-signaling pathways in macrophages culminating in the induction of several genes including TLR-2 and hypothesize that this could have a significant impact on macrophage activation and contribute to amoebic pathogenesis. |
| 256 | 14630697 | Moreover, cells pretreated with an inhibitor of p38 kinase (SB 208530) inhibited Gal-lectin induced TLR-2 mRNA expression by 40%. |
| 257 | 14630697 | We conclude that the Gal-lectin activates NF-kappaB and MAP kinase-signaling pathways in macrophages culminating in the induction of several genes including TLR-2 and hypothesize that this could have a significant impact on macrophage activation and contribute to amoebic pathogenesis. |
| 258 | 14764714 | We found that OMPC and Hib-OMPC engaged human Toll-like receptor 2 (TLR2) expressed in human embryonic kidney (HEK) cells, inducing IL-8 production, and engaged mouse TLR2 on bone marrow-derived dendritic cells, inducing TNF release. |
| 259 | 14764714 | Engagement of TLR2 by Hib-OMPC was MyD88 dependent, as Hib-OMPC-induced TNF production was ablated in MyD88 knockout (KO) mice. |
| 260 | 14764714 | Splenocytes from OMPC-immunized TLR2 KO mice also produced significantly less IL-6 and TNF-alpha than those from wild-type mice. |
| 261 | 14764714 | Hib-OMPC is unique among glycoconjugate vaccines by engaging TLR2, and the ability of Hib-OMPC to elicit protective levels of Abs after one dose may be related to TLR2-mediated induction and regulation of cytokines produced by T cells and macrophages in addition to the peptide/MHC II-dependent recruitment of T cell help commonly afforded by carrier proteins. |
| 262 | 14764714 | We found that OMPC and Hib-OMPC engaged human Toll-like receptor 2 (TLR2) expressed in human embryonic kidney (HEK) cells, inducing IL-8 production, and engaged mouse TLR2 on bone marrow-derived dendritic cells, inducing TNF release. |
| 263 | 14764714 | Engagement of TLR2 by Hib-OMPC was MyD88 dependent, as Hib-OMPC-induced TNF production was ablated in MyD88 knockout (KO) mice. |
| 264 | 14764714 | Splenocytes from OMPC-immunized TLR2 KO mice also produced significantly less IL-6 and TNF-alpha than those from wild-type mice. |
| 265 | 14764714 | Hib-OMPC is unique among glycoconjugate vaccines by engaging TLR2, and the ability of Hib-OMPC to elicit protective levels of Abs after one dose may be related to TLR2-mediated induction and regulation of cytokines produced by T cells and macrophages in addition to the peptide/MHC II-dependent recruitment of T cell help commonly afforded by carrier proteins. |
| 266 | 14764714 | We found that OMPC and Hib-OMPC engaged human Toll-like receptor 2 (TLR2) expressed in human embryonic kidney (HEK) cells, inducing IL-8 production, and engaged mouse TLR2 on bone marrow-derived dendritic cells, inducing TNF release. |
| 267 | 14764714 | Engagement of TLR2 by Hib-OMPC was MyD88 dependent, as Hib-OMPC-induced TNF production was ablated in MyD88 knockout (KO) mice. |
| 268 | 14764714 | Splenocytes from OMPC-immunized TLR2 KO mice also produced significantly less IL-6 and TNF-alpha than those from wild-type mice. |
| 269 | 14764714 | Hib-OMPC is unique among glycoconjugate vaccines by engaging TLR2, and the ability of Hib-OMPC to elicit protective levels of Abs after one dose may be related to TLR2-mediated induction and regulation of cytokines produced by T cells and macrophages in addition to the peptide/MHC II-dependent recruitment of T cell help commonly afforded by carrier proteins. |
| 270 | 14764714 | We found that OMPC and Hib-OMPC engaged human Toll-like receptor 2 (TLR2) expressed in human embryonic kidney (HEK) cells, inducing IL-8 production, and engaged mouse TLR2 on bone marrow-derived dendritic cells, inducing TNF release. |
| 271 | 14764714 | Engagement of TLR2 by Hib-OMPC was MyD88 dependent, as Hib-OMPC-induced TNF production was ablated in MyD88 knockout (KO) mice. |
| 272 | 14764714 | Splenocytes from OMPC-immunized TLR2 KO mice also produced significantly less IL-6 and TNF-alpha than those from wild-type mice. |
| 273 | 14764714 | Hib-OMPC is unique among glycoconjugate vaccines by engaging TLR2, and the ability of Hib-OMPC to elicit protective levels of Abs after one dose may be related to TLR2-mediated induction and regulation of cytokines produced by T cells and macrophages in addition to the peptide/MHC II-dependent recruitment of T cell help commonly afforded by carrier proteins. |
| 274 | 15067049 | A Toll-like receptor 2 ligand stimulates Th2 responses in vivo, via induction of extracellular signal-regulated kinase mitogen-activated protein kinase and c-Fos in dendritic cells. |
| 275 | 15067049 | Thus, Escherichia coli LPS (TLR-4 stimulus), activates DCs to produce abundant IL-12(p70), but little IL-10, and stimulates Th1 and Tc1 responses. |
| 276 | 15067049 | In contrast, Pam-3-cys (TLR-2 stimulus) elicits less IL-12(p70), but abundant IL-10, and favors Th2 and T cytotoxic 2 (Tc2) responses. |
| 277 | 15067049 | Thus, Pam-3-cys induces enhanced extracellular signal-regulated kinase signaling, compared with LPS, resulting in suppressed IL-12(p70) and enhanced IL-10 production, as well as enhanced induction of the transcription factor, c-Fos. |
| 278 | 15067049 | Interestingly, DCs from c-fos(-/-) mice produce more IL-12(p70), but less IL-10, compared with control DCs. |
| 279 | 15067049 | A Toll-like receptor 2 ligand stimulates Th2 responses in vivo, via induction of extracellular signal-regulated kinase mitogen-activated protein kinase and c-Fos in dendritic cells. |
| 280 | 15067049 | Thus, Escherichia coli LPS (TLR-4 stimulus), activates DCs to produce abundant IL-12(p70), but little IL-10, and stimulates Th1 and Tc1 responses. |
| 281 | 15067049 | In contrast, Pam-3-cys (TLR-2 stimulus) elicits less IL-12(p70), but abundant IL-10, and favors Th2 and T cytotoxic 2 (Tc2) responses. |
| 282 | 15067049 | Thus, Pam-3-cys induces enhanced extracellular signal-regulated kinase signaling, compared with LPS, resulting in suppressed IL-12(p70) and enhanced IL-10 production, as well as enhanced induction of the transcription factor, c-Fos. |
| 283 | 15067049 | Interestingly, DCs from c-fos(-/-) mice produce more IL-12(p70), but less IL-10, compared with control DCs. |
| 284 | 15158187 | In this work, we used a murine model of systemic C. albicans infection, in which resistance to reinfection with virulent wild-type cells is induced by prior exposure of mice to a low-virulence agerminative strain of C. albicans (primary sublethal infection), to study the influence of TLR2 gene deletion on (i) the ability to develop an acquired resistance upon vaccination; (ii) the development of the acquired humoral response; and (iii) the production of Th1 cytokines IFN-gamma, IL-12 and TNF-alpha. |
| 285 | 15193414 | By screening a combinatorial lipohexapeptide amide collection in an in vitro IL-8 induction assay, we systematically evaluated the potential of 19 proteinogenic amino acids in the peptide moiety of Pam3Cys-lipopeptides to interact with TLR2. |
| 286 | 15193414 | Lipopeptides with modifications in the core structure of the unusual amino acid S-glycerylcysteine were synthesized and tested for IL-8 induction via TLR2. |
| 287 | 15193414 | By screening a combinatorial lipohexapeptide amide collection in an in vitro IL-8 induction assay, we systematically evaluated the potential of 19 proteinogenic amino acids in the peptide moiety of Pam3Cys-lipopeptides to interact with TLR2. |
| 288 | 15193414 | Lipopeptides with modifications in the core structure of the unusual amino acid S-glycerylcysteine were synthesized and tested for IL-8 induction via TLR2. |
| 289 | 15195559 | Mtb H37Rv infection were found to downregulate the bcl-2, vitamin D receptor, interferon regulatory factor 3, cytochrome c oxidase, gene expression by 2-, 3-, 3-, 2.5-fold, respectively, while the clinical strain infection leads to upregulate the SOD2, SOD3, serine protease, toll-like receptor 2, signal transducer and activator (STAT1), hypoxia-inducible factor 22, 2.9-, 2.5-, 2.5-, 2.2-, 2.4-, 5.9-fold respectively. |
| 290 | 15322203 | IL-6 and IL-10 induction from dendritic cells in response to Mycobacterium tuberculosis is predominantly dependent on TLR2-mediated recognition. |
| 291 | 15322203 | In this study, we therefore determined the dependency on TLR2 and TLR4 for M. tuberculosis-induced cytokine production by murine dendritic cells. |
| 292 | 15322203 | A key new finding of this study is that production of IL-6 and IL-10 from dendritic cells in response to M. tuberculosis is principally dependent on TLR2. |
| 293 | 15322203 | The study also indicates that M. tuberculosis can induce IL-12 production in the absence of either TLR2 or TLR4, suggesting redundancy or possibly involvement of other receptors in IL-12 production. |
| 294 | 15322203 | In addition, the data also reveal that lack of TLR2 or TLR4 does not impact on dendritic cell maturation or on their ability to influence the polarity of differentiating naive T cells. |
| 295 | 15322203 | Collectively, data presented here provide a mechanistic insight for the contribution of TLR2 and TLR4 to tuberculosis disease progression and offer strategies for regulating IL-6 and IL-10 production in dendritic cell-based vaccine strategies. |
| 296 | 15322203 | IL-6 and IL-10 induction from dendritic cells in response to Mycobacterium tuberculosis is predominantly dependent on TLR2-mediated recognition. |
| 297 | 15322203 | In this study, we therefore determined the dependency on TLR2 and TLR4 for M. tuberculosis-induced cytokine production by murine dendritic cells. |
| 298 | 15322203 | A key new finding of this study is that production of IL-6 and IL-10 from dendritic cells in response to M. tuberculosis is principally dependent on TLR2. |
| 299 | 15322203 | The study also indicates that M. tuberculosis can induce IL-12 production in the absence of either TLR2 or TLR4, suggesting redundancy or possibly involvement of other receptors in IL-12 production. |
| 300 | 15322203 | In addition, the data also reveal that lack of TLR2 or TLR4 does not impact on dendritic cell maturation or on their ability to influence the polarity of differentiating naive T cells. |
| 301 | 15322203 | Collectively, data presented here provide a mechanistic insight for the contribution of TLR2 and TLR4 to tuberculosis disease progression and offer strategies for regulating IL-6 and IL-10 production in dendritic cell-based vaccine strategies. |
| 302 | 15322203 | IL-6 and IL-10 induction from dendritic cells in response to Mycobacterium tuberculosis is predominantly dependent on TLR2-mediated recognition. |
| 303 | 15322203 | In this study, we therefore determined the dependency on TLR2 and TLR4 for M. tuberculosis-induced cytokine production by murine dendritic cells. |
| 304 | 15322203 | A key new finding of this study is that production of IL-6 and IL-10 from dendritic cells in response to M. tuberculosis is principally dependent on TLR2. |
| 305 | 15322203 | The study also indicates that M. tuberculosis can induce IL-12 production in the absence of either TLR2 or TLR4, suggesting redundancy or possibly involvement of other receptors in IL-12 production. |
| 306 | 15322203 | In addition, the data also reveal that lack of TLR2 or TLR4 does not impact on dendritic cell maturation or on their ability to influence the polarity of differentiating naive T cells. |
| 307 | 15322203 | Collectively, data presented here provide a mechanistic insight for the contribution of TLR2 and TLR4 to tuberculosis disease progression and offer strategies for regulating IL-6 and IL-10 production in dendritic cell-based vaccine strategies. |
| 308 | 15322203 | IL-6 and IL-10 induction from dendritic cells in response to Mycobacterium tuberculosis is predominantly dependent on TLR2-mediated recognition. |
| 309 | 15322203 | In this study, we therefore determined the dependency on TLR2 and TLR4 for M. tuberculosis-induced cytokine production by murine dendritic cells. |
| 310 | 15322203 | A key new finding of this study is that production of IL-6 and IL-10 from dendritic cells in response to M. tuberculosis is principally dependent on TLR2. |
| 311 | 15322203 | The study also indicates that M. tuberculosis can induce IL-12 production in the absence of either TLR2 or TLR4, suggesting redundancy or possibly involvement of other receptors in IL-12 production. |
| 312 | 15322203 | In addition, the data also reveal that lack of TLR2 or TLR4 does not impact on dendritic cell maturation or on their ability to influence the polarity of differentiating naive T cells. |
| 313 | 15322203 | Collectively, data presented here provide a mechanistic insight for the contribution of TLR2 and TLR4 to tuberculosis disease progression and offer strategies for regulating IL-6 and IL-10 production in dendritic cell-based vaccine strategies. |
| 314 | 15380043 | Induction of proliferation and IFN-gamma secretion of CTL lines by Lip-OspA was independent of T cell receptor (TCR) engagement but was considerably enhanced after suboptimal TCR activation and was inhibitable by monoclonal antibodies against TLR-2. |
| 315 | 15482852 | Porin of Shigella dysenteriae type 1 increased the mRNA levels for Toll-like receptor (TLR) 2 and TLR6 by 1.5- and 2.9-fold respectively, of peritoneal cavity B-1a and B-1b cells, implicating that coexpression of TLR2 and TLR6 is essential as a combinatorial repertoire for recognition of porin by the B-1 cells. |
| 316 | 15482852 | Among the two key TLRs, TLR2 and TLR4, which are primarily responsible for recognizing majority of the bacterial products, TLR2 and not TLR4, participates in porin recognition. |
| 317 | 15482852 | TLR2 got increased on both the B-1 cell populations whereas the TLR4 expression remained unaffected. |
| 318 | 15482852 | Both of the B-1 cell populations expressed strongly the mRNA for NF-kappaB in the presence of porin, that was 2.4-fold more than untreated control, conforming to the earlier finding that coexpression of TLR2 and TLR6, resulted in robust NF-kappaB activation for signaling. |
| 319 | 15482852 | CD80 expression got enhanced on the B-1a cells whereas CD86 got solely expressed on B-1b cells. |
| 320 | 15482852 | The porin-mediated induction of IgA was augmented by interleukin-6 on B-1a and B-1b cells, by 2.4- and 2.6-fold, respectively. |
| 321 | 15482852 | Porin of Shigella dysenteriae type 1 increased the mRNA levels for Toll-like receptor (TLR) 2 and TLR6 by 1.5- and 2.9-fold respectively, of peritoneal cavity B-1a and B-1b cells, implicating that coexpression of TLR2 and TLR6 is essential as a combinatorial repertoire for recognition of porin by the B-1 cells. |
| 322 | 15482852 | Among the two key TLRs, TLR2 and TLR4, which are primarily responsible for recognizing majority of the bacterial products, TLR2 and not TLR4, participates in porin recognition. |
| 323 | 15482852 | TLR2 got increased on both the B-1 cell populations whereas the TLR4 expression remained unaffected. |
| 324 | 15482852 | Both of the B-1 cell populations expressed strongly the mRNA for NF-kappaB in the presence of porin, that was 2.4-fold more than untreated control, conforming to the earlier finding that coexpression of TLR2 and TLR6, resulted in robust NF-kappaB activation for signaling. |
| 325 | 15482852 | CD80 expression got enhanced on the B-1a cells whereas CD86 got solely expressed on B-1b cells. |
| 326 | 15482852 | The porin-mediated induction of IgA was augmented by interleukin-6 on B-1a and B-1b cells, by 2.4- and 2.6-fold, respectively. |
| 327 | 15482852 | Porin of Shigella dysenteriae type 1 increased the mRNA levels for Toll-like receptor (TLR) 2 and TLR6 by 1.5- and 2.9-fold respectively, of peritoneal cavity B-1a and B-1b cells, implicating that coexpression of TLR2 and TLR6 is essential as a combinatorial repertoire for recognition of porin by the B-1 cells. |
| 328 | 15482852 | Among the two key TLRs, TLR2 and TLR4, which are primarily responsible for recognizing majority of the bacterial products, TLR2 and not TLR4, participates in porin recognition. |
| 329 | 15482852 | TLR2 got increased on both the B-1 cell populations whereas the TLR4 expression remained unaffected. |
| 330 | 15482852 | Both of the B-1 cell populations expressed strongly the mRNA for NF-kappaB in the presence of porin, that was 2.4-fold more than untreated control, conforming to the earlier finding that coexpression of TLR2 and TLR6, resulted in robust NF-kappaB activation for signaling. |
| 331 | 15482852 | CD80 expression got enhanced on the B-1a cells whereas CD86 got solely expressed on B-1b cells. |
| 332 | 15482852 | The porin-mediated induction of IgA was augmented by interleukin-6 on B-1a and B-1b cells, by 2.4- and 2.6-fold, respectively. |
| 333 | 15482852 | Porin of Shigella dysenteriae type 1 increased the mRNA levels for Toll-like receptor (TLR) 2 and TLR6 by 1.5- and 2.9-fold respectively, of peritoneal cavity B-1a and B-1b cells, implicating that coexpression of TLR2 and TLR6 is essential as a combinatorial repertoire for recognition of porin by the B-1 cells. |
| 334 | 15482852 | Among the two key TLRs, TLR2 and TLR4, which are primarily responsible for recognizing majority of the bacterial products, TLR2 and not TLR4, participates in porin recognition. |
| 335 | 15482852 | TLR2 got increased on both the B-1 cell populations whereas the TLR4 expression remained unaffected. |
| 336 | 15482852 | Both of the B-1 cell populations expressed strongly the mRNA for NF-kappaB in the presence of porin, that was 2.4-fold more than untreated control, conforming to the earlier finding that coexpression of TLR2 and TLR6, resulted in robust NF-kappaB activation for signaling. |
| 337 | 15482852 | CD80 expression got enhanced on the B-1a cells whereas CD86 got solely expressed on B-1b cells. |
| 338 | 15482852 | The porin-mediated induction of IgA was augmented by interleukin-6 on B-1a and B-1b cells, by 2.4- and 2.6-fold, respectively. |
| 339 | 15489266 | The vaccines are totally synthetic, serve as their own adjuvant, and are composed of (i) a single helper T cell epitope, (ii) a target epitope that is either recognized by CD8+ T cells or B cells, and (iii) a Toll-like receptor 2-targeting lipid moiety, S-[2,3-bis(palmitoyloxy)propyl]cysteine, that is situated between the peptide epitopes to form a branched configuration. |
| 340 | 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. |
| 341 | 15550117 | In contrast, LPS, poly(I:C) and CpG DNA, but not zymosan, induced functional CD8+ T-cell responses against OVA; peptidoglycan (TLR2/?) |
| 342 | 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. |
| 343 | 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. |
| 344 | 15550117 | In contrast, LPS, poly(I:C) and CpG DNA, but not zymosan, induced functional CD8+ T-cell responses against OVA; peptidoglycan (TLR2/?) |
| 345 | 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. |
| 346 | 15557620 | We investigated the mechanisms of adjuvanticity of the Mycoplasma-derived macrophage-activating 2-kDa lipopeptide (MALP-2), which binds to the heterodimer formed by the Toll-like receptors 2 and 6 (TLR2 and -6), at the level of the murine nasal mucosa-associated lymphoid tissues (NALT). |
| 347 | 15557620 | We observed an early up-regulated expression of IP-10, MCP-1, MCP-3, MIP-1alpha, MIP-2, and CCR-2 which was reversed within 36 h. |
| 348 | 15606799 | Porin of Shigella dysenteriae type 1 increased the mRNA levels for Toll-like receptors TLR2 and TLR6, by 1.8-fold and twofold, respectively, in peritoneal cavity B-2 cells from C57BL/6 mice, implicating that the co-expression of TLR2 and TLR6 occurs as a combinatorial repertoire in response to porin. |
| 349 | 15606799 | Among the two key TLRs, TLR2 and TLR4, which are primarily responsible for recognizing the majority of bacterial products, TLR2 alone participates in porin recognition. |
| 350 | 15606799 | TLR2 expression was increased on B-2 cells, whereas the expression of TLR4 remained unaffected. |
| 351 | 15606799 | The porin-mediated inductions of IgG2a and IgA were augmented by interleukin-6 on B-2 cells, by 2.7- and 1.6-fold, respectively. |
| 352 | 15606799 | Porin of Shigella dysenteriae type 1 increased the mRNA levels for Toll-like receptors TLR2 and TLR6, by 1.8-fold and twofold, respectively, in peritoneal cavity B-2 cells from C57BL/6 mice, implicating that the co-expression of TLR2 and TLR6 occurs as a combinatorial repertoire in response to porin. |
| 353 | 15606799 | Among the two key TLRs, TLR2 and TLR4, which are primarily responsible for recognizing the majority of bacterial products, TLR2 alone participates in porin recognition. |
| 354 | 15606799 | TLR2 expression was increased on B-2 cells, whereas the expression of TLR4 remained unaffected. |
| 355 | 15606799 | The porin-mediated inductions of IgG2a and IgA were augmented by interleukin-6 on B-2 cells, by 2.7- and 1.6-fold, respectively. |
| 356 | 15606799 | Porin of Shigella dysenteriae type 1 increased the mRNA levels for Toll-like receptors TLR2 and TLR6, by 1.8-fold and twofold, respectively, in peritoneal cavity B-2 cells from C57BL/6 mice, implicating that the co-expression of TLR2 and TLR6 occurs as a combinatorial repertoire in response to porin. |
| 357 | 15606799 | Among the two key TLRs, TLR2 and TLR4, which are primarily responsible for recognizing the majority of bacterial products, TLR2 alone participates in porin recognition. |
| 358 | 15606799 | TLR2 expression was increased on B-2 cells, whereas the expression of TLR4 remained unaffected. |
| 359 | 15606799 | The porin-mediated inductions of IgG2a and IgA were augmented by interleukin-6 on B-2 cells, by 2.7- and 1.6-fold, respectively. |
| 360 | 15760459 | Mycobacterium bovis bacille Calmette Guerin infection of human neutrophils induces CXCL8 secretion by MyD88-dependent TLR2 and TLR4 activation. |
| 361 | 15760459 | BCG induced transcription and secretion of the chemokine CXCL8, by signalling through Toll-like receptors TLR2 and TLR4, in conjunction with the adaptor protein myeloid differentiation factor 88 (MyD88). |
| 362 | 15760459 | Anti-TLR2 antibody blocked the early phase of CXCL8 and MyD88 induction. |
| 363 | 15760459 | Mycobacterium bovis bacille Calmette Guerin infection of human neutrophils induces CXCL8 secretion by MyD88-dependent TLR2 and TLR4 activation. |
| 364 | 15760459 | BCG induced transcription and secretion of the chemokine CXCL8, by signalling through Toll-like receptors TLR2 and TLR4, in conjunction with the adaptor protein myeloid differentiation factor 88 (MyD88). |
| 365 | 15760459 | Anti-TLR2 antibody blocked the early phase of CXCL8 and MyD88 induction. |
| 366 | 15809303 | Furthermore, we show that whereas mycobacterial heat shock protein 65 signals exclusively through Toll-like receptor 4, heat shock protein 70 also signals through Toll-like receptor 2. |
| 367 | 15809303 | Mycobacterial heat shock protein 65-induced NF-kappaB activation was MyD88-, TIRAP-, TRIF-, and TRAM-dependent and required the presence of MD-2. |
| 368 | 15882532 | Also, no donor-dependecy was found to highly purified lipoteichoic acid from the Gram-positive bacteria Bacillus subtilis and Staphylococcus aureus, known to be mediated via TLR-2 and TLR-6. |
| 369 | 16116197 | All PPS-containing preparations induced IL-6 and TNF-alpha from wild-type, but not TLR2-/-, macrophages. |
| 370 | 16116197 | The commercial 23-valent PPS vaccine, Pneumovax-23 also contained TLR ligands (TLR2 and TLR4), which were absolutely critical for the IgG-inducing activity of the vaccine in mice. |
| 371 | 16129524 | Are mineral adjuvants triggering TLR2/TLR4 on dendritic cells by a secondary cascade reaction in vivo through the action of heat shock proteins and danger signals? |
| 372 | 16426010 | We recently demonstrated that the pattern recognition receptors (PRRs) toll-like receptor 2 (TLR2), TLR4, and CD14 are expressed in mouse colonic epithelium in a compartmentalized manner. |
| 373 | 16426010 | Interestingly, while TLR2, TLR4, and CD14 were up-regulated in the inflamed colon, TLR5 was down-regulated at both the mRNA and protein levels. |
| 374 | 16426010 | Additional in vitro studies using a mouse cell line, Colon-26, showed that gamma interferon (IFN-gamma) time- and dose-dependently down-regulates TLR5. |
| 375 | 16426010 | TLR5 expression is down-regulated in vivo during acute and chronic DSS-induced colitis, in contrast to the expression of TLR2, TLR4, and CD14. |
| 376 | 16426010 | Finally, IFN-gamma may be involved in down-regulating TLR5 expression. |
| 377 | 16426010 | We recently demonstrated that the pattern recognition receptors (PRRs) toll-like receptor 2 (TLR2), TLR4, and CD14 are expressed in mouse colonic epithelium in a compartmentalized manner. |
| 378 | 16426010 | Interestingly, while TLR2, TLR4, and CD14 were up-regulated in the inflamed colon, TLR5 was down-regulated at both the mRNA and protein levels. |
| 379 | 16426010 | Additional in vitro studies using a mouse cell line, Colon-26, showed that gamma interferon (IFN-gamma) time- and dose-dependently down-regulates TLR5. |
| 380 | 16426010 | TLR5 expression is down-regulated in vivo during acute and chronic DSS-induced colitis, in contrast to the expression of TLR2, TLR4, and CD14. |
| 381 | 16426010 | Finally, IFN-gamma may be involved in down-regulating TLR5 expression. |
| 382 | 16426010 | We recently demonstrated that the pattern recognition receptors (PRRs) toll-like receptor 2 (TLR2), TLR4, and CD14 are expressed in mouse colonic epithelium in a compartmentalized manner. |
| 383 | 16426010 | Interestingly, while TLR2, TLR4, and CD14 were up-regulated in the inflamed colon, TLR5 was down-regulated at both the mRNA and protein levels. |
| 384 | 16426010 | Additional in vitro studies using a mouse cell line, Colon-26, showed that gamma interferon (IFN-gamma) time- and dose-dependently down-regulates TLR5. |
| 385 | 16426010 | TLR5 expression is down-regulated in vivo during acute and chronic DSS-induced colitis, in contrast to the expression of TLR2, TLR4, and CD14. |
| 386 | 16426010 | Finally, IFN-gamma may be involved in down-regulating TLR5 expression. |
| 387 | 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. |
| 388 | 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. |
| 389 | 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. |
| 390 | 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. |
| 391 | 16467329 | Mononuclear cells from Peyer's patches were isolated to determine the CD-206 and TLR-2 receptors. |
| 392 | 16467329 | In histological slices we determined the number of IgA+, CD4+, CD8+, and CD3+ cells and two cytokines (interleulin-5 [IL-5] and IL-6). |
| 393 | 16467329 | CD-206 and TLR-2 increased with respect to the untreated control. |
| 394 | 16467329 | The main immune cells activated after oral L. casei administration were those of the innate immune response, with an increase in the specific markers of these cells (CD-206 and TLR-2), with no modification in the number of T cells. |
| 395 | 16467329 | Mononuclear cells from Peyer's patches were isolated to determine the CD-206 and TLR-2 receptors. |
| 396 | 16467329 | In histological slices we determined the number of IgA+, CD4+, CD8+, and CD3+ cells and two cytokines (interleulin-5 [IL-5] and IL-6). |
| 397 | 16467329 | CD-206 and TLR-2 increased with respect to the untreated control. |
| 398 | 16467329 | The main immune cells activated after oral L. casei administration were those of the innate immune response, with an increase in the specific markers of these cells (CD-206 and TLR-2), with no modification in the number of T cells. |
| 399 | 16467329 | Mononuclear cells from Peyer's patches were isolated to determine the CD-206 and TLR-2 receptors. |
| 400 | 16467329 | In histological slices we determined the number of IgA+, CD4+, CD8+, and CD3+ cells and two cytokines (interleulin-5 [IL-5] and IL-6). |
| 401 | 16467329 | CD-206 and TLR-2 increased with respect to the untreated control. |
| 402 | 16467329 | The main immune cells activated after oral L. casei administration were those of the innate immune response, with an increase in the specific markers of these cells (CD-206 and TLR-2), with no modification in the number of T cells. |
| 403 | 16509590 | Lipolanthionine peptides act as inhibitors of TLR2-mediated IL-8 secretion. |
| 404 | 16509590 | Lipoproteins from gram-positive and -negative bacteria, mycoplasma, and shorter synthetic lipopeptide analogues activate cells of the innate immune system via the Toll-like receptor TLR2/TLR1 or TLR2/TLR6 heterodimers. |
| 405 | 16509590 | A collection of analytically defined lipolanthionine peptide amides exhibited an inhibitory effect of the TLR2-mediated IL-8 secretion when applied in high molar excess to the agonistic synthetic lipopeptide Pam3Cys-Ser-(Lys)4-OH. |
| 406 | 16509590 | Lipolanthionine peptides act as inhibitors of TLR2-mediated IL-8 secretion. |
| 407 | 16509590 | Lipoproteins from gram-positive and -negative bacteria, mycoplasma, and shorter synthetic lipopeptide analogues activate cells of the innate immune system via the Toll-like receptor TLR2/TLR1 or TLR2/TLR6 heterodimers. |
| 408 | 16509590 | A collection of analytically defined lipolanthionine peptide amides exhibited an inhibitory effect of the TLR2-mediated IL-8 secretion when applied in high molar excess to the agonistic synthetic lipopeptide Pam3Cys-Ser-(Lys)4-OH. |
| 409 | 16509590 | Lipolanthionine peptides act as inhibitors of TLR2-mediated IL-8 secretion. |
| 410 | 16509590 | Lipoproteins from gram-positive and -negative bacteria, mycoplasma, and shorter synthetic lipopeptide analogues activate cells of the innate immune system via the Toll-like receptor TLR2/TLR1 or TLR2/TLR6 heterodimers. |
| 411 | 16509590 | A collection of analytically defined lipolanthionine peptide amides exhibited an inhibitory effect of the TLR2-mediated IL-8 secretion when applied in high molar excess to the agonistic synthetic lipopeptide Pam3Cys-Ser-(Lys)4-OH. |
| 412 | 16513388 | MyD88 knockout (KO) mice, but not TLR2-, TLR4- or TLR9-deficient mice, rapidly succumbed following in vivo bacterial infection via the intradermal route even with a very low dose of LVS (5 x 10(1)) that was 100,000-fold less than the LD(50) of normal wild-type (WT) mice. |
| 413 | 16513388 | By day 5 after LVS infection, bacterial organ burdens were 5-6 logs higher in MyD88 knockout mice; further, unlike infected WT mice, levels of interferon-gamma in the sera of LVS-infected MyD88 KO were undetectable. |
| 414 | 16522788 | Nucleotide-binding oligomerization domain 2 (Nod2) pathways are known to interact with Toll-like receptor 2 (TLR2) and TLR4, which are pattern recognition receptors for Candida albicans. |
| 415 | 16543948 | Yeast zymosan, a stimulus for TLR2 and dectin-1, induces regulatory antigen-presenting cells and immunological tolerance. |
| 416 | 16543948 | Here, we show that zymosan, a stimulus for TLR2 and dectin-1, regulates cytokine secretion in DCs and macrophages to induce immunological tolerance. |
| 417 | 16543948 | First, zymosan induces DCs to secrete abundant IL-10 but little IL-6 and IL-12(p70). |
| 418 | 16543948 | Induction of IL-10 is dependent on TLR2- and dectin-1-mediated activation of ERK MAPK via a mechanism independent of the activation protein 1 (AP-1) transcription factor c-Fos. |
| 419 | 16543948 | Such DCs stimulate antigen-specific CD4+ T cells poorly due to IL-10 and the lack of IL-6. |
| 420 | 16543948 | Finally, coinjection of zymosan with OVA plus LPS suppresses the response to OVA via a mechanism dependent on IL-10, TGF-beta, and lack of IL-6. |
| 421 | 16543948 | Together, our data demonstrate that zymosan stimulates IL-10+ IL-12(p70)- IL-6low regulatory DCs and TGF-beta+ macrophages to induce immunological tolerance. |
| 422 | 16543948 | Yeast zymosan, a stimulus for TLR2 and dectin-1, induces regulatory antigen-presenting cells and immunological tolerance. |
| 423 | 16543948 | Here, we show that zymosan, a stimulus for TLR2 and dectin-1, regulates cytokine secretion in DCs and macrophages to induce immunological tolerance. |
| 424 | 16543948 | First, zymosan induces DCs to secrete abundant IL-10 but little IL-6 and IL-12(p70). |
| 425 | 16543948 | Induction of IL-10 is dependent on TLR2- and dectin-1-mediated activation of ERK MAPK via a mechanism independent of the activation protein 1 (AP-1) transcription factor c-Fos. |
| 426 | 16543948 | Such DCs stimulate antigen-specific CD4+ T cells poorly due to IL-10 and the lack of IL-6. |
| 427 | 16543948 | Finally, coinjection of zymosan with OVA plus LPS suppresses the response to OVA via a mechanism dependent on IL-10, TGF-beta, and lack of IL-6. |
| 428 | 16543948 | Together, our data demonstrate that zymosan stimulates IL-10+ IL-12(p70)- IL-6low regulatory DCs and TGF-beta+ macrophages to induce immunological tolerance. |
| 429 | 16543948 | Yeast zymosan, a stimulus for TLR2 and dectin-1, induces regulatory antigen-presenting cells and immunological tolerance. |
| 430 | 16543948 | Here, we show that zymosan, a stimulus for TLR2 and dectin-1, regulates cytokine secretion in DCs and macrophages to induce immunological tolerance. |
| 431 | 16543948 | First, zymosan induces DCs to secrete abundant IL-10 but little IL-6 and IL-12(p70). |
| 432 | 16543948 | Induction of IL-10 is dependent on TLR2- and dectin-1-mediated activation of ERK MAPK via a mechanism independent of the activation protein 1 (AP-1) transcription factor c-Fos. |
| 433 | 16543948 | Such DCs stimulate antigen-specific CD4+ T cells poorly due to IL-10 and the lack of IL-6. |
| 434 | 16543948 | Finally, coinjection of zymosan with OVA plus LPS suppresses the response to OVA via a mechanism dependent on IL-10, TGF-beta, and lack of IL-6. |
| 435 | 16543948 | Together, our data demonstrate that zymosan stimulates IL-10+ IL-12(p70)- IL-6low regulatory DCs and TGF-beta+ macrophages to induce immunological tolerance. |
| 436 | 16548886 | In this study we analyse the interaction of the MP from Candida albicans (MP65) with dendritic cells (DC) and demonstrate that MP65 stimulates DC and induces the release of TNF-alpha, IL-6 and the activation of IL-12 gene, with maximal value 6 h post treatment. |
| 437 | 16548886 | The latter effect is partly mediated by toll-like receptor 2 (TLR2) and TLR4, and the MyD88-dependent pathway is involved in the process. |
| 438 | 16574669 | Induction of kappaB-driven transcriptional activity by 2.5 mug ml(-1) F. tularensis LPS isolated by phenol-water and ether-water extraction, was observed in cells transfected with Toll-like receptor (TLR) 4 and MD-2, although CD14 was required for optimal induction. |
| 439 | 16574669 | Conversely, TLR2, TLR2/TLR1 or TLR2/TLR6 transfected cells did not show kappaB-driven transcriptional activity in the presence of F. tularensis LPS. |
| 440 | 16574669 | Concentrations of 5-10 mug ml(-1) F. tularensis LPS elicited a similar pattern of mRNA and protein induction than 0.1 mug ml(-1) E. coli LPS, including the expression of CXC chemokines (IL-8, Gro and IFN-gamma-inducible protein-10); CC chemokines (monocyte chemoattractant protein-1 and -2, macrophage-derived chemoattractant, macrophage inflammatory protein-1alpha and -1beta and RANTES (regulated upon activation, normal T cell expressed and secreted) and pro-inflammatory cytokines (IL-6 and tumor necrosis factor alpha). |
| 441 | 16750567 | Besides TLRs, mRNA for MyD88 and TRAF6, and nuclear translocation of NF-kappaB were enhanced that indicate their involvement in tandem in the activity of porin. |
| 442 | 16750567 | The protein selectively up-regulated CD80 on the activated MPhi together with MHC class II molecule and CD40, and had no effect on CD86 expression. |
| 443 | 16750567 | The porin-induced profile of MIP-1alpha, MIP-1beta and RANTES showed strong bias for chemokines correlated with M1 polarization. |
| 444 | 16750567 | Intracellular expression and release of TNF-alpha and IL-12 in presence of porin was found to be TLR2 and NF-kappaB dependent. |
| 445 | 16750567 | Induction of TNF-alpha and IL-12 along with the chemokine profile suggests type I polarization of the MPhi that would influence Th1-type response. |
| 446 | 16895974 | Using cells derived from TLR2-deficient mice and in vitro transfection assays, we demonstrated that this response was mediated by TLR2 and did not require the LPS-binding protein. |
| 447 | 16895974 | F. tularensis appeared to activate TLR2/TLR1 and TLR2/TLR6 heterodimers. |
| 448 | 16895974 | IL-1beta secretion, a reflection of caspase-1 activation, was induced by live but not heat-killed F. tularensis, despite the fact that both forms of the bacterium equally induced the IL-1beta transcript. |
| 449 | 16920494 | The role of TLRs during infection with Mycobacterium bovis Bacillus Calmette-Guérin (BCG) has been evaluated for TLR2 and TLR4 only. |
| 450 | 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. |
| 451 | 16920494 | The degree of activation and stimulation was determined by TNFalpha, IL-6 and IL-12p40 ELISA. |
| 452 | 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. |
| 453 | 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. |
| 454 | 16920494 | The role of TLRs during infection with Mycobacterium bovis Bacillus Calmette-Guérin (BCG) has been evaluated for TLR2 and TLR4 only. |
| 455 | 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. |
| 456 | 16920494 | The degree of activation and stimulation was determined by TNFalpha, IL-6 and IL-12p40 ELISA. |
| 457 | 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. |
| 458 | 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. |
| 459 | 16920494 | The role of TLRs during infection with Mycobacterium bovis Bacillus Calmette-Guérin (BCG) has been evaluated for TLR2 and TLR4 only. |
| 460 | 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. |
| 461 | 16920494 | The degree of activation and stimulation was determined by TNFalpha, IL-6 and IL-12p40 ELISA. |
| 462 | 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. |
| 463 | 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. |
| 464 | 16920494 | The role of TLRs during infection with Mycobacterium bovis Bacillus Calmette-Guérin (BCG) has been evaluated for TLR2 and TLR4 only. |
| 465 | 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. |
| 466 | 16920494 | The degree of activation and stimulation was determined by TNFalpha, IL-6 and IL-12p40 ELISA. |
| 467 | 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. |
| 468 | 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. |
| 469 | 16940524 | The HIV-VLP-activated MDDCs show enhanced Th1- and Th2-specific cytokine production, and the effects of HIV-VLPs on MDDCs are not mediated through Toll-like receptors 2 and 4 (TLR2 and -4) signaling. |
| 470 | 16973959 | The TLR pathway was mediated by TLR2 and MyD88, leading to the production of proinflammatory cytokines, whereas activation of the TLR-independent pathway resulted in the secretion of IFN-beta. |
| 471 | 16988256 | Because it is known that SOCS are induced by IL-10 and that B. burgdorferi and its lipoproteins most likely interact via TLR2 or the heterodimers TLR2/1 and/or TLR2/6, we hypothesized that SOCS are induced by IL-10 and B. burgdorferi and its lipoproteins in macrophages and that SOCS may mediate the inhibition by IL-10 of concomitantly elicited cytokines. |
| 472 | 16988256 | We report here that mouse J774 macrophages incubated with IL-10 and added B. burgdorferi spirochetes (freeze-thawed, live, or sonicated) or lipidated outer surface protein A (L-OspA) augmented their SOCS1/SOCS3 mRNA and protein expression, with SOCS3 being more abundant. |
| 473 | 16988256 | Pam(3)Cys, a synthetic lipopeptide, also induced SOCS1/SOCS3 expression under these conditions, but unlipidated OspA was ineffective. |
| 474 | 16988256 | Neither endogenous IL-10 nor the translation inhibitor cycloheximide blocked SOCS1/SOCS3 induction by B. burgdorferi and its lipoproteins, indicating that the expression of other genes is not required. |
| 475 | 16988256 | This temporally correlated with the IL-10-mediated inhibition of the inflammatory cytokines IL-1beta, IL-6, IL-12p40, IL-18, and tumor necrosis factor alpha. |
| 476 | 16988256 | Our data are evidence to suggest that expression of SOCS is part of the mechanism of IL-10-mediated inhibition of inflammatory cytokines elicited by B. burgdorferi and its lipoproteins. |
| 477 | 17049413 | Among other receptors, toll like receptor (TLR)-2 and TLR-4 have been suggested to be involved in HSP70-mediated signalling. |
| 478 | 17049413 | In the present study, we have extended the study with other microbial HSPs (mHSPs) and considered of interest to assess the influence of TLR-2 and TLR-4 in mHSP-promoted responses. |
| 479 | 17049413 | To test this, we evaluated the adjuvant effect of various mHSP molecules in TLR-2(-/-), TLR-4(-/-) and MyD88(-/-) mice. |
| 480 | 17049413 | Interestingly, Tc70 was found to induce in vivo and in vitro responses in both TLR-2(-/-) and TLR-4(-/-) mice. |
| 481 | 17049413 | Among other receptors, toll like receptor (TLR)-2 and TLR-4 have been suggested to be involved in HSP70-mediated signalling. |
| 482 | 17049413 | In the present study, we have extended the study with other microbial HSPs (mHSPs) and considered of interest to assess the influence of TLR-2 and TLR-4 in mHSP-promoted responses. |
| 483 | 17049413 | To test this, we evaluated the adjuvant effect of various mHSP molecules in TLR-2(-/-), TLR-4(-/-) and MyD88(-/-) mice. |
| 484 | 17049413 | Interestingly, Tc70 was found to induce in vivo and in vitro responses in both TLR-2(-/-) and TLR-4(-/-) mice. |
| 485 | 17049413 | Among other receptors, toll like receptor (TLR)-2 and TLR-4 have been suggested to be involved in HSP70-mediated signalling. |
| 486 | 17049413 | In the present study, we have extended the study with other microbial HSPs (mHSPs) and considered of interest to assess the influence of TLR-2 and TLR-4 in mHSP-promoted responses. |
| 487 | 17049413 | To test this, we evaluated the adjuvant effect of various mHSP molecules in TLR-2(-/-), TLR-4(-/-) and MyD88(-/-) mice. |
| 488 | 17049413 | Interestingly, Tc70 was found to induce in vivo and in vitro responses in both TLR-2(-/-) and TLR-4(-/-) mice. |
| 489 | 17055123 | Furthermore, the C16 lipopeptide was the most effective in activating dendritic cells, measured by up regulation of surface MHC Class II molecules, and also in activating NF-kappaB in a Toll-like receptor-2 (TLR2)-dependent manner. |
| 490 | 17077175 | In this study, we examined different lipid structures from bacterial or non-bacterial sources coupled to peptides representing influenza viral epitopes recognized by CD8(+) and CD4(+) T cells. |
| 491 | 17077175 | Mice immunized with the TLR2-binding lipopeptides showed greatly enhanced numbers of specific IFN-gamma-secreting CD8(+) T cells at the site of infection after i.n. exposure to virus, which resulted in enhanced protection of the pneumonic lung. |
| 492 | 17113914 | The ability of OM-197-MP-AC to induce maturation of human and mouse DC and macrophages was dependent on TLR4, not TLR2. |
| 493 | 17363432 | In other work, we have found that the mannose receptor as well as the toll-like receptors TLR2 and TLR4 may have a role in recognizing glycosylated coccidioidal antigens. |
| 494 | 17374422 | Mice immunized with the Protollin vaccine displayed polarized Th1 responses with augmented IFNgamma/IL-5 ratios in RSV-restimulated lung and spleen cell preparations compared with animals that received antigen alone. |
| 495 | 17374422 | This new model will permit us to dissect the respective roles of the TLR2 and TLR4 ligands contained in the vaccine using TLR knock-out animals established on the C57Bl/6 background. |
| 496 | 17383632 | It appears that TLR2/4 agonists induce a well controlled tumor necrosis factor-alpha (TNF-alpha) secretion, at plasma levels known to permeabilize neoangiogenic tumor vessels to the passage of cytotoxic drugs. |
| 497 | 17383632 | Moreover, TLR2/4 agonists induce inducible nitric oxide synthase (iNOS) expression, and nitric oxide is able to induce apoptosis of chemotherapy-resistant tumor cell clones. |
| 498 | 17383632 | It appears that TLR2/4 agonists induce a well controlled tumor necrosis factor-alpha (TNF-alpha) secretion, at plasma levels known to permeabilize neoangiogenic tumor vessels to the passage of cytotoxic drugs. |
| 499 | 17383632 | Moreover, TLR2/4 agonists induce inducible nitric oxide synthase (iNOS) expression, and nitric oxide is able to induce apoptosis of chemotherapy-resistant tumor cell clones. |
| 500 | 17420241 | When it was examined for binding to murine bone marrow-derived dendritic cells (DCs), the dltA mutant exhibited 200- to 400-fold less binding than the parent but similar levels of binding were shown for Toll-like receptor 2 (TLR2) knockout DCs and HEp-2 cells. |
| 501 | 17420241 | LTA purified from the bacteria induced tumor necrosis factor-alpha and IL-6 production from wild-type DCs but not from TLR2 knockout DCs, and the mutant LTA induced a significantly smaller amount of these two cytokines. |
| 502 | 17420241 | When it was examined for binding to murine bone marrow-derived dendritic cells (DCs), the dltA mutant exhibited 200- to 400-fold less binding than the parent but similar levels of binding were shown for Toll-like receptor 2 (TLR2) knockout DCs and HEp-2 cells. |
| 503 | 17420241 | LTA purified from the bacteria induced tumor necrosis factor-alpha and IL-6 production from wild-type DCs but not from TLR2 knockout DCs, and the mutant LTA induced a significantly smaller amount of these two cytokines. |
| 504 | 17451442 | An oral Salmonella vaccine promotes the down-regulation of cell surface Toll-like receptor 4 (TLR4) and TLR2 expression in mice. |
| 505 | 17451442 | The populations of cell surface Toll-like receptor 4 (TLR4) and TLR2 on peritoneal macrophages decreased at week 6 after immunization. |
| 506 | 17451442 | An oral Salmonella vaccine promotes the down-regulation of cell surface Toll-like receptor 4 (TLR4) and TLR2 expression in mice. |
| 507 | 17451442 | The populations of cell surface Toll-like receptor 4 (TLR4) and TLR2 on peritoneal macrophages decreased at week 6 after immunization. |
| 508 | 17499405 | Human receptors of innate immunity (CD14, TLR2) are promising targets for novel recombinant immunoglobulin-based vaccine candidates. |
| 509 | 17499405 | We have here constructed recombinant scFv-based vaccine candidate proteins (vaccibodies) that target human TLR2 and CD14 for delivery of large antigens. |
| 510 | 17499405 | The TLR2- and CD14-specific vaccibodies bound their respective target receptors expressed on transfected CHO cells and PBMC. |
| 511 | 17499405 | In the presence of monocytes, TLR2- and CD14-specific vaccibodies having either Ckappa or TetC as antigenic unit were 100-10,000 more efficient at stimulating T cell clones in vitro compared to non-targeted vaccibodies expressing the same antigens. |
| 512 | 17499405 | The results show that TLR2 and CD14 are efficient targets for delivery of antigen to APC for stimulation of HLA class II-restricted CD4(+) T cells. |
| 513 | 17499405 | Human receptors of innate immunity (CD14, TLR2) are promising targets for novel recombinant immunoglobulin-based vaccine candidates. |
| 514 | 17499405 | We have here constructed recombinant scFv-based vaccine candidate proteins (vaccibodies) that target human TLR2 and CD14 for delivery of large antigens. |
| 515 | 17499405 | The TLR2- and CD14-specific vaccibodies bound their respective target receptors expressed on transfected CHO cells and PBMC. |
| 516 | 17499405 | In the presence of monocytes, TLR2- and CD14-specific vaccibodies having either Ckappa or TetC as antigenic unit were 100-10,000 more efficient at stimulating T cell clones in vitro compared to non-targeted vaccibodies expressing the same antigens. |
| 517 | 17499405 | The results show that TLR2 and CD14 are efficient targets for delivery of antigen to APC for stimulation of HLA class II-restricted CD4(+) T cells. |
| 518 | 17499405 | Human receptors of innate immunity (CD14, TLR2) are promising targets for novel recombinant immunoglobulin-based vaccine candidates. |
| 519 | 17499405 | We have here constructed recombinant scFv-based vaccine candidate proteins (vaccibodies) that target human TLR2 and CD14 for delivery of large antigens. |
| 520 | 17499405 | The TLR2- and CD14-specific vaccibodies bound their respective target receptors expressed on transfected CHO cells and PBMC. |
| 521 | 17499405 | In the presence of monocytes, TLR2- and CD14-specific vaccibodies having either Ckappa or TetC as antigenic unit were 100-10,000 more efficient at stimulating T cell clones in vitro compared to non-targeted vaccibodies expressing the same antigens. |
| 522 | 17499405 | The results show that TLR2 and CD14 are efficient targets for delivery of antigen to APC for stimulation of HLA class II-restricted CD4(+) T cells. |
| 523 | 17499405 | Human receptors of innate immunity (CD14, TLR2) are promising targets for novel recombinant immunoglobulin-based vaccine candidates. |
| 524 | 17499405 | We have here constructed recombinant scFv-based vaccine candidate proteins (vaccibodies) that target human TLR2 and CD14 for delivery of large antigens. |
| 525 | 17499405 | The TLR2- and CD14-specific vaccibodies bound their respective target receptors expressed on transfected CHO cells and PBMC. |
| 526 | 17499405 | In the presence of monocytes, TLR2- and CD14-specific vaccibodies having either Ckappa or TetC as antigenic unit were 100-10,000 more efficient at stimulating T cell clones in vitro compared to non-targeted vaccibodies expressing the same antigens. |
| 527 | 17499405 | The results show that TLR2 and CD14 are efficient targets for delivery of antigen to APC for stimulation of HLA class II-restricted CD4(+) T cells. |
| 528 | 17499405 | Human receptors of innate immunity (CD14, TLR2) are promising targets for novel recombinant immunoglobulin-based vaccine candidates. |
| 529 | 17499405 | We have here constructed recombinant scFv-based vaccine candidate proteins (vaccibodies) that target human TLR2 and CD14 for delivery of large antigens. |
| 530 | 17499405 | The TLR2- and CD14-specific vaccibodies bound their respective target receptors expressed on transfected CHO cells and PBMC. |
| 531 | 17499405 | In the presence of monocytes, TLR2- and CD14-specific vaccibodies having either Ckappa or TetC as antigenic unit were 100-10,000 more efficient at stimulating T cell clones in vitro compared to non-targeted vaccibodies expressing the same antigens. |
| 532 | 17499405 | The results show that TLR2 and CD14 are efficient targets for delivery of antigen to APC for stimulation of HLA class II-restricted CD4(+) T cells. |
| 533 | 17507120 | We further found that the MyD88-dependent TLR2 signal partially mediates SRV-induced mucosal immunity, with the exception of TLR4- and TLR5-governed innate immunity. |
| 534 | 17517865 | We reported previously that F. tularensis live vaccine strain (LVS) elicited strong, dose-dependent NF-kappaB reporter activity in Toll-like receptor 2 (TLR2)-expressing HEK293T cells and proinflammatory gene expression in primary murine macrophages. |
| 535 | 17517865 | Colocalization of intracellular F. tularensis LVS, TLR2, and MyD88 was visualized by confocal microscopy. |
| 536 | 17517865 | F. tularensis LVS replicates in macrophages; however, bacterial replication was not required for TLR2 signaling because LVSDeltaguaA, an F. tularensis LVS guanine auxotroph that fails to replicate in the absence of exogenous guanine, activated NF-kappaB in TLR2-transfected HEK293T cells and induced cytokine expression in wild-type macrophages comparably to wild-type F. tularensis LVS. |
| 537 | 17517865 | We reported previously that F. tularensis live vaccine strain (LVS) elicited strong, dose-dependent NF-kappaB reporter activity in Toll-like receptor 2 (TLR2)-expressing HEK293T cells and proinflammatory gene expression in primary murine macrophages. |
| 538 | 17517865 | Colocalization of intracellular F. tularensis LVS, TLR2, and MyD88 was visualized by confocal microscopy. |
| 539 | 17517865 | F. tularensis LVS replicates in macrophages; however, bacterial replication was not required for TLR2 signaling because LVSDeltaguaA, an F. tularensis LVS guanine auxotroph that fails to replicate in the absence of exogenous guanine, activated NF-kappaB in TLR2-transfected HEK293T cells and induced cytokine expression in wild-type macrophages comparably to wild-type F. tularensis LVS. |
| 540 | 17517865 | We reported previously that F. tularensis live vaccine strain (LVS) elicited strong, dose-dependent NF-kappaB reporter activity in Toll-like receptor 2 (TLR2)-expressing HEK293T cells and proinflammatory gene expression in primary murine macrophages. |
| 541 | 17517865 | Colocalization of intracellular F. tularensis LVS, TLR2, and MyD88 was visualized by confocal microscopy. |
| 542 | 17517865 | F. tularensis LVS replicates in macrophages; however, bacterial replication was not required for TLR2 signaling because LVSDeltaguaA, an F. tularensis LVS guanine auxotroph that fails to replicate in the absence of exogenous guanine, activated NF-kappaB in TLR2-transfected HEK293T cells and induced cytokine expression in wild-type macrophages comparably to wild-type F. tularensis LVS. |
| 543 | 17570527 | HlyA oligomer-treated murine B-1a cells up-regulated TLR2 and involved the signaling molecules MyD88, TRAF6 and NF-kappaB. |
| 544 | 17570527 | Apoptosis was detected in majority of the monomer-treated cells that involved caspase-9 and caspase-3. |
| 545 | 17570535 | Here we report on the construction of a fusion protein consisting of a tuberculosis vaccine candidate mycolyl-transferase antigen 85A (Ag85A, Rv3804c) coupled to the outer membrane lipoprotein I (OprI) from Pseudomonas (P.) aeruginosa, a documented TLR2/TLR4 trigger. |
| 546 | 17570535 | Intranasal priming of C57BL/6 mice with live, attenuated Mycobacterium bovis bacille Calmette-Guérin (BCG) vaccine, followed by intranasal boosting with OprI-Ag85A increased systemic and local antigen-specific interferon (IFN)-gamma and interleukin (IL)-2 responses in spleen, draining cervical and mediastinal lymph nodes and particularly in lung tissue, as compared to responses in mice only vaccinated with BCG vaccine. |
| 547 | 17576158 | Higher doses of lentivirus, however, resulted in upregulation of adhesion, costimulatory, and HLA molecules, as well as in increased allostimulatory capacity and secretion of interleukin (IL)-6, IL-8, and tumor necrosis factor-alpha. |
| 548 | 17576158 | Production of IL-12 p70, IL-10, and interferon-alpha was observed only at extremely high doses. |
| 549 | 17576158 | A Toll-like receptor (TLR)-driven luciferase reporter assay showed dose-dependent activation of TLR2, TLR3, and TLR8, which was independent of the pseudotype, production, or transduction protocol and was abrogated on heat inactivation. |
| 550 | 17651955 | T. cruzi triggers both MyD88-dependent and TRIF-dependent innate activation pathways in macrophages and dendritic cells. |
| 551 | 17651955 | TLR-2 and TLR-9 recognize GPI anchors and parasite DNA, respectively; however other, as yet undefined receptors and ligands, also appear to be involved in innate recognition. |
| 552 | 17713026 | It has been shown that a single parenteral administration of vaccine containing bacterial ligands for TLRI, TLR2, TLR4, TLR6, and TLR9 in mice induced rapid (24 h after administration) and effective (100%), but short-term (96 h) protection against lethal challenge with Salmonella typhimurium. |
| 553 | 17804688 | CD14+ antigen-presenting cells in human dermis are less mature than their CD1a+ counterparts. |
| 554 | 17804688 | We recently demonstrated that three antigen-presenting cell (APC) subsets exist in the healthy human dermis, CD14(+) and CD1a(+) dermal APCs and migratory dermal Langerhans cells. |
| 555 | 17804688 | Here, we extend these findings by defining CD208 as an exclusive marker of migratory dermal Langerhans cells, confirming that migratory dermal Langerhans cells (CD1a(high) CD207(+) CD208(+)) and CD1a(+) dermal APCs (CD1a(mid) CD207(-) CD208(-)) are two distinct APC populations. |
| 556 | 17804688 | Using flow cytometry and multicolor fluorescence immunohistochemistry, we demonstrated that there were striking differences between CD1a(+) and CD14(+) dermal APCs in their expression of pattern recognition receptors and maturation markers. |
| 557 | 17804688 | Expression of Toll-like receptor (TLR) 2, CD206 and CD209 was largely restricted to CD14(+) dermal APCs. |
| 558 | 17804688 | Consistent with these observations, most CD14(+) dermal APCs expressed an immature phenotype when compared with CD1a(+) dermal APCs, which expressed high levels of the maturation marker CD83 on their cell surface. |
| 559 | 17804688 | However, a subset of CD14(+) dermal APCs also expressed cell-surface CD83, associated with a loss of cell-surface TLR2, suggesting that they have the capacity to mature. |
| 560 | 17804688 | CD14(+) dermal APCs are therefore the dominant cutaneous APC population capable of sensing ligands recognized by CD206, CD209 and TLR2 and subsequently may have the potential to mature. |
| 561 | 17804688 | CD68 expression was largely restricted to a subset of CD14(+) dermal APCs, while both CD14(+) and CD1a(+) dermal APCs expressed CD11b and CD11c. |
| 562 | 17804688 | CD14+ antigen-presenting cells in human dermis are less mature than their CD1a+ counterparts. |
| 563 | 17804688 | We recently demonstrated that three antigen-presenting cell (APC) subsets exist in the healthy human dermis, CD14(+) and CD1a(+) dermal APCs and migratory dermal Langerhans cells. |
| 564 | 17804688 | Here, we extend these findings by defining CD208 as an exclusive marker of migratory dermal Langerhans cells, confirming that migratory dermal Langerhans cells (CD1a(high) CD207(+) CD208(+)) and CD1a(+) dermal APCs (CD1a(mid) CD207(-) CD208(-)) are two distinct APC populations. |
| 565 | 17804688 | Using flow cytometry and multicolor fluorescence immunohistochemistry, we demonstrated that there were striking differences between CD1a(+) and CD14(+) dermal APCs in their expression of pattern recognition receptors and maturation markers. |
| 566 | 17804688 | Expression of Toll-like receptor (TLR) 2, CD206 and CD209 was largely restricted to CD14(+) dermal APCs. |
| 567 | 17804688 | Consistent with these observations, most CD14(+) dermal APCs expressed an immature phenotype when compared with CD1a(+) dermal APCs, which expressed high levels of the maturation marker CD83 on their cell surface. |
| 568 | 17804688 | However, a subset of CD14(+) dermal APCs also expressed cell-surface CD83, associated with a loss of cell-surface TLR2, suggesting that they have the capacity to mature. |
| 569 | 17804688 | CD14(+) dermal APCs are therefore the dominant cutaneous APC population capable of sensing ligands recognized by CD206, CD209 and TLR2 and subsequently may have the potential to mature. |
| 570 | 17804688 | CD68 expression was largely restricted to a subset of CD14(+) dermal APCs, while both CD14(+) and CD1a(+) dermal APCs expressed CD11b and CD11c. |
| 571 | 17989335 | Mycobacterium bovis bacillus Calmette-Guerin induces CCL5 secretion via the Toll-like receptor 2-NF-kappaB and -Jun N-terminal kinase signaling pathways. |
| 572 | 17989335 | In this study, we report that stimulation of HEK293 cells expressing human TLR2 with M. bovis BCG resulted in increased CCL2 and CCL5 secretion, as determined by an enzyme-linked immunosorbent assay. |
| 573 | 17989335 | M. bovis BCG infection resulted in the activation of c-Jun N-terminal kinase (JNK), and the inhibition of JNK activity had a significant effect on M. bovis BCG-dependent CCL5 secretion in TLR2-expressing cells but no effect on M. bovis BCG-dependent CCL2 secretion from infected HEK293 cells expressing human TLR2. |
| 574 | 17989335 | The M. bovis BCG-induced CCL5 release was attenuated by sulfasalazine (a well-described inhibitor of NF-kappaB activity), BAY 11-7082 (an IkappaB phosphorylation inhibitor), and ALLN (a well-described inhibitor of NF-kappaB activation that prevents degradation of IkappaB and eventually results in a lack of translocated NF-kappaB in the nucleus). |
| 575 | 17989335 | In addition, stimulation of TLR2-expressing cells with M. bovis BCG resulted in translocation of NF-kappaB subunits from the cytoplasmic to the nuclear fraction, and stimulation of cells with M. bovis BCG activated IkappaB kinase alphabeta. |
| 576 | 17989335 | These findings indicate that M. bovis BCG induces CCL5 production through mechanisms that include a TLR2-dependent component that requires JNK and NF-kappaB activities. |
| 577 | 17989335 | Mycobacterium bovis bacillus Calmette-Guerin induces CCL5 secretion via the Toll-like receptor 2-NF-kappaB and -Jun N-terminal kinase signaling pathways. |
| 578 | 17989335 | In this study, we report that stimulation of HEK293 cells expressing human TLR2 with M. bovis BCG resulted in increased CCL2 and CCL5 secretion, as determined by an enzyme-linked immunosorbent assay. |
| 579 | 17989335 | M. bovis BCG infection resulted in the activation of c-Jun N-terminal kinase (JNK), and the inhibition of JNK activity had a significant effect on M. bovis BCG-dependent CCL5 secretion in TLR2-expressing cells but no effect on M. bovis BCG-dependent CCL2 secretion from infected HEK293 cells expressing human TLR2. |
| 580 | 17989335 | The M. bovis BCG-induced CCL5 release was attenuated by sulfasalazine (a well-described inhibitor of NF-kappaB activity), BAY 11-7082 (an IkappaB phosphorylation inhibitor), and ALLN (a well-described inhibitor of NF-kappaB activation that prevents degradation of IkappaB and eventually results in a lack of translocated NF-kappaB in the nucleus). |
| 581 | 17989335 | In addition, stimulation of TLR2-expressing cells with M. bovis BCG resulted in translocation of NF-kappaB subunits from the cytoplasmic to the nuclear fraction, and stimulation of cells with M. bovis BCG activated IkappaB kinase alphabeta. |
| 582 | 17989335 | These findings indicate that M. bovis BCG induces CCL5 production through mechanisms that include a TLR2-dependent component that requires JNK and NF-kappaB activities. |
| 583 | 17989335 | Mycobacterium bovis bacillus Calmette-Guerin induces CCL5 secretion via the Toll-like receptor 2-NF-kappaB and -Jun N-terminal kinase signaling pathways. |
| 584 | 17989335 | In this study, we report that stimulation of HEK293 cells expressing human TLR2 with M. bovis BCG resulted in increased CCL2 and CCL5 secretion, as determined by an enzyme-linked immunosorbent assay. |
| 585 | 17989335 | M. bovis BCG infection resulted in the activation of c-Jun N-terminal kinase (JNK), and the inhibition of JNK activity had a significant effect on M. bovis BCG-dependent CCL5 secretion in TLR2-expressing cells but no effect on M. bovis BCG-dependent CCL2 secretion from infected HEK293 cells expressing human TLR2. |
| 586 | 17989335 | The M. bovis BCG-induced CCL5 release was attenuated by sulfasalazine (a well-described inhibitor of NF-kappaB activity), BAY 11-7082 (an IkappaB phosphorylation inhibitor), and ALLN (a well-described inhibitor of NF-kappaB activation that prevents degradation of IkappaB and eventually results in a lack of translocated NF-kappaB in the nucleus). |
| 587 | 17989335 | In addition, stimulation of TLR2-expressing cells with M. bovis BCG resulted in translocation of NF-kappaB subunits from the cytoplasmic to the nuclear fraction, and stimulation of cells with M. bovis BCG activated IkappaB kinase alphabeta. |
| 588 | 17989335 | These findings indicate that M. bovis BCG induces CCL5 production through mechanisms that include a TLR2-dependent component that requires JNK and NF-kappaB activities. |
| 589 | 17989335 | Mycobacterium bovis bacillus Calmette-Guerin induces CCL5 secretion via the Toll-like receptor 2-NF-kappaB and -Jun N-terminal kinase signaling pathways. |
| 590 | 17989335 | In this study, we report that stimulation of HEK293 cells expressing human TLR2 with M. bovis BCG resulted in increased CCL2 and CCL5 secretion, as determined by an enzyme-linked immunosorbent assay. |
| 591 | 17989335 | M. bovis BCG infection resulted in the activation of c-Jun N-terminal kinase (JNK), and the inhibition of JNK activity had a significant effect on M. bovis BCG-dependent CCL5 secretion in TLR2-expressing cells but no effect on M. bovis BCG-dependent CCL2 secretion from infected HEK293 cells expressing human TLR2. |
| 592 | 17989335 | The M. bovis BCG-induced CCL5 release was attenuated by sulfasalazine (a well-described inhibitor of NF-kappaB activity), BAY 11-7082 (an IkappaB phosphorylation inhibitor), and ALLN (a well-described inhibitor of NF-kappaB activation that prevents degradation of IkappaB and eventually results in a lack of translocated NF-kappaB in the nucleus). |
| 593 | 17989335 | In addition, stimulation of TLR2-expressing cells with M. bovis BCG resulted in translocation of NF-kappaB subunits from the cytoplasmic to the nuclear fraction, and stimulation of cells with M. bovis BCG activated IkappaB kinase alphabeta. |
| 594 | 17989335 | These findings indicate that M. bovis BCG induces CCL5 production through mechanisms that include a TLR2-dependent component that requires JNK and NF-kappaB activities. |
| 595 | 17989335 | Mycobacterium bovis bacillus Calmette-Guerin induces CCL5 secretion via the Toll-like receptor 2-NF-kappaB and -Jun N-terminal kinase signaling pathways. |
| 596 | 17989335 | In this study, we report that stimulation of HEK293 cells expressing human TLR2 with M. bovis BCG resulted in increased CCL2 and CCL5 secretion, as determined by an enzyme-linked immunosorbent assay. |
| 597 | 17989335 | M. bovis BCG infection resulted in the activation of c-Jun N-terminal kinase (JNK), and the inhibition of JNK activity had a significant effect on M. bovis BCG-dependent CCL5 secretion in TLR2-expressing cells but no effect on M. bovis BCG-dependent CCL2 secretion from infected HEK293 cells expressing human TLR2. |
| 598 | 17989335 | The M. bovis BCG-induced CCL5 release was attenuated by sulfasalazine (a well-described inhibitor of NF-kappaB activity), BAY 11-7082 (an IkappaB phosphorylation inhibitor), and ALLN (a well-described inhibitor of NF-kappaB activation that prevents degradation of IkappaB and eventually results in a lack of translocated NF-kappaB in the nucleus). |
| 599 | 17989335 | In addition, stimulation of TLR2-expressing cells with M. bovis BCG resulted in translocation of NF-kappaB subunits from the cytoplasmic to the nuclear fraction, and stimulation of cells with M. bovis BCG activated IkappaB kinase alphabeta. |
| 600 | 17989335 | These findings indicate that M. bovis BCG induces CCL5 production through mechanisms that include a TLR2-dependent component that requires JNK and NF-kappaB activities. |
| 601 | 18220804 | Furthermore hyperlipidemic mice deficient in TLR2, TLR4, and MyD88 signaling exhibit diminished inflammatory responses and decreased atherosclerosis. |
| 602 | 18220804 | Furthermore, we have demonstrated that P. gingivalis infection accelerates atherosclerosis in hyperlipidemic mice with an associated increase in expression of TLR2 and TLR4 in atherosclerotic lesions. |
| 603 | 18220804 | Furthermore hyperlipidemic mice deficient in TLR2, TLR4, and MyD88 signaling exhibit diminished inflammatory responses and decreased atherosclerosis. |
| 604 | 18220804 | Furthermore, we have demonstrated that P. gingivalis infection accelerates atherosclerosis in hyperlipidemic mice with an associated increase in expression of TLR2 and TLR4 in atherosclerotic lesions. |
| 605 | 18287580 | Role of protein tyrosine kinase and Erk1/2 activities in the Toll-like receptor 2-induced cellular activation of murine B cells by neisserial porin. |
| 606 | 18287580 | PorB was able to induce (i) protein tyrosine kinase (PTK) activity, (ii) the phosphorylation of Erk1 and Erk2, and (iii) IkappaB-alpha phosphorylation, leading to NF-kappaB nuclear translocation in B cells in a TLR2-dependent manner. |
| 607 | 18287580 | PorB-induced NF-kappaB nuclear translocation was not dependent on either PTK or Erk1/2 activities. |
| 608 | 18287580 | However, B-cell proliferation and the induction of increased surface expression of CD86 by PorB were dependent on PTK activity and not Erk1/2 activation. |
| 609 | 18287580 | In conclusion, PorB acts through TLR2 as a B-cell mitogen, triggering tyrosine phosphorylation of various cellular proteins that are involved in proliferation and CD86 expression, as well as the phosphorylation of Erk1/2, which is not necessary for CD86 upregulation or the proliferation of B cells. |
| 610 | 18287580 | Role of protein tyrosine kinase and Erk1/2 activities in the Toll-like receptor 2-induced cellular activation of murine B cells by neisserial porin. |
| 611 | 18287580 | PorB was able to induce (i) protein tyrosine kinase (PTK) activity, (ii) the phosphorylation of Erk1 and Erk2, and (iii) IkappaB-alpha phosphorylation, leading to NF-kappaB nuclear translocation in B cells in a TLR2-dependent manner. |
| 612 | 18287580 | PorB-induced NF-kappaB nuclear translocation was not dependent on either PTK or Erk1/2 activities. |
| 613 | 18287580 | However, B-cell proliferation and the induction of increased surface expression of CD86 by PorB were dependent on PTK activity and not Erk1/2 activation. |
| 614 | 18287580 | In conclusion, PorB acts through TLR2 as a B-cell mitogen, triggering tyrosine phosphorylation of various cellular proteins that are involved in proliferation and CD86 expression, as well as the phosphorylation of Erk1/2, which is not necessary for CD86 upregulation or the proliferation of B cells. |
| 615 | 18287580 | Role of protein tyrosine kinase and Erk1/2 activities in the Toll-like receptor 2-induced cellular activation of murine B cells by neisserial porin. |
| 616 | 18287580 | PorB was able to induce (i) protein tyrosine kinase (PTK) activity, (ii) the phosphorylation of Erk1 and Erk2, and (iii) IkappaB-alpha phosphorylation, leading to NF-kappaB nuclear translocation in B cells in a TLR2-dependent manner. |
| 617 | 18287580 | PorB-induced NF-kappaB nuclear translocation was not dependent on either PTK or Erk1/2 activities. |
| 618 | 18287580 | However, B-cell proliferation and the induction of increased surface expression of CD86 by PorB were dependent on PTK activity and not Erk1/2 activation. |
| 619 | 18287580 | In conclusion, PorB acts through TLR2 as a B-cell mitogen, triggering tyrosine phosphorylation of various cellular proteins that are involved in proliferation and CD86 expression, as well as the phosphorylation of Erk1/2, which is not necessary for CD86 upregulation or the proliferation of B cells. |
| 620 | 18413606 | The peptide was administered to BALB/c mice three times at monthly intervals, either alone or in the context of a synthetic lipopeptide vaccine candidate (P25-P2C-HPV) produced by linkage of the HPV peptide with a broadly recognized T helper epitope (P25) and the Toll-like receptor-2 (TLR2) ligand dipalmitoyl-S-glyceryl cysteine (P2C). |
| 621 | 18413606 | The L2-specific antibody response depended on MHC class II, CD40, and MyD88 signaling. |
| 622 | 18453609 | The observation that intracellular Ft LVS colocalizes with TLR2 and MyD88 inside macrophages suggested that Ft LVS might signal from within the phagosome. |
| 623 | 18453609 | IL-1beta secretion was also diminished in Ft LVS-infected IFN-beta(-/-) macrophages. rIFN-beta failed to restore IL-1beta secretion in LVSDeltaiglC-infected macrophages, suggesting that signals in addition to IFN-beta are required for assembly of the inflammasome and activation of caspase-1. |
| 624 | 18490734 | Before or after AAC, animals received BCG, TLR4 agonist, IFN-gamma, or TLR4 antagonist i.p. |
| 625 | 18490734 | BCG decreased the expression of TLR2 or TLR4 on the heart tissue but TLR4 agonist increased the expression of TLR2 or TLR4 on the immune cells that infiltrate into the heart tissue. |
| 626 | 18490734 | This led to an increased expression ratio of IFN-gamma/TGF-beta in the heart. |
| 627 | 18641352 | Adenovirus vector-induced innate inflammatory mediators, MAPK signaling, as well as adaptive immune responses are dependent upon both TLR2 and TLR9 in vivo. |
| 628 | 18641352 | The complexity of Ad-induced innate immune responses was confirmed when we also found that both TLR2 and MyD88 functions are required for the sustained activation of ERK1/2. |
| 629 | 18641352 | Finally, we found that several Ad-induced innate immune responses are dependent on both TLR2 and TLR9. |
| 630 | 18641352 | Adenovirus vector-induced innate inflammatory mediators, MAPK signaling, as well as adaptive immune responses are dependent upon both TLR2 and TLR9 in vivo. |
| 631 | 18641352 | The complexity of Ad-induced innate immune responses was confirmed when we also found that both TLR2 and MyD88 functions are required for the sustained activation of ERK1/2. |
| 632 | 18641352 | Finally, we found that several Ad-induced innate immune responses are dependent on both TLR2 and TLR9. |
| 633 | 18641352 | Adenovirus vector-induced innate inflammatory mediators, MAPK signaling, as well as adaptive immune responses are dependent upon both TLR2 and TLR9 in vivo. |
| 634 | 18641352 | The complexity of Ad-induced innate immune responses was confirmed when we also found that both TLR2 and MyD88 functions are required for the sustained activation of ERK1/2. |
| 635 | 18641352 | Finally, we found that several Ad-induced innate immune responses are dependent on both TLR2 and TLR9. |
| 636 | 18686103 | Since T-regulatory cells and other T-cell subsets express TLR2, and TLR2 engagement modifies functionality and activation state of these cells, we speculate that most effects induced by natural and chemically derived ZPS may be explained by their TLR2 agonist properties, presumably through the combined action on TLR2-expressing APCs and T cells. |
| 637 | 18948575 | In this study, we showed that direct TLR2-myeloid differentiating factor 88 (MyD88) signaling in CD8 T cells was also required for their efficient clonal expansion by promoting the survival of activated T cells on vaccinia viral infection in vivo. |
| 638 | 18948575 | Furthermore, we observed that direct TLR2 ligation on CD8 T cells promoted CD8 T-cell proliferation and survival in vitro in a manner dependent on the phosphatidylinositol 3-kinase (PI3K)-Akt pathway activation and that activation of Akt controlled memory cell formation in vivo. |
| 639 | 18948575 | In this study, we showed that direct TLR2-myeloid differentiating factor 88 (MyD88) signaling in CD8 T cells was also required for their efficient clonal expansion by promoting the survival of activated T cells on vaccinia viral infection in vivo. |
| 640 | 18948575 | Furthermore, we observed that direct TLR2 ligation on CD8 T cells promoted CD8 T-cell proliferation and survival in vitro in a manner dependent on the phosphatidylinositol 3-kinase (PI3K)-Akt pathway activation and that activation of Akt controlled memory cell formation in vivo. |
| 641 | 19013492 | TLR4 and MyD88 control protection and pulmonary granulocytic recruitment in a murine intranasal RSV immunization and challenge model. |
| 642 | 19013492 | An intranasal vaccine composed of Toll-like receptor 2 (TLR2) ligand Neisseria meningitidis outer membrane proteins and Toll-like receptor 4 (TLR4) ligand Shigella flexneri lipopolysaccharide (LPS) (Protollin) and enriched respiratory syncytial virus (RSV) proteins (eRSV) has been demonstrated to promote balanced Th1/Th2 responses without eosinophil recruitment and to protect against challenge in mouse models. |
| 643 | 19013492 | We used TLR2, TLR4 and myeloid differentiation factor 88 (MyD88) knock-out (-/-) mice to investigate the roles of these signalling pathways on immunogenicity, protection and pulmonary infiltrates following RSV immunization and challenge. |
| 644 | 19013492 | In contrast, an intact MyD88 pathway was crucial to elicit a balanced type 1:type 2 immune response, characterized by increased splenocyte production of antigen-induced IFNgamma and IL-10 with concomitant reduction of IL5, IgG2a isotype switching and abrogation of pulmonary eosinophil recruitment following challenge. |
| 645 | 19013492 | Both TLR4 and MyD88-signalling were required for optimal protection against challenge. |
| 646 | 19013492 | The upregulation of early signalling molecules IFN-beta, TNFalpha, CD40 and CD86 were studied in splenocytes isolated from naïve TLR2, TLR4 and MyD88-/- mice following stimulation with vaccine components. |
| 647 | 19013492 | Splenocytes from TLR4-/- mice displayed reduced IFN-beta while those of MyD88-/- mice elicited less TNFalpha and lower expression of CD40 and CD86 on CD11c+ cells. |
| 648 | 19013492 | Together, our results suggest that optimal immunogenicity and protection against RSV without risk of enhanced pulmonary inflammation requires intact TLR4/MyD88-dependent signalling. |
| 649 | 19013492 | TLR4 and MyD88 control protection and pulmonary granulocytic recruitment in a murine intranasal RSV immunization and challenge model. |
| 650 | 19013492 | An intranasal vaccine composed of Toll-like receptor 2 (TLR2) ligand Neisseria meningitidis outer membrane proteins and Toll-like receptor 4 (TLR4) ligand Shigella flexneri lipopolysaccharide (LPS) (Protollin) and enriched respiratory syncytial virus (RSV) proteins (eRSV) has been demonstrated to promote balanced Th1/Th2 responses without eosinophil recruitment and to protect against challenge in mouse models. |
| 651 | 19013492 | We used TLR2, TLR4 and myeloid differentiation factor 88 (MyD88) knock-out (-/-) mice to investigate the roles of these signalling pathways on immunogenicity, protection and pulmonary infiltrates following RSV immunization and challenge. |
| 652 | 19013492 | In contrast, an intact MyD88 pathway was crucial to elicit a balanced type 1:type 2 immune response, characterized by increased splenocyte production of antigen-induced IFNgamma and IL-10 with concomitant reduction of IL5, IgG2a isotype switching and abrogation of pulmonary eosinophil recruitment following challenge. |
| 653 | 19013492 | Both TLR4 and MyD88-signalling were required for optimal protection against challenge. |
| 654 | 19013492 | The upregulation of early signalling molecules IFN-beta, TNFalpha, CD40 and CD86 were studied in splenocytes isolated from naïve TLR2, TLR4 and MyD88-/- mice following stimulation with vaccine components. |
| 655 | 19013492 | Splenocytes from TLR4-/- mice displayed reduced IFN-beta while those of MyD88-/- mice elicited less TNFalpha and lower expression of CD40 and CD86 on CD11c+ cells. |
| 656 | 19013492 | Together, our results suggest that optimal immunogenicity and protection against RSV without risk of enhanced pulmonary inflammation requires intact TLR4/MyD88-dependent signalling. |
| 657 | 19013492 | TLR4 and MyD88 control protection and pulmonary granulocytic recruitment in a murine intranasal RSV immunization and challenge model. |
| 658 | 19013492 | An intranasal vaccine composed of Toll-like receptor 2 (TLR2) ligand Neisseria meningitidis outer membrane proteins and Toll-like receptor 4 (TLR4) ligand Shigella flexneri lipopolysaccharide (LPS) (Protollin) and enriched respiratory syncytial virus (RSV) proteins (eRSV) has been demonstrated to promote balanced Th1/Th2 responses without eosinophil recruitment and to protect against challenge in mouse models. |
| 659 | 19013492 | We used TLR2, TLR4 and myeloid differentiation factor 88 (MyD88) knock-out (-/-) mice to investigate the roles of these signalling pathways on immunogenicity, protection and pulmonary infiltrates following RSV immunization and challenge. |
| 660 | 19013492 | In contrast, an intact MyD88 pathway was crucial to elicit a balanced type 1:type 2 immune response, characterized by increased splenocyte production of antigen-induced IFNgamma and IL-10 with concomitant reduction of IL5, IgG2a isotype switching and abrogation of pulmonary eosinophil recruitment following challenge. |
| 661 | 19013492 | Both TLR4 and MyD88-signalling were required for optimal protection against challenge. |
| 662 | 19013492 | The upregulation of early signalling molecules IFN-beta, TNFalpha, CD40 and CD86 were studied in splenocytes isolated from naïve TLR2, TLR4 and MyD88-/- mice following stimulation with vaccine components. |
| 663 | 19013492 | Splenocytes from TLR4-/- mice displayed reduced IFN-beta while those of MyD88-/- mice elicited less TNFalpha and lower expression of CD40 and CD86 on CD11c+ cells. |
| 664 | 19013492 | Together, our results suggest that optimal immunogenicity and protection against RSV without risk of enhanced pulmonary inflammation requires intact TLR4/MyD88-dependent signalling. |
| 665 | 19027958 | Chirality of TLR-2 ligand Pam3CysSK4 in fully synthetic peptide conjugates critically influences the induction of specific CD8+ T-cells. |
| 666 | 19027958 | In the current study we have investigated the behaviour of two diastereomers of the TLR-2 ligand Pam(3)CSK(4) (Pam) derivatives, namely the R- and S-epimers at C-2 of the glycerol moiety. |
| 667 | 19027958 | In summary we show that the favourable effects of the Pam(R)-configuration of TLR-2 ligand can be attributed to direct effects on dendritic cells resulting in enhancement of CD8(+) T-cell responses. |
| 668 | 19027958 | Chirality of TLR-2 ligand Pam3CysSK4 in fully synthetic peptide conjugates critically influences the induction of specific CD8+ T-cells. |
| 669 | 19027958 | In the current study we have investigated the behaviour of two diastereomers of the TLR-2 ligand Pam(3)CSK(4) (Pam) derivatives, namely the R- and S-epimers at C-2 of the glycerol moiety. |
| 670 | 19027958 | In summary we show that the favourable effects of the Pam(R)-configuration of TLR-2 ligand can be attributed to direct effects on dendritic cells resulting in enhancement of CD8(+) T-cell responses. |
| 671 | 19027958 | Chirality of TLR-2 ligand Pam3CysSK4 in fully synthetic peptide conjugates critically influences the induction of specific CD8+ T-cells. |
| 672 | 19027958 | In the current study we have investigated the behaviour of two diastereomers of the TLR-2 ligand Pam(3)CSK(4) (Pam) derivatives, namely the R- and S-epimers at C-2 of the glycerol moiety. |
| 673 | 19027958 | In summary we show that the favourable effects of the Pam(R)-configuration of TLR-2 ligand can be attributed to direct effects on dendritic cells resulting in enhancement of CD8(+) T-cell responses. |
| 674 | 19054578 | In this study, we evaluated the patterns of TLR2-, TLR3- and TLR9-expressing antigen presenting cells (APCs) in spleen and blood of gnotobiotic (Gn) pigs after colonization with a mixture of two strains of lactic acid bacteria (LAB), Lactobacillus acidophilus and Lactobacillus reuteri or infection with the virulent human rotavirus (HRV) Wa strain. |
| 675 | 19054578 | We demonstrated that LAB induced strong TLR2-expressing APC responses in blood and spleen, HRV induced a TLR3 response in spleen, and TLR9 responses were induced by either HRV (in spleen) or LAB (in blood). |
| 676 | 19054578 | LAB and HRV have an additive effect on TLR2- and TLR9-expressing APC responses, consistent with the adjuvant effect of LAB. |
| 677 | 19054578 | LAB enhanced the IFN-gamma and IL-4 responses in serum, but it had a suppressive effect on the TLR3- and TLR9-expressing CD14- APC responses in spleen and the serum IFN-alpha response induced by HRV. |
| 678 | 19054578 | These results elucidated the systemic TLR2-, TLR3-, and TLR9-expressing monocyte/macrophage and cDC responses after HRV infection, LAB colonization, and the two combined. |
| 679 | 19054578 | In this study, we evaluated the patterns of TLR2-, TLR3- and TLR9-expressing antigen presenting cells (APCs) in spleen and blood of gnotobiotic (Gn) pigs after colonization with a mixture of two strains of lactic acid bacteria (LAB), Lactobacillus acidophilus and Lactobacillus reuteri or infection with the virulent human rotavirus (HRV) Wa strain. |
| 680 | 19054578 | We demonstrated that LAB induced strong TLR2-expressing APC responses in blood and spleen, HRV induced a TLR3 response in spleen, and TLR9 responses were induced by either HRV (in spleen) or LAB (in blood). |
| 681 | 19054578 | LAB and HRV have an additive effect on TLR2- and TLR9-expressing APC responses, consistent with the adjuvant effect of LAB. |
| 682 | 19054578 | LAB enhanced the IFN-gamma and IL-4 responses in serum, but it had a suppressive effect on the TLR3- and TLR9-expressing CD14- APC responses in spleen and the serum IFN-alpha response induced by HRV. |
| 683 | 19054578 | These results elucidated the systemic TLR2-, TLR3-, and TLR9-expressing monocyte/macrophage and cDC responses after HRV infection, LAB colonization, and the two combined. |
| 684 | 19054578 | In this study, we evaluated the patterns of TLR2-, TLR3- and TLR9-expressing antigen presenting cells (APCs) in spleen and blood of gnotobiotic (Gn) pigs after colonization with a mixture of two strains of lactic acid bacteria (LAB), Lactobacillus acidophilus and Lactobacillus reuteri or infection with the virulent human rotavirus (HRV) Wa strain. |
| 685 | 19054578 | We demonstrated that LAB induced strong TLR2-expressing APC responses in blood and spleen, HRV induced a TLR3 response in spleen, and TLR9 responses were induced by either HRV (in spleen) or LAB (in blood). |
| 686 | 19054578 | LAB and HRV have an additive effect on TLR2- and TLR9-expressing APC responses, consistent with the adjuvant effect of LAB. |
| 687 | 19054578 | LAB enhanced the IFN-gamma and IL-4 responses in serum, but it had a suppressive effect on the TLR3- and TLR9-expressing CD14- APC responses in spleen and the serum IFN-alpha response induced by HRV. |
| 688 | 19054578 | These results elucidated the systemic TLR2-, TLR3-, and TLR9-expressing monocyte/macrophage and cDC responses after HRV infection, LAB colonization, and the two combined. |
| 689 | 19054578 | In this study, we evaluated the patterns of TLR2-, TLR3- and TLR9-expressing antigen presenting cells (APCs) in spleen and blood of gnotobiotic (Gn) pigs after colonization with a mixture of two strains of lactic acid bacteria (LAB), Lactobacillus acidophilus and Lactobacillus reuteri or infection with the virulent human rotavirus (HRV) Wa strain. |
| 690 | 19054578 | We demonstrated that LAB induced strong TLR2-expressing APC responses in blood and spleen, HRV induced a TLR3 response in spleen, and TLR9 responses were induced by either HRV (in spleen) or LAB (in blood). |
| 691 | 19054578 | LAB and HRV have an additive effect on TLR2- and TLR9-expressing APC responses, consistent with the adjuvant effect of LAB. |
| 692 | 19054578 | LAB enhanced the IFN-gamma and IL-4 responses in serum, but it had a suppressive effect on the TLR3- and TLR9-expressing CD14- APC responses in spleen and the serum IFN-alpha response induced by HRV. |
| 693 | 19054578 | These results elucidated the systemic TLR2-, TLR3-, and TLR9-expressing monocyte/macrophage and cDC responses after HRV infection, LAB colonization, and the two combined. |
| 694 | 19056540 | Considering the importance of CD14 - TLR2/TLR4 interactions in macrophage signalling, we determined the polymorphism of TLR2 and TLR4 genes as well as macrophage expression of TLR2 for the volunteers with and without skin reactivity to PPD. |
| 695 | 19056540 | A significant increase in CD14 density was observed on macrophages stimulated with PPD and LPS but not with live BCG bacilli. |
| 696 | 19056540 | However, we could see no association between the polymorphisms of TLR4 (Asp299Gly and Thr399Ile) and TLR2 genes (Arg753Gln and Arg677Trp) and skin responses to PPD. |
| 697 | 19056540 | Considering the importance of CD14 - TLR2/TLR4 interactions in macrophage signalling, we determined the polymorphism of TLR2 and TLR4 genes as well as macrophage expression of TLR2 for the volunteers with and without skin reactivity to PPD. |
| 698 | 19056540 | A significant increase in CD14 density was observed on macrophages stimulated with PPD and LPS but not with live BCG bacilli. |
| 699 | 19056540 | However, we could see no association between the polymorphisms of TLR4 (Asp299Gly and Thr399Ile) and TLR2 genes (Arg753Gln and Arg677Trp) and skin responses to PPD. |
| 700 | 19058846 | Interestingly, we demonstrate that OMPLL-DNA and RMPLL-DNA are able to mediate dendritic cell activation via toll-like receptor 2 as opposed to mannan alone which mediates via toll-like receptor 4. |
| 701 | 19107191 | The 60 kDa heat shock protein (HSP60) has been reported to influence T-cell responses in two ways: as a ligand of toll-like receptor 2 signalling and as an antigen. |
| 702 | 19107191 | Presentation of HSP60 by activated T cells was found to be MHC-restricted and dependent on accessory molecules - CD28, CD80 and CD86. |
| 703 | 19107191 | Anti-ergotypic T cells responded to T-cell HSP60 by proliferation and secreted IFNgamma and TGFbeta1. |
| 704 | 19107191 | In vivo, adoptive transfer of an anti-ergotypic HSP60-specific T-cell line led to decreased secretion of IFNgamma by arthritogenic T cells and ameliorated adjuvant arthritis (AA). |
| 705 | 19109135 | Activated human neonatal CD8+ T cells are subject to immunomodulation by direct TLR2 or TLR5 stimulation. |
| 706 | 19109135 | In concert with TCR stimulation, only Pam(3)Cys (palmitoyl-3-Cys-Ser-(Lys)(4)) and flagellin monomers significantly enhanced proliferation, CD25(+) expression, IL-2, IFN-gamma, TNF-alpha, and intracellular granzyme B expression. |
| 707 | 19109135 | TLR2 and TLR5 mRNA was detected in the CD8(+) T cells. |
| 708 | 19109135 | Blocking studies confirmed that the increase in IFN-gamma production was by the direct triggering of surface TLR2 or TLR5. |
| 709 | 19109135 | The simultaneous exposure of CD8(+) T cells to both TLR agonists had an additive effect on IFN-gamma production. |
| 710 | 19109135 | Activated human neonatal CD8+ T cells are subject to immunomodulation by direct TLR2 or TLR5 stimulation. |
| 711 | 19109135 | In concert with TCR stimulation, only Pam(3)Cys (palmitoyl-3-Cys-Ser-(Lys)(4)) and flagellin monomers significantly enhanced proliferation, CD25(+) expression, IL-2, IFN-gamma, TNF-alpha, and intracellular granzyme B expression. |
| 712 | 19109135 | TLR2 and TLR5 mRNA was detected in the CD8(+) T cells. |
| 713 | 19109135 | Blocking studies confirmed that the increase in IFN-gamma production was by the direct triggering of surface TLR2 or TLR5. |
| 714 | 19109135 | The simultaneous exposure of CD8(+) T cells to both TLR agonists had an additive effect on IFN-gamma production. |
| 715 | 19109135 | Activated human neonatal CD8+ T cells are subject to immunomodulation by direct TLR2 or TLR5 stimulation. |
| 716 | 19109135 | In concert with TCR stimulation, only Pam(3)Cys (palmitoyl-3-Cys-Ser-(Lys)(4)) and flagellin monomers significantly enhanced proliferation, CD25(+) expression, IL-2, IFN-gamma, TNF-alpha, and intracellular granzyme B expression. |
| 717 | 19109135 | TLR2 and TLR5 mRNA was detected in the CD8(+) T cells. |
| 718 | 19109135 | Blocking studies confirmed that the increase in IFN-gamma production was by the direct triggering of surface TLR2 or TLR5. |
| 719 | 19109135 | The simultaneous exposure of CD8(+) T cells to both TLR agonists had an additive effect on IFN-gamma production. |
| 720 | 19129756 | A genital tract peptide epitope vaccine targeting TLR-2 efficiently induces local and systemic CD8+ T cells and protects against herpes simplex virus type 2 challenge. |
| 721 | 19129756 | To test this hypothesis, we intravaginally (IVAG) immunized wild-type B6, TLR-2 (TLR2(-/-)) or myeloid differentiation factor 88 deficient (MyD88(-/-)) mice with a herpes simplex virus type 2 (HSV-2) CD8+ T-cell peptide epitope extended by a palmitic acid moiety (a TLR-2 agonist). |
| 722 | 19129756 | Moreover, lipopeptide-immunized TLR2(-/-) and MyD88(-/-) mice developed significantly less HSV-specific CD8+ T-cell response, earlier death, faster disease progression, and higher vaginal HSV-2 titers compared to lipopeptide-immunized wild-type B6 mice. |
| 723 | 19129756 | A genital tract peptide epitope vaccine targeting TLR-2 efficiently induces local and systemic CD8+ T cells and protects against herpes simplex virus type 2 challenge. |
| 724 | 19129756 | To test this hypothesis, we intravaginally (IVAG) immunized wild-type B6, TLR-2 (TLR2(-/-)) or myeloid differentiation factor 88 deficient (MyD88(-/-)) mice with a herpes simplex virus type 2 (HSV-2) CD8+ T-cell peptide epitope extended by a palmitic acid moiety (a TLR-2 agonist). |
| 725 | 19129756 | Moreover, lipopeptide-immunized TLR2(-/-) and MyD88(-/-) mice developed significantly less HSV-specific CD8+ T-cell response, earlier death, faster disease progression, and higher vaginal HSV-2 titers compared to lipopeptide-immunized wild-type B6 mice. |
| 726 | 19129756 | A genital tract peptide epitope vaccine targeting TLR-2 efficiently induces local and systemic CD8+ T cells and protects against herpes simplex virus type 2 challenge. |
| 727 | 19129756 | To test this hypothesis, we intravaginally (IVAG) immunized wild-type B6, TLR-2 (TLR2(-/-)) or myeloid differentiation factor 88 deficient (MyD88(-/-)) mice with a herpes simplex virus type 2 (HSV-2) CD8+ T-cell peptide epitope extended by a palmitic acid moiety (a TLR-2 agonist). |
| 728 | 19129756 | Moreover, lipopeptide-immunized TLR2(-/-) and MyD88(-/-) mice developed significantly less HSV-specific CD8+ T-cell response, earlier death, faster disease progression, and higher vaginal HSV-2 titers compared to lipopeptide-immunized wild-type B6 mice. |
| 729 | 19130558 | TLR2 and TLR4 signaling shapes specific antibody responses to Salmonella typhi antigens. |
| 730 | 19186221 | As compared to healthy controls, patients were characterized with down-regulation of TLR2 and TLR4/CD14 complex on PB monocytes (p<0.01), decreased share of CD14+CD16+ DCs precursors (p<0.01), decreased CD86 expression on PB DCs (p<0.05) and a Th2 shift of cytokine profile. |
| 731 | 19186221 | Respivax modulated differentially the surface expression of pattern-recognition receptors on PB monocytes, increasing TLR2 and CD14 without affecting TLR4 expression. |
| 732 | 19186221 | As compared to healthy controls, patients were characterized with down-regulation of TLR2 and TLR4/CD14 complex on PB monocytes (p<0.01), decreased share of CD14+CD16+ DCs precursors (p<0.01), decreased CD86 expression on PB DCs (p<0.05) and a Th2 shift of cytokine profile. |
| 733 | 19186221 | Respivax modulated differentially the surface expression of pattern-recognition receptors on PB monocytes, increasing TLR2 and CD14 without affecting TLR4 expression. |
| 734 | 19198566 | By interacting with STAT1 and Jak1, the viral P and V proteins prevent the type I interferon receptor (IFNAR) signalling. |
| 735 | 19198566 | The H protein binds to TLR2, which then transduces an activation signal and CD150 expression in monocytes. |
| 736 | 19252500 | We show that two pathogen recognition receptors, Toll-like receptor 2 (TLR2) and dectin-1, recognizing the same microbial stimulus, stimulate distinct innate and adaptive responses. |
| 737 | 19252500 | TLR2 signaling induced splenic dendritic cells (DCs) to express the retinoic acid metabolizing enzyme retinaldehyde dehydrogenase type 2 and interleukin-10 (IL-10) and to metabolize vitamin A and stimulate Foxp3(+) T regulatory cells (T(reg) cells). |
| 738 | 19252500 | Retinoic acid acted on DCs to induce suppressor of cytokine signaling-3 expression, which suppressed activation of p38 mitogen-activated protein kinase and proinflammatory cytokines. |
| 739 | 19252500 | Consistent with this finding, TLR2 signaling induced T(reg) cells and suppressed IL-23 and T helper type 17 (T(H)17) and T(H)1-mediated autoimmune responses in vivo. |
| 740 | 19252500 | In contrast, dectin-1 signaling mostly induced IL-23 and proinflammatory cytokines and augmented T(H)17 and T(H)1-mediated autoimmune responses in vivo. |
| 741 | 19252500 | We show that two pathogen recognition receptors, Toll-like receptor 2 (TLR2) and dectin-1, recognizing the same microbial stimulus, stimulate distinct innate and adaptive responses. |
| 742 | 19252500 | TLR2 signaling induced splenic dendritic cells (DCs) to express the retinoic acid metabolizing enzyme retinaldehyde dehydrogenase type 2 and interleukin-10 (IL-10) and to metabolize vitamin A and stimulate Foxp3(+) T regulatory cells (T(reg) cells). |
| 743 | 19252500 | Retinoic acid acted on DCs to induce suppressor of cytokine signaling-3 expression, which suppressed activation of p38 mitogen-activated protein kinase and proinflammatory cytokines. |
| 744 | 19252500 | Consistent with this finding, TLR2 signaling induced T(reg) cells and suppressed IL-23 and T helper type 17 (T(H)17) and T(H)1-mediated autoimmune responses in vivo. |
| 745 | 19252500 | In contrast, dectin-1 signaling mostly induced IL-23 and proinflammatory cytokines and augmented T(H)17 and T(H)1-mediated autoimmune responses in vivo. |
| 746 | 19252500 | We show that two pathogen recognition receptors, Toll-like receptor 2 (TLR2) and dectin-1, recognizing the same microbial stimulus, stimulate distinct innate and adaptive responses. |
| 747 | 19252500 | TLR2 signaling induced splenic dendritic cells (DCs) to express the retinoic acid metabolizing enzyme retinaldehyde dehydrogenase type 2 and interleukin-10 (IL-10) and to metabolize vitamin A and stimulate Foxp3(+) T regulatory cells (T(reg) cells). |
| 748 | 19252500 | Retinoic acid acted on DCs to induce suppressor of cytokine signaling-3 expression, which suppressed activation of p38 mitogen-activated protein kinase and proinflammatory cytokines. |
| 749 | 19252500 | Consistent with this finding, TLR2 signaling induced T(reg) cells and suppressed IL-23 and T helper type 17 (T(H)17) and T(H)1-mediated autoimmune responses in vivo. |
| 750 | 19252500 | In contrast, dectin-1 signaling mostly induced IL-23 and proinflammatory cytokines and augmented T(H)17 and T(H)1-mediated autoimmune responses in vivo. |
| 751 | 19273561 | These two beta-glucans failed to stimulate TNF-alpha in Dectin-1 (beta-glucan receptor) knockout BMDCs. |
| 752 | 19273561 | The upregulation of TNF-alpha and downregulation of IL-12p70 required Dectin-1, but not IL-10. |
| 753 | 19273561 | Finally, costimulation of BMDCs with YGPs and either the TLR9 ligand, CpG, or the TLR2/1 ligand, Pam(3)CSK(4), resulted in upregulated secretion of IL-1alpha and IL-10 and downregulated secretion of IL-1beta, IL-6, and IFN-gamma-inducible protein 10 but had no significant effects on IL-12p40, keratinocyte-derived chemokine, monocyte chemotactic protein 1, or macrophage inflammatory protein alpha, compared with the TLR ligand alone. |
| 754 | 19309560 | F1, V, and F1-V proteins engaged TLR2 signalling and activated IL-6 and CXCL-8 production by monocytes, without affecting the expression of TNF-alpha, IL-12, IL-10, IL-1beta, and CXCL10. |
| 755 | 19330258 | Genetic polymorphisms in vitamin D receptor, vitamin D-binding protein, Toll-like receptor 2, nitric oxide synthase 2, and interferon-gamma genes and its association with susceptibility to tuberculosis. |
| 756 | 19330258 | Many studies have focused on the candidate genes for tuberculosis susceptibility ranging from those expressed in several cells from the innate or adaptive immune system such as Toll-like receptors, cytokines (TNF-alpha, TGF-beta, IFN-gamma, IL-1b, IL-1RA, IL-12, IL-10), nitric oxide synthase and vitamin D, both nuclear receptors and their carrier, the vitamin D-binding protein (VDBP). |
| 757 | 19330258 | Thus, in this mini-review, we summarize the current state of investigation on some of the genetic determinants, such as the candidate polymorphisms of vitamin D, VDBP, Toll-like receptor, nitric oxide synthase 2 and interferon-gamma genes, to generate resistance or susceptibility to M. tuberculosis infection. |
| 758 | 19543380 | Analyses of the cytokine production profile of macrophages isolated from knockout mice deficient in Toll-like receptors (TLRs) or in the adapter molecules MyD88 and TRIF revealed a critical role for TLR2, TLR6 and MyD88 in the production of IFNbeta-independent chemokines. |
| 759 | 19543380 | Reduced expression of RIG-I, MDA-5 and IPS-1 by shRNAs indicated that sensing of MVA by RLR and production of IFNbeta and IFNbeta-dependent chemokines was controlled by the MDA-5 and IPS-1 pathway in the macrophage. |
| 760 | 19543380 | Transcription of the Il1b gene was markedly impaired in TLR2(-/-) and MyD88(-/-) BMDM, whereas mature and secreted IL-1beta was massively reduced in NALP3(-/-) BMDMs or in human THP-1 macrophages with reduced expression of NALP3, ASC or caspase-1 by shRNAs. |
| 761 | 19543380 | Innate immune sensing of MVA and production of chemokines, IFNbeta and IL-1beta by macrophages is mediated by the TLR2-TLR6-MyD88, MDA-5-IPS-1 and NALP3 inflammasome pathways. |
| 762 | 19543380 | Analyses of the cytokine production profile of macrophages isolated from knockout mice deficient in Toll-like receptors (TLRs) or in the adapter molecules MyD88 and TRIF revealed a critical role for TLR2, TLR6 and MyD88 in the production of IFNbeta-independent chemokines. |
| 763 | 19543380 | Reduced expression of RIG-I, MDA-5 and IPS-1 by shRNAs indicated that sensing of MVA by RLR and production of IFNbeta and IFNbeta-dependent chemokines was controlled by the MDA-5 and IPS-1 pathway in the macrophage. |
| 764 | 19543380 | Transcription of the Il1b gene was markedly impaired in TLR2(-/-) and MyD88(-/-) BMDM, whereas mature and secreted IL-1beta was massively reduced in NALP3(-/-) BMDMs or in human THP-1 macrophages with reduced expression of NALP3, ASC or caspase-1 by shRNAs. |
| 765 | 19543380 | Innate immune sensing of MVA and production of chemokines, IFNbeta and IL-1beta by macrophages is mediated by the TLR2-TLR6-MyD88, MDA-5-IPS-1 and NALP3 inflammasome pathways. |
| 766 | 19543380 | Analyses of the cytokine production profile of macrophages isolated from knockout mice deficient in Toll-like receptors (TLRs) or in the adapter molecules MyD88 and TRIF revealed a critical role for TLR2, TLR6 and MyD88 in the production of IFNbeta-independent chemokines. |
| 767 | 19543380 | Reduced expression of RIG-I, MDA-5 and IPS-1 by shRNAs indicated that sensing of MVA by RLR and production of IFNbeta and IFNbeta-dependent chemokines was controlled by the MDA-5 and IPS-1 pathway in the macrophage. |
| 768 | 19543380 | Transcription of the Il1b gene was markedly impaired in TLR2(-/-) and MyD88(-/-) BMDM, whereas mature and secreted IL-1beta was massively reduced in NALP3(-/-) BMDMs or in human THP-1 macrophages with reduced expression of NALP3, ASC or caspase-1 by shRNAs. |
| 769 | 19543380 | Innate immune sensing of MVA and production of chemokines, IFNbeta and IL-1beta by macrophages is mediated by the TLR2-TLR6-MyD88, MDA-5-IPS-1 and NALP3 inflammasome pathways. |
| 770 | 19553557 | Lipoprotein lipase and hydrofluoric acid deactivate both bacterial lipoproteins and lipoteichoic acids, but platelet-activating factor-acetylhydrolase degrades only lipoteichoic acids. |
| 771 | 19553557 | To identify the Toll-like receptor 2 ligand critically involved in infections with gram-positive bacteria, lipoprotein lipase (LPL) or hydrogen peroxide (H(2)O(2)) is often used to selectively inactivate lipoproteins, and hydrofluoric acid (HF) or platelet-activating factor-acetylhydrolase (PAF-AH) is used to selectively inactivate lipoteichoic acid (LTA). |
| 772 | 19553557 | We investigated the reaction specificities by using two synthetic lipoproteins (Pam(3)CSK(4) and FSL-1) and LTAs from pneumococci and staphylococci. |
| 773 | 19553557 | Changes in the structures of the two synthetic proteins and the LTAs were monitored by mass spectrometry, and biological activity changes were evaluated by measuring tumor necrosis factor alpha production by mouse macrophage cells (RAW 264.7) following stimulation. |
| 774 | 19553557 | PAF-AH inactivated LTA without reducing the biological activities of Pam(3)CSK(4) and FSL-1. |
| 775 | 19553557 | Our results indicate that treatment with 1% H(2)O(2) for 6 h at 37 degrees C inactivates Pam(3)CSK(4), FSL-1, and LTA by more than 80%. |
| 776 | 19553557 | Although HF, LPL, and H(2)O(2) treatments degrade and inactivate both lipopeptides and LTA, PAF-AH selectively inactivated LTA with no effect on the biological and structural properties of the two lipopeptides. |
| 777 | 19578160 | When used as an extraneous vaccine, one critical interaction which must occur for an immune response to be generated is the interaction between gp96 and the antigen presenting cell (APC) surface receptors (CD91, SR-A, TLR-2, and TLR-4). |
| 778 | 19694614 | Toll-like receptor-2 (TLR-2) agonist, Pam(3)Cys, was synthesized and coupled to CM-TMC through a polyethylene glycol (PEG) spacer. |
| 779 | 19694614 | In vitro studies using phorbol 12-myristyl 13-acetate (PMA) stimulated macrophage-like THP-1 (mTHP-1) cells were focused on cytotoxicity of both polymers and particles, and their potential to stimulate IL-8 release via the TLR-2 pathway. |
| 780 | 19694614 | Toll-like receptor-2 (TLR-2) agonist, Pam(3)Cys, was synthesized and coupled to CM-TMC through a polyethylene glycol (PEG) spacer. |
| 781 | 19694614 | In vitro studies using phorbol 12-myristyl 13-acetate (PMA) stimulated macrophage-like THP-1 (mTHP-1) cells were focused on cytotoxicity of both polymers and particles, and their potential to stimulate IL-8 release via the TLR-2 pathway. |
| 782 | 19752746 | Vaccination of melanoma patients with Melan-A/Mart-1 peptide and Klebsiella outer membrane protein p40 as an adjuvant. |
| 783 | 19752746 | Here we investigated the novel Toll-like receptor2 ligand P40, the outer membrane protein A derived from Klebsiella pneumoniae. |
| 784 | 19752746 | Seventeen human leukocyte antigen-A*0201 positive stage III/IV melanoma patients were vaccinated with P40 and Melan-A/Mart-1 peptide subcutaneously in monthly intervals. |
| 785 | 19752746 | Melan-A/Mart-1 specific CD8 T cells were analyzed ex vivo, with positive results in 6 of 14 evaluable patients. |
| 786 | 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. |
| 787 | 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. |
| 788 | 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. |
| 789 | 19793902 | Mycoplasma genitalium-derived lipid-associated membrane proteins activate NF-kappaB through toll-like receptors 1, 2, and 6 and CD14 in a MyD88-dependent pathway. |
| 790 | 19793902 | However, the interaction of M. genitalium-derived LAMPs as pathogenic agents with Toll-like receptors (TLRs) and the signaling pathways responsible for active inflammation and NF-kappaB activation have not been fully elucidated. |
| 791 | 19793902 | In this study, LAMPs induced the production of tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) in a dose-dependent manner. |
| 792 | 19793902 | Blocking assays showed that TLR2- and CD14-neutralizing antibodies reduced the expression of TNF-alpha and IL-6 in THP-1 cells. |
| 793 | 19793902 | Furthermore, LAMP-induced NF-kappaB activation was increased in 293T cells transfected with TLR2 plasmid. |
| 794 | 19793902 | The activity of NF-kappaB was synergically augmented by cotransfected TLR1, TLR6, and CD14. |
| 795 | 19793902 | Additionally, LAMPs were shown to inhibit NF-kappaB expression by cotransfection with dominant-negative MyD88 and TLR2 plasmids. |
| 796 | 19793902 | These results suggest that M. genitalium-derived LAMPs activate NF-kappaB via TLR1, TLR2, TLR6, and CD14 in a MyD88-dependent pathway. |
| 797 | 19793902 | Mycoplasma genitalium-derived lipid-associated membrane proteins activate NF-kappaB through toll-like receptors 1, 2, and 6 and CD14 in a MyD88-dependent pathway. |
| 798 | 19793902 | However, the interaction of M. genitalium-derived LAMPs as pathogenic agents with Toll-like receptors (TLRs) and the signaling pathways responsible for active inflammation and NF-kappaB activation have not been fully elucidated. |
| 799 | 19793902 | In this study, LAMPs induced the production of tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) in a dose-dependent manner. |
| 800 | 19793902 | Blocking assays showed that TLR2- and CD14-neutralizing antibodies reduced the expression of TNF-alpha and IL-6 in THP-1 cells. |
| 801 | 19793902 | Furthermore, LAMP-induced NF-kappaB activation was increased in 293T cells transfected with TLR2 plasmid. |
| 802 | 19793902 | The activity of NF-kappaB was synergically augmented by cotransfected TLR1, TLR6, and CD14. |
| 803 | 19793902 | Additionally, LAMPs were shown to inhibit NF-kappaB expression by cotransfection with dominant-negative MyD88 and TLR2 plasmids. |
| 804 | 19793902 | These results suggest that M. genitalium-derived LAMPs activate NF-kappaB via TLR1, TLR2, TLR6, and CD14 in a MyD88-dependent pathway. |
| 805 | 19793902 | Mycoplasma genitalium-derived lipid-associated membrane proteins activate NF-kappaB through toll-like receptors 1, 2, and 6 and CD14 in a MyD88-dependent pathway. |
| 806 | 19793902 | However, the interaction of M. genitalium-derived LAMPs as pathogenic agents with Toll-like receptors (TLRs) and the signaling pathways responsible for active inflammation and NF-kappaB activation have not been fully elucidated. |
| 807 | 19793902 | In this study, LAMPs induced the production of tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) in a dose-dependent manner. |
| 808 | 19793902 | Blocking assays showed that TLR2- and CD14-neutralizing antibodies reduced the expression of TNF-alpha and IL-6 in THP-1 cells. |
| 809 | 19793902 | Furthermore, LAMP-induced NF-kappaB activation was increased in 293T cells transfected with TLR2 plasmid. |
| 810 | 19793902 | The activity of NF-kappaB was synergically augmented by cotransfected TLR1, TLR6, and CD14. |
| 811 | 19793902 | Additionally, LAMPs were shown to inhibit NF-kappaB expression by cotransfection with dominant-negative MyD88 and TLR2 plasmids. |
| 812 | 19793902 | These results suggest that M. genitalium-derived LAMPs activate NF-kappaB via TLR1, TLR2, TLR6, and CD14 in a MyD88-dependent pathway. |
| 813 | 19793902 | Mycoplasma genitalium-derived lipid-associated membrane proteins activate NF-kappaB through toll-like receptors 1, 2, and 6 and CD14 in a MyD88-dependent pathway. |
| 814 | 19793902 | However, the interaction of M. genitalium-derived LAMPs as pathogenic agents with Toll-like receptors (TLRs) and the signaling pathways responsible for active inflammation and NF-kappaB activation have not been fully elucidated. |
| 815 | 19793902 | In this study, LAMPs induced the production of tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) in a dose-dependent manner. |
| 816 | 19793902 | Blocking assays showed that TLR2- and CD14-neutralizing antibodies reduced the expression of TNF-alpha and IL-6 in THP-1 cells. |
| 817 | 19793902 | Furthermore, LAMP-induced NF-kappaB activation was increased in 293T cells transfected with TLR2 plasmid. |
| 818 | 19793902 | The activity of NF-kappaB was synergically augmented by cotransfected TLR1, TLR6, and CD14. |
| 819 | 19793902 | Additionally, LAMPs were shown to inhibit NF-kappaB expression by cotransfection with dominant-negative MyD88 and TLR2 plasmids. |
| 820 | 19793902 | These results suggest that M. genitalium-derived LAMPs activate NF-kappaB via TLR1, TLR2, TLR6, and CD14 in a MyD88-dependent pathway. |
| 821 | 19822632 | Toll-like receptor 2, TLR4, and TLR9 were each essential for generating robust cytokine and antibody responses. |
| 822 | 19828771 | V. parvula LPS stimulated tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) release in human peripheral blood mononuclear cells (PBMC) in a dose-dependent manner. |
| 823 | 19828771 | Pretreatment of cells with a TLR4 antagonist significantly reduced TNF-alpha and IL-6 production in PBMC stimulated with either Veillonella or Escherichia coli LPS. |
| 824 | 19828771 | TNF-alpha, IL-1beta, IL-6, and IL-10 were released in wild-type and TLR2(-/-), but not TLR4(-/-), mouse macrophage cultures. |
| 825 | 19828771 | V. parvula LPS was able to activate the human PBMC p38 mitogen-activated protein kinase (MAPK). |
| 826 | 19828771 | A specific p38 MAPK inhibitor strongly inhibited V. parvula LPS-induced TNF-alpha, IL-1beta, IL-6, and IL-10. |
| 827 | 19828771 | V. parvula LPS-stimulated cytokine induction, as well as p38 MAPK activation, are TLR4-dependent features. |
| 828 | 20045502 | In the current study, we investigated the ability of our lipopeptides to activate nuclear factor-kappaB (NF-kappaB) in a toll-like receptor-2 (TLR2)-dependent manner as the possible mode of action and reported the structure-function requirements for novel TLR2 targeting lipopeptides based on LAAs. |
| 829 | 20087927 | There was a synergistic increase in cytokine production (TNF-alpha, IL-6, IL-10, and IFN-beta) in BM-DCs, together with an increase in the expression of co-stimulatory molecules (CD86 and CD40) in response to co-treatment with poly(I:C) and zymosan. |
| 830 | 20087927 | The results of the current study suggest that one of the mechanisms by which zymosan enhances the adjuvant activity of poly(I:C) is through increased cytokine production by DCs involving the synergistic activation of poly(I:C)-induced TLR3- and zymosan-induced TLR2-mediated signaling pathways. |
| 831 | 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. |
| 832 | 20130107 | Interferon-gamma secretion is induced in IL-12 stimulated human NK cells by recognition of Helicobacter pylori or TLR2 ligands. |
| 833 | 20130107 | We found that inhibition of MyD88 homodimerization resulted in decreased production of IFN-γ and that inhibition of the p38 MAPK decreased the production as well as the secretion of IFN-γ. |
| 834 | 20145703 | This molecule, which was termed lipopeptidophosphoglycan (LPPG), is recognized through TLR2 and TLR4 and leads to the release of cytokines from human monocytes, macrophages, and dendritic cells; LPPG-activated dendritic cells have increased expression of costimulatory molecules. |
| 835 | 20200188 | The objective of this study was to investigate the effects of glucose-based peritoneal dialysis (PD) fluids and icodextrin-based PD fluids on the expression of Toll-like receptor 2 (TLR2)/TLR4 and subsequent ligand-induced mitogen-activated protein kinase (MAPK) and NF-kappaB signaling and tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA expression in human peritoneal mesothelial cells (HPMCs). |
| 836 | 20200188 | TLR2/TLR4 expression was determined by real-time PCR, Western blotting, and an immunofluorescence assay. |
| 837 | 20200188 | In addition, cells were pretreated with different PD solutions and then incubated with Pam3CSK4 or lipopolysaccharide (LPS), and the degrees of MAPK and NF-kappaB activation were reflected by detecting the phosphorylation levels of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), p38, and p65, using a Western blot method. |
| 838 | 20200188 | TNF-alpha and IL-1beta mRNA expression was measured by real-time PCR. |
| 839 | 20200188 | Glucose-based peritoneal dialysis fluids suppressed the expression of TLR2 and TLR4 proteins in HPMCs. |
| 840 | 20200188 | Challenge of cells with either Pam3CSK4 or LPS resulted in impaired TNF-alpha and IL-1beta production. |
| 841 | 20200188 | Moreover, reduced TLR2 and TLR4 levels in glucose-based peritoneal dialysis solution-treated mesothelial cells were accompanied by reduced p42/44 (ERK1/2), JNK, p38 MAPK, and NF-kappaB p65 phosphorylation upon TLR ligand engagement. |
| 842 | 20200188 | No significant changes in MAPK and NF-kappaB signaling and TNF-alpha and IL-1beta mRNA expression were observed in icodextrin-based PD solution-treated mesothelial cells. |
| 843 | 20200188 | Glucose-based PD solution, but not icodextrin-based PD solution, downregulates expression of TLR2/TLR4 by human peritoneal mesothelial cells and triggers hyporesponsiveness to pathogen-associated molecular patterns. |
| 844 | 20200188 | The objective of this study was to investigate the effects of glucose-based peritoneal dialysis (PD) fluids and icodextrin-based PD fluids on the expression of Toll-like receptor 2 (TLR2)/TLR4 and subsequent ligand-induced mitogen-activated protein kinase (MAPK) and NF-kappaB signaling and tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA expression in human peritoneal mesothelial cells (HPMCs). |
| 845 | 20200188 | TLR2/TLR4 expression was determined by real-time PCR, Western blotting, and an immunofluorescence assay. |
| 846 | 20200188 | In addition, cells were pretreated with different PD solutions and then incubated with Pam3CSK4 or lipopolysaccharide (LPS), and the degrees of MAPK and NF-kappaB activation were reflected by detecting the phosphorylation levels of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), p38, and p65, using a Western blot method. |
| 847 | 20200188 | TNF-alpha and IL-1beta mRNA expression was measured by real-time PCR. |
| 848 | 20200188 | Glucose-based peritoneal dialysis fluids suppressed the expression of TLR2 and TLR4 proteins in HPMCs. |
| 849 | 20200188 | Challenge of cells with either Pam3CSK4 or LPS resulted in impaired TNF-alpha and IL-1beta production. |
| 850 | 20200188 | Moreover, reduced TLR2 and TLR4 levels in glucose-based peritoneal dialysis solution-treated mesothelial cells were accompanied by reduced p42/44 (ERK1/2), JNK, p38 MAPK, and NF-kappaB p65 phosphorylation upon TLR ligand engagement. |
| 851 | 20200188 | No significant changes in MAPK and NF-kappaB signaling and TNF-alpha and IL-1beta mRNA expression were observed in icodextrin-based PD solution-treated mesothelial cells. |
| 852 | 20200188 | Glucose-based PD solution, but not icodextrin-based PD solution, downregulates expression of TLR2/TLR4 by human peritoneal mesothelial cells and triggers hyporesponsiveness to pathogen-associated molecular patterns. |
| 853 | 20200188 | The objective of this study was to investigate the effects of glucose-based peritoneal dialysis (PD) fluids and icodextrin-based PD fluids on the expression of Toll-like receptor 2 (TLR2)/TLR4 and subsequent ligand-induced mitogen-activated protein kinase (MAPK) and NF-kappaB signaling and tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA expression in human peritoneal mesothelial cells (HPMCs). |
| 854 | 20200188 | TLR2/TLR4 expression was determined by real-time PCR, Western blotting, and an immunofluorescence assay. |
| 855 | 20200188 | In addition, cells were pretreated with different PD solutions and then incubated with Pam3CSK4 or lipopolysaccharide (LPS), and the degrees of MAPK and NF-kappaB activation were reflected by detecting the phosphorylation levels of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), p38, and p65, using a Western blot method. |
| 856 | 20200188 | TNF-alpha and IL-1beta mRNA expression was measured by real-time PCR. |
| 857 | 20200188 | Glucose-based peritoneal dialysis fluids suppressed the expression of TLR2 and TLR4 proteins in HPMCs. |
| 858 | 20200188 | Challenge of cells with either Pam3CSK4 or LPS resulted in impaired TNF-alpha and IL-1beta production. |
| 859 | 20200188 | Moreover, reduced TLR2 and TLR4 levels in glucose-based peritoneal dialysis solution-treated mesothelial cells were accompanied by reduced p42/44 (ERK1/2), JNK, p38 MAPK, and NF-kappaB p65 phosphorylation upon TLR ligand engagement. |
| 860 | 20200188 | No significant changes in MAPK and NF-kappaB signaling and TNF-alpha and IL-1beta mRNA expression were observed in icodextrin-based PD solution-treated mesothelial cells. |
| 861 | 20200188 | Glucose-based PD solution, but not icodextrin-based PD solution, downregulates expression of TLR2/TLR4 by human peritoneal mesothelial cells and triggers hyporesponsiveness to pathogen-associated molecular patterns. |
| 862 | 20200188 | The objective of this study was to investigate the effects of glucose-based peritoneal dialysis (PD) fluids and icodextrin-based PD fluids on the expression of Toll-like receptor 2 (TLR2)/TLR4 and subsequent ligand-induced mitogen-activated protein kinase (MAPK) and NF-kappaB signaling and tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA expression in human peritoneal mesothelial cells (HPMCs). |
| 863 | 20200188 | TLR2/TLR4 expression was determined by real-time PCR, Western blotting, and an immunofluorescence assay. |
| 864 | 20200188 | In addition, cells were pretreated with different PD solutions and then incubated with Pam3CSK4 or lipopolysaccharide (LPS), and the degrees of MAPK and NF-kappaB activation were reflected by detecting the phosphorylation levels of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), p38, and p65, using a Western blot method. |
| 865 | 20200188 | TNF-alpha and IL-1beta mRNA expression was measured by real-time PCR. |
| 866 | 20200188 | Glucose-based peritoneal dialysis fluids suppressed the expression of TLR2 and TLR4 proteins in HPMCs. |
| 867 | 20200188 | Challenge of cells with either Pam3CSK4 or LPS resulted in impaired TNF-alpha and IL-1beta production. |
| 868 | 20200188 | Moreover, reduced TLR2 and TLR4 levels in glucose-based peritoneal dialysis solution-treated mesothelial cells were accompanied by reduced p42/44 (ERK1/2), JNK, p38 MAPK, and NF-kappaB p65 phosphorylation upon TLR ligand engagement. |
| 869 | 20200188 | No significant changes in MAPK and NF-kappaB signaling and TNF-alpha and IL-1beta mRNA expression were observed in icodextrin-based PD solution-treated mesothelial cells. |
| 870 | 20200188 | Glucose-based PD solution, but not icodextrin-based PD solution, downregulates expression of TLR2/TLR4 by human peritoneal mesothelial cells and triggers hyporesponsiveness to pathogen-associated molecular patterns. |
| 871 | 20200188 | The objective of this study was to investigate the effects of glucose-based peritoneal dialysis (PD) fluids and icodextrin-based PD fluids on the expression of Toll-like receptor 2 (TLR2)/TLR4 and subsequent ligand-induced mitogen-activated protein kinase (MAPK) and NF-kappaB signaling and tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA expression in human peritoneal mesothelial cells (HPMCs). |
| 872 | 20200188 | TLR2/TLR4 expression was determined by real-time PCR, Western blotting, and an immunofluorescence assay. |
| 873 | 20200188 | In addition, cells were pretreated with different PD solutions and then incubated with Pam3CSK4 or lipopolysaccharide (LPS), and the degrees of MAPK and NF-kappaB activation were reflected by detecting the phosphorylation levels of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), p38, and p65, using a Western blot method. |
| 874 | 20200188 | TNF-alpha and IL-1beta mRNA expression was measured by real-time PCR. |
| 875 | 20200188 | Glucose-based peritoneal dialysis fluids suppressed the expression of TLR2 and TLR4 proteins in HPMCs. |
| 876 | 20200188 | Challenge of cells with either Pam3CSK4 or LPS resulted in impaired TNF-alpha and IL-1beta production. |
| 877 | 20200188 | Moreover, reduced TLR2 and TLR4 levels in glucose-based peritoneal dialysis solution-treated mesothelial cells were accompanied by reduced p42/44 (ERK1/2), JNK, p38 MAPK, and NF-kappaB p65 phosphorylation upon TLR ligand engagement. |
| 878 | 20200188 | No significant changes in MAPK and NF-kappaB signaling and TNF-alpha and IL-1beta mRNA expression were observed in icodextrin-based PD solution-treated mesothelial cells. |
| 879 | 20200188 | Glucose-based PD solution, but not icodextrin-based PD solution, downregulates expression of TLR2/TLR4 by human peritoneal mesothelial cells and triggers hyporesponsiveness to pathogen-associated molecular patterns. |
| 880 | 20213311 | Treponema denticola suppresses expression of human beta-defensin-2 in gingival epithelial cells through inhibition of TNFalpha production and TLR2 activation. |
| 881 | 20213311 | We previously reported that Treponema denticola, a periodontal pathogen, suppressed the expression of human beta-defensins (HBDs) and IL-8 in human gingival epithelial cells. |
| 882 | 20213311 | Time courses of suppression revealed that T. denticola suppressed HBD-2 expression only at late time points, which was accompanied with the suppression of TNFalpha production. |
| 883 | 20213311 | Neutralization of TNFalpha with an antibody abrogated the suppressive effect of T. denticola on HBD-2. |
| 884 | 20213311 | Knock-down of toll-like receptor (TLR) 2 via RNA interference reversed the suppressive effect of T. denticola on the expression of HBD-3, but not on the production of TNFalpha. |
| 885 | 20213311 | Collectively, T. denticola suppresses the expression of HBD-2 in gingival epithelial cells by inhibiting the TLR2 axis and TNFalpha production, which may contribute to the pathogenesis of periodontitis by T. denticola. |
| 886 | 20213311 | Treponema denticola suppresses expression of human beta-defensin-2 in gingival epithelial cells through inhibition of TNFalpha production and TLR2 activation. |
| 887 | 20213311 | We previously reported that Treponema denticola, a periodontal pathogen, suppressed the expression of human beta-defensins (HBDs) and IL-8 in human gingival epithelial cells. |
| 888 | 20213311 | Time courses of suppression revealed that T. denticola suppressed HBD-2 expression only at late time points, which was accompanied with the suppression of TNFalpha production. |
| 889 | 20213311 | Neutralization of TNFalpha with an antibody abrogated the suppressive effect of T. denticola on HBD-2. |
| 890 | 20213311 | Knock-down of toll-like receptor (TLR) 2 via RNA interference reversed the suppressive effect of T. denticola on the expression of HBD-3, but not on the production of TNFalpha. |
| 891 | 20213311 | Collectively, T. denticola suppresses the expression of HBD-2 in gingival epithelial cells by inhibiting the TLR2 axis and TNFalpha production, which may contribute to the pathogenesis of periodontitis by T. denticola. |
| 892 | 20445007 | The current studies used the Toll-like receptor 2 (TLR2) agonist palmitoyl(3)-cysteine-serine-lysine(4) (PAM) or the TLR4 agonist lipopolysaccharide (LPS) to stimulate human whole blood and determine whether postponing the addition of the GC dexamethasone (DEX) limits its ability to decrease cytokine production. |
| 893 | 20445007 | Twenty-four hours after stimulation, tumor necrosis factor (TNF), interleukin-1beta (IL-1beta), IL-6, and IL-8 levels were measured, in addition to the cytokine inhibitors IL-1 soluble receptor II (SRII), IL-1 receptor antagonist, and TNF SRII. |
| 894 | 20445007 | PAM stimulation also induced IL-1beta, IL-6, and IL-8. |
| 895 | 20445007 | Delaying the addition of DEX until 6 h after LPS stimulation failed to decrease TNF or IL-6. |
| 896 | 20445007 | In contrast, delayed DEX addition significantly suppressed PAM-induced IL-1beta, IL-6, or IL-8 and also suppressed LPS-induced IL-1beta and IL-8. |
| 897 | 20504771 | TLR2, in cooperation with either TLR1 or TLR6, mediates responses to a wide variety of microbial products as well as products of host tissue damage. |
| 898 | 20504771 | In an effort to understand the structural basis of TLR2 recognition and uncover novel TLR2 agonists, a synthetic chemical library of 24,000 compounds was screened using an IL-8-driven luciferase reporter in cells expressing these human receptors. |
| 899 | 20504771 | The screening yielded several novel TLR2-dependent activators that utilize TLR1, TLR6, or both as co-receptors. |
| 900 | 20504771 | TLR2, in cooperation with either TLR1 or TLR6, mediates responses to a wide variety of microbial products as well as products of host tissue damage. |
| 901 | 20504771 | In an effort to understand the structural basis of TLR2 recognition and uncover novel TLR2 agonists, a synthetic chemical library of 24,000 compounds was screened using an IL-8-driven luciferase reporter in cells expressing these human receptors. |
| 902 | 20504771 | The screening yielded several novel TLR2-dependent activators that utilize TLR1, TLR6, or both as co-receptors. |
| 903 | 20504771 | TLR2, in cooperation with either TLR1 or TLR6, mediates responses to a wide variety of microbial products as well as products of host tissue damage. |
| 904 | 20504771 | In an effort to understand the structural basis of TLR2 recognition and uncover novel TLR2 agonists, a synthetic chemical library of 24,000 compounds was screened using an IL-8-driven luciferase reporter in cells expressing these human receptors. |
| 905 | 20504771 | The screening yielded several novel TLR2-dependent activators that utilize TLR1, TLR6, or both as co-receptors. |
| 906 | 20599915 | Ursolic acid isolated from Uncaria rhynchophylla activates human dendritic cells via TLR2 and/or TLR4 and induces the production of IFN-gamma by CD4+ naïve T cells. |
| 907 | 20599915 | The expression levels of CD1a, CD80, CD83, CD86, HLA-DR and CCR7 on Ursolic acid-primed dendritic cells was slightly enhanced. |
| 908 | 20599915 | Moreover, Ursolic acid-primed dendritic cells expressed levels of mRNA coding for both TLR2 and TLR4. |
| 909 | 20599915 | The majority of cells produced considerable interferon-gamma (IFN-gamma), but also small amounts of interleukin (IL-4)-4. |
| 910 | 20599915 | Ursolic acid-primed dendritic cells have an intermediate migratory capacity towards CCL19 and CCL21. |
| 911 | 20599915 | These results suggest that Ursolic acid modulates human dendritic cells function in a fashion that favors Th1 polarization via the activation of IL-12p70 dependent on TLR2 and/or TLR4, and may be used on dendritic cells-based vaccines for cancer immunotherapy. |
| 912 | 20599915 | Ursolic acid isolated from Uncaria rhynchophylla activates human dendritic cells via TLR2 and/or TLR4 and induces the production of IFN-gamma by CD4+ naïve T cells. |
| 913 | 20599915 | The expression levels of CD1a, CD80, CD83, CD86, HLA-DR and CCR7 on Ursolic acid-primed dendritic cells was slightly enhanced. |
| 914 | 20599915 | Moreover, Ursolic acid-primed dendritic cells expressed levels of mRNA coding for both TLR2 and TLR4. |
| 915 | 20599915 | The majority of cells produced considerable interferon-gamma (IFN-gamma), but also small amounts of interleukin (IL-4)-4. |
| 916 | 20599915 | Ursolic acid-primed dendritic cells have an intermediate migratory capacity towards CCL19 and CCL21. |
| 917 | 20599915 | These results suggest that Ursolic acid modulates human dendritic cells function in a fashion that favors Th1 polarization via the activation of IL-12p70 dependent on TLR2 and/or TLR4, and may be used on dendritic cells-based vaccines for cancer immunotherapy. |
| 918 | 20599915 | Ursolic acid isolated from Uncaria rhynchophylla activates human dendritic cells via TLR2 and/or TLR4 and induces the production of IFN-gamma by CD4+ naïve T cells. |
| 919 | 20599915 | The expression levels of CD1a, CD80, CD83, CD86, HLA-DR and CCR7 on Ursolic acid-primed dendritic cells was slightly enhanced. |
| 920 | 20599915 | Moreover, Ursolic acid-primed dendritic cells expressed levels of mRNA coding for both TLR2 and TLR4. |
| 921 | 20599915 | The majority of cells produced considerable interferon-gamma (IFN-gamma), but also small amounts of interleukin (IL-4)-4. |
| 922 | 20599915 | Ursolic acid-primed dendritic cells have an intermediate migratory capacity towards CCL19 and CCL21. |
| 923 | 20599915 | These results suggest that Ursolic acid modulates human dendritic cells function in a fashion that favors Th1 polarization via the activation of IL-12p70 dependent on TLR2 and/or TLR4, and may be used on dendritic cells-based vaccines for cancer immunotherapy. |
| 924 | 20610663 | Since Toll-like receptor 2 (TLR2), TLR4, and TLR9 activation have been involved in HIV-1 recrudescence, we sought to determine the role of these TLRs in HIV-1 reactivation induced by the periodontal pathogens Fusobacterium nucleatum and Porphyromonas gingivalis using BF24 monocytes/macrophages stably transfected with the HIV-1 promoter driving chloramphenicol acetyltransferase (CAT) expression and THP89GFP cells, a model of HIV-1 latency. |
| 925 | 20610663 | We demonstrated that TLR9 activation by F. nucleatum and TLR2 activation by both bacteria appear to be involved in HIV-1 reactivation; however, TLR4 activation had no effect. |
| 926 | 20610663 | Moreover, the autocrine activity of tumor necrosis factor alpha (TNF-alpha) but not interleukin-1beta (IL-1beta) produced in response to bacteria could impact viral reactivation. |
| 927 | 20610663 | The transcription factors NF-kappaB and Sp1 appear to be positively regulating HIV-1 reactivation induced by these oral pathogens. |
| 928 | 20610663 | These results suggest that oral Gram-negative bacteria (F. nucleatum and P. gingivalis) associated with oral and systemic chronic inflammatory disorders enhance HIV-1 reactivation in monocytes/macrophages through TLR2 and TLR9 activation in a mechanism that appears to be transcriptionally regulated. |
| 929 | 20610663 | Since Toll-like receptor 2 (TLR2), TLR4, and TLR9 activation have been involved in HIV-1 recrudescence, we sought to determine the role of these TLRs in HIV-1 reactivation induced by the periodontal pathogens Fusobacterium nucleatum and Porphyromonas gingivalis using BF24 monocytes/macrophages stably transfected with the HIV-1 promoter driving chloramphenicol acetyltransferase (CAT) expression and THP89GFP cells, a model of HIV-1 latency. |
| 930 | 20610663 | We demonstrated that TLR9 activation by F. nucleatum and TLR2 activation by both bacteria appear to be involved in HIV-1 reactivation; however, TLR4 activation had no effect. |
| 931 | 20610663 | Moreover, the autocrine activity of tumor necrosis factor alpha (TNF-alpha) but not interleukin-1beta (IL-1beta) produced in response to bacteria could impact viral reactivation. |
| 932 | 20610663 | The transcription factors NF-kappaB and Sp1 appear to be positively regulating HIV-1 reactivation induced by these oral pathogens. |
| 933 | 20610663 | These results suggest that oral Gram-negative bacteria (F. nucleatum and P. gingivalis) associated with oral and systemic chronic inflammatory disorders enhance HIV-1 reactivation in monocytes/macrophages through TLR2 and TLR9 activation in a mechanism that appears to be transcriptionally regulated. |
| 934 | 20610663 | Since Toll-like receptor 2 (TLR2), TLR4, and TLR9 activation have been involved in HIV-1 recrudescence, we sought to determine the role of these TLRs in HIV-1 reactivation induced by the periodontal pathogens Fusobacterium nucleatum and Porphyromonas gingivalis using BF24 monocytes/macrophages stably transfected with the HIV-1 promoter driving chloramphenicol acetyltransferase (CAT) expression and THP89GFP cells, a model of HIV-1 latency. |
| 935 | 20610663 | We demonstrated that TLR9 activation by F. nucleatum and TLR2 activation by both bacteria appear to be involved in HIV-1 reactivation; however, TLR4 activation had no effect. |
| 936 | 20610663 | Moreover, the autocrine activity of tumor necrosis factor alpha (TNF-alpha) but not interleukin-1beta (IL-1beta) produced in response to bacteria could impact viral reactivation. |
| 937 | 20610663 | The transcription factors NF-kappaB and Sp1 appear to be positively regulating HIV-1 reactivation induced by these oral pathogens. |
| 938 | 20610663 | These results suggest that oral Gram-negative bacteria (F. nucleatum and P. gingivalis) associated with oral and systemic chronic inflammatory disorders enhance HIV-1 reactivation in monocytes/macrophages through TLR2 and TLR9 activation in a mechanism that appears to be transcriptionally regulated. |
| 939 | 20631332 | Our results revealed that poly(anhydride) NPs also act as agonists of various Toll-like receptors (TLRs) (TLR2, -4, and -5), triggering a Th1-profile cytokine release (gamma interferon [IFN-gamma], 478 pg/ml versus 39.6 pg/ml from negative control; interleukin-12 [IL-12], 40 pg/ml versus 7.2 pg/ml from negative control) and, after incubation with dendritic cells, inducing a 2.5- to 3.5-fold increase of CD54 and CD86 costimulatory molecule expression. |
| 940 | 20660347 | In these studies we observed that M. tuberculosis, which expresses agonists of both TLR9 and TLR2, did not induce production of IFN-alpha/beta or cross processing by murine DCs. |
| 941 | 20660347 | Inhibition of the response to one TLR by another may affect the ultimate response to pathogens like M. tuberculosis that express agonists of multiple TLRs, including TLR2 and TLR9. |
| 942 | 20660347 | In these studies we observed that M. tuberculosis, which expresses agonists of both TLR9 and TLR2, did not induce production of IFN-alpha/beta or cross processing by murine DCs. |
| 943 | 20660347 | Inhibition of the response to one TLR by another may affect the ultimate response to pathogens like M. tuberculosis that express agonists of multiple TLRs, including TLR2 and TLR9. |
| 944 | 20696947 | Emerging reports reveal that activating Toll-like receptor-2 (TLR2)-MyD88 signals in CD8 T lymphocytes enhances cytokine production and cytotoxicity; however, the signaling pathway remains undefined. |
| 945 | 20696947 | We found that TLR2 engagement on T-cell receptor transgenic CD8 OT-1 T cells increased T-bet transcription factor levels consequently, augmenting effector transcript and protein levels both in vivo and in vitro. |
| 946 | 20696947 | In contrast, TLR2 agonist did not costimulate TLR2(-/-)OT-1 or MyD88(-/-)OT-1 T cells. |
| 947 | 20696947 | Inhibiting mTOR, Akt, or protein kinase C in T cells abolished the costimulatory effects of the TLR2 agonist. |
| 948 | 20696947 | Emerging reports reveal that activating Toll-like receptor-2 (TLR2)-MyD88 signals in CD8 T lymphocytes enhances cytokine production and cytotoxicity; however, the signaling pathway remains undefined. |
| 949 | 20696947 | We found that TLR2 engagement on T-cell receptor transgenic CD8 OT-1 T cells increased T-bet transcription factor levels consequently, augmenting effector transcript and protein levels both in vivo and in vitro. |
| 950 | 20696947 | In contrast, TLR2 agonist did not costimulate TLR2(-/-)OT-1 or MyD88(-/-)OT-1 T cells. |
| 951 | 20696947 | Inhibiting mTOR, Akt, or protein kinase C in T cells abolished the costimulatory effects of the TLR2 agonist. |
| 952 | 20696947 | Emerging reports reveal that activating Toll-like receptor-2 (TLR2)-MyD88 signals in CD8 T lymphocytes enhances cytokine production and cytotoxicity; however, the signaling pathway remains undefined. |
| 953 | 20696947 | We found that TLR2 engagement on T-cell receptor transgenic CD8 OT-1 T cells increased T-bet transcription factor levels consequently, augmenting effector transcript and protein levels both in vivo and in vitro. |
| 954 | 20696947 | In contrast, TLR2 agonist did not costimulate TLR2(-/-)OT-1 or MyD88(-/-)OT-1 T cells. |
| 955 | 20696947 | Inhibiting mTOR, Akt, or protein kinase C in T cells abolished the costimulatory effects of the TLR2 agonist. |
| 956 | 20696947 | Emerging reports reveal that activating Toll-like receptor-2 (TLR2)-MyD88 signals in CD8 T lymphocytes enhances cytokine production and cytotoxicity; however, the signaling pathway remains undefined. |
| 957 | 20696947 | We found that TLR2 engagement on T-cell receptor transgenic CD8 OT-1 T cells increased T-bet transcription factor levels consequently, augmenting effector transcript and protein levels both in vivo and in vitro. |
| 958 | 20696947 | In contrast, TLR2 agonist did not costimulate TLR2(-/-)OT-1 or MyD88(-/-)OT-1 T cells. |
| 959 | 20696947 | Inhibiting mTOR, Akt, or protein kinase C in T cells abolished the costimulatory effects of the TLR2 agonist. |
| 960 | 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. |
| 961 | 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. |
| 962 | 20719993 | In these cells, stimulation of TLR3 and TLR4 by their ligands suppressed HIV-1 expression partly through type I interferon (IFN). |
| 963 | 20719993 | The bacteria with suppressive effects preferentially stimulated TLR4, whereas the ones with enhancing effects stimulated TLR2. |
| 964 | 20808895 | The synthetic bacterial lipopeptide Pam3-Cys-Ser-Lys4 (Pam3CSK4), the prototype ligand for the heterodimeric TLR1/TLR2 complex, enhanced RSV infection in primary epithelial, myeloid and lymphoid cells. |
| 965 | 20809414 | Dimerization between either of the two avian TLR2 species and TLR1La or 1Lb permits recognition of the same broad range of molecules as recognized by mammalian TLR2 dimerized with either TLR1, 6 and 10. |
| 966 | 20809414 | Components of downstream TLR signaling are also mostly conserved but with some losses in avian species; notably, TRAM is absent in avian genomes and, hence, the TRIF/TRAM-dependent signaling pathway utilized by mammals in LPS activation appears to be absent in birds. |
| 967 | 20826612 | The concentrations of several chemoattractants for neutrophils (CXCL1, CXCL2, CXCL3, CXCL8, and C5a) increased in milk after challenge, and the highest increases followed challenge with the combination of MDP and LTA. |
| 968 | 20826612 | Nucleotide-binding oligomerization domain 2 (NOD2), a major sensor of MDP, was expressed (mRNA) in bovine mammary tissue and by bMEpC in culture. |
| 969 | 20826612 | The production of interleukin-8 (IL-8) following the stimulation of bMEpC by LTA and MDP was dependent on the activation of NF-κB. |
| 970 | 20826612 | LTA-induced IL-8 production did not depend on platelet-activating factor receptor (PAFR), as the PAFR antagonist WEB2086 was without effect. |
| 971 | 20826612 | Although the levels of expression of the inflammatory cytokines tumor necrosis factor alpha (TNF-α) and IL-1β were increased by LTA and MDP at the mRNA level, no protein could be detected in the bMEpC culture supernatant. |
| 972 | 20826612 | Overall, this study indicates that the TLR2 and NOD2 pathways could cooperate to trigger an innate immune response to S. aureus mastitis. |
| 973 | 20875795 | Immunological basis of M13 phage vaccine: Regulation under MyD88 and TLR9 signaling. |
| 974 | 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. |
| 975 | 20877154 | Transcription of TLR2, TLR4, and TLR9 mRNA on canine CD21(+) cells was confirmed by reverse-transcript polymerase chain reaction (RT-PCR). |
| 976 | 20877154 | Quantification of IL-6, IL-10, and IL-12p40 mRNA transcription on canine CD21(+) cells revealed that CpG-ODNs enhanced IL-6 mRNA transcription but not IL-10 and IL-12p40 mRNA transcription (P<0.05 compared with control-ODNs). |
| 977 | 20947433 | We demonstrate that TLR2 ligands induce CCR9 and CCR10 expression by circulating B cells and increased chemotaxis to cognate chemokines CCL25 and CCL28 suggesting that TLR2 induces B cell homing to the gastrointestinal tract. |
| 978 | 21056473 | In this study we investigate the feasibility of generating self-adjuvanting vaccines capable of inducing high titre antibody responses following the covalent attachment of the TLR2 agonist Pam(2)Cys to intact proteins. |
| 979 | 21098227 | In this study, we demonstrate that the induction of TNF and IL-6 expression by LVS in mouse bone marrow-derived macrophages was markedly enhanced when PI3K activity was inhibited by either of the well-known chemical inhibitors, wortmannin or LY294002. |
| 980 | 21098227 | The enhanced cytokine expression was accompanied by enhanced activation of p38 MAPK and ERK1/2, both of which were critical for LVS-induced expression of TNF and IL-6. |
| 981 | 21098227 | LVS-induced MAPK activation and cytokine production were TLR2- and MyD88- dependent. |
| 982 | 21098227 | PI3K/Akt activation was MyD88-dependent, but was surprisingly TLR2-independent. |
| 983 | 21098227 | LVS infection also rapidly induced MAPK phosphatase-1 (MKP-1) expression; PI3K and TLR2 signaling were required. |
| 984 | 21098227 | Peak levels of MKP-1 correlated closely with the decline in p38 MAPK and ERK1/2 phosphorylation. |
| 985 | 21098227 | These data suggest that infection by LVS restrains the TLR2-triggered proinflammatory response via parallel activation of PI3K, leading to enhanced MKP-1 expression, accelerated deactivation of MAPKs, and suppression of proinflammatory cytokine production. |
| 986 | 21098227 | In this study, we demonstrate that the induction of TNF and IL-6 expression by LVS in mouse bone marrow-derived macrophages was markedly enhanced when PI3K activity was inhibited by either of the well-known chemical inhibitors, wortmannin or LY294002. |
| 987 | 21098227 | The enhanced cytokine expression was accompanied by enhanced activation of p38 MAPK and ERK1/2, both of which were critical for LVS-induced expression of TNF and IL-6. |
| 988 | 21098227 | LVS-induced MAPK activation and cytokine production were TLR2- and MyD88- dependent. |
| 989 | 21098227 | PI3K/Akt activation was MyD88-dependent, but was surprisingly TLR2-independent. |
| 990 | 21098227 | LVS infection also rapidly induced MAPK phosphatase-1 (MKP-1) expression; PI3K and TLR2 signaling were required. |
| 991 | 21098227 | Peak levels of MKP-1 correlated closely with the decline in p38 MAPK and ERK1/2 phosphorylation. |
| 992 | 21098227 | These data suggest that infection by LVS restrains the TLR2-triggered proinflammatory response via parallel activation of PI3K, leading to enhanced MKP-1 expression, accelerated deactivation of MAPKs, and suppression of proinflammatory cytokine production. |
| 993 | 21156751 | TLR2 deficiency by compromising p19 (IL-23) expression limits Th 17 cell responses to Mycobacterium tuberculosis. |
| 994 | 21156751 | Consistent with the decreased numbers of T(h)17 cells in the lungs of infected TLR2-deficient animals, we observed reduced expression of CXCL9, CXCL10 and CXCL11, chemokines involved in recall responses to M. tuberculosis. |
| 995 | 21156751 | TLR2 deficiency by compromising p19 (IL-23) expression limits Th 17 cell responses to Mycobacterium tuberculosis. |
| 996 | 21156751 | Consistent with the decreased numbers of T(h)17 cells in the lungs of infected TLR2-deficient animals, we observed reduced expression of CXCL9, CXCL10 and CXCL11, chemokines involved in recall responses to M. tuberculosis. |
| 997 | 21159924 | The IL-12 production was a consequence of the ligation of those recombinant proteins with Toll-like receptor 2. |
| 998 | 21159924 | The M. tuberculosis-derived and M. leprae-derived recombinant proteins activated naïve T cells of both CD4 and CD8 subsets, but M. tuberculosis-derived proteins were superior to M. leprae-derived proteins and fusion proteins were superior to MMP, regardless of the origin of the protein. |
| 999 | 21159924 | Memory-type CD4(+) T cells obtained from BCG-vaccinated healthy individuals seem to be primed with MMP-MTB by the vaccination, and both M. tuberculosis-derived recombinant proteins produced perforin-producing CD8(+) T cells from memory-type CD8(+) T cells. |
| 1000 | 21159925 | Toll-like receptor 4 gene (TLR4), but not TLR2, polymorphisms modify the risk of tonsillar disease due to Streptococcus pyogenes and Haemophilus influenzae. |
| 1001 | 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. |
| 1002 | 21173782 | Results showed that TLR2(-/-), TLR4(-/-)and TLR7(-/-) mice survived ECTV infection whereas MyD88(-/-) and TLR9(-/-)mice, in contrast, were highly susceptible. |
| 1003 | 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. |
| 1004 | 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. |
| 1005 | 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. |
| 1006 | 21188584 | Bacterial cell wall polysaccharides, such as PGN, bind and activate TLR-2, NOD2 and PGRP on monocytes/macrophages and activate inflammation. |
| 1007 | 21188584 | MTP, MDP, and lysine-less PGN bind to TLR-2, 87-113. |
| 1008 | 21191086 | Meningococcal CPS induced a dose-dependent release of cytokines (TNF-α, IL-6, IL-8, and CXCL10) and NO from human and murine macrophages, respectively. |
| 1009 | 21191086 | CPS induced IL-8 release from HEK cells stably transfected with TLR2/6, TLR2, TLR2/CD14, and TLR4/MD-2/CD14 but not HEK cells alone. mAb to TLR2 but not an isotype control antibody blocked CPS-induced IL-8 release from HEK-TLR2/6-transfected cells. |
| 1010 | 21191086 | A significant reduction in TNF-α and IL-8 release was seen when THP-1- and HEK-TLR4/MD-2-CD14- but not HEK-TLR2- or HEK-TLR2/6-transfected cells were stimulated with CPS in the presence of Eritoran (E5564), a lipid A antagonist that binds to MD-2, and a similar reduction in NO and TNF-α release was also seen in RAW 264.7 cells in the presence of Eritoran. |
| 1011 | 21191086 | CD14 and LBP enhanced CPS bioactivity, and NF-κB was, as anticipated, the major signaling pathway. |
| 1012 | 21199392 | For this purpose, serum concentration of interleukin 2 (IL2), interleukin 10 (IL10), interferon-gamma (IFNG), Toll-like receptor 2 (TLR2) and Toll-like receptor 9 (TLR9) were measured in blood samples obtained from F(2) piglets (n = 334) of a Duroc × Piétrain resource population (DUPI) after Mycoplasma hypopneumoniae (Mh), tetanus toxoid (TT) and Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) vaccination at 6, 9 and 15 weeks of age. |
| 1013 | 21203418 | Differential effect of TLR2 and TLR4 on the immune response after immunization with a vaccine against Neisseria meningitidis or Bordetella pertussis. |
| 1014 | 21203418 | Innate and adaptive immune responses were compared between wild type mice and mice deficient in TLR2, TLR4, or TRIF. |
| 1015 | 21203418 | TRIF-deficient and TLR4-deficient mice showed impaired immunity after immunization. |
| 1016 | 21203418 | Together our data demonstrate that TLR4 activation contributes to the immunogenicity of the N. meningitidis OMV vaccine and the whole cell pertussis vaccine, but that TLR2 activation is not required. |
| 1017 | 21203418 | Differential effect of TLR2 and TLR4 on the immune response after immunization with a vaccine against Neisseria meningitidis or Bordetella pertussis. |
| 1018 | 21203418 | Innate and adaptive immune responses were compared between wild type mice and mice deficient in TLR2, TLR4, or TRIF. |
| 1019 | 21203418 | TRIF-deficient and TLR4-deficient mice showed impaired immunity after immunization. |
| 1020 | 21203418 | Together our data demonstrate that TLR4 activation contributes to the immunogenicity of the N. meningitidis OMV vaccine and the whole cell pertussis vaccine, but that TLR2 activation is not required. |
| 1021 | 21203418 | Differential effect of TLR2 and TLR4 on the immune response after immunization with a vaccine against Neisseria meningitidis or Bordetella pertussis. |
| 1022 | 21203418 | Innate and adaptive immune responses were compared between wild type mice and mice deficient in TLR2, TLR4, or TRIF. |
| 1023 | 21203418 | TRIF-deficient and TLR4-deficient mice showed impaired immunity after immunization. |
| 1024 | 21203418 | Together our data demonstrate that TLR4 activation contributes to the immunogenicity of the N. meningitidis OMV vaccine and the whole cell pertussis vaccine, but that TLR2 activation is not required. |
| 1025 | 21236236 | Compared to the mice unvaccinated or vaccinated with empty plasmid, CD11c(+) cells at the dLN from naïve B6 mice expressed prominent IL-12 mRNA after the T.g.HSP70 gene vaccine. |
| 1026 | 21236236 | Also, CD4(+) cells at the dLN from the mice expressed prominent interferon-γ, but not IL-4 or IL-17, mRNA at a maximum level at day 5 following vaccination. |
| 1027 | 21236236 | This T.g.HSP70 gene vaccine-induced DC activation and Th1 polarization were also observed in TRIF-deficient mice, but not MyD88-deficient mice with B6 background indicating the involvement of TLR4/MyD88 signal transduction cascade in the vaccine effects with T.g.HSP70 gene. |
| 1028 | 21236236 | The T.g.HSP70 gene vaccine (twice at a 2-week interval) has been shown to limit T. gondii loads in the mesenteric LN of WT, TLR2-deficient and TRIF-deficient mice, but neither TLR4-deficient nor MyD88-deficient mice, at an acute phase of toxoplasmosis. |
| 1029 | 21236236 | The T.g.HSP70 gene vaccine also limited cyst number in the brains of WT, TLR2-deficient and TRIF-deficient mice, but not TLR4-deficient mice at a chronic phase of toxoplasmosis. |
| 1030 | 21236236 | Compared to the mice unvaccinated or vaccinated with empty plasmid, CD11c(+) cells at the dLN from naïve B6 mice expressed prominent IL-12 mRNA after the T.g.HSP70 gene vaccine. |
| 1031 | 21236236 | Also, CD4(+) cells at the dLN from the mice expressed prominent interferon-γ, but not IL-4 or IL-17, mRNA at a maximum level at day 5 following vaccination. |
| 1032 | 21236236 | This T.g.HSP70 gene vaccine-induced DC activation and Th1 polarization were also observed in TRIF-deficient mice, but not MyD88-deficient mice with B6 background indicating the involvement of TLR4/MyD88 signal transduction cascade in the vaccine effects with T.g.HSP70 gene. |
| 1033 | 21236236 | The T.g.HSP70 gene vaccine (twice at a 2-week interval) has been shown to limit T. gondii loads in the mesenteric LN of WT, TLR2-deficient and TRIF-deficient mice, but neither TLR4-deficient nor MyD88-deficient mice, at an acute phase of toxoplasmosis. |
| 1034 | 21236236 | The T.g.HSP70 gene vaccine also limited cyst number in the brains of WT, TLR2-deficient and TRIF-deficient mice, but not TLR4-deficient mice at a chronic phase of toxoplasmosis. |
| 1035 | 21288993 | Both B. breve and lactobacilli induced cytokines in a Toll-like receptor 9 (TLR9)-dependent manner, while the lower inflammatory profile of B. breve was due to inhibitory effects of TLR2. |
| 1036 | 21288993 | No role for TLR4, NOD2, and C-type lectin receptors was apparent. |
| 1037 | 21388684 | Here we demonstrated that the polymorphisms resulting in amino acid changes TLR5(R148L), TLR5(P402L), and TLR2(V703M) attenuated the responses to SC by the cells transfected with the TLR genes. |
| 1038 | 21424379 | The major alleles of coding SNPs in the TLR2 (rs3804100) and TLR4 (rs5030710) genes were associated with a dose-related increase (660 vs. 892 mIU/ml, p = 0.002) and a dose-related decrease (2,209 vs. 830 mIU/ml, p = 0.001) in measles-specific antibodies, respectively. |
| 1039 | 21424379 | We observed an additional 12 associations (p < 0.01) between coding (nonsynonymous and synonymous) polymorphisms within the TLRs (TLR2, 7, and 8), IKBKE, TICAM1, NFKBIA, IRAK2, and KIAA1542 genes and variations in measles-specific IL-2, IL-6, IFN-α, IFN-γ, IFNλ-1, and TNF-α secretion levels. |
| 1040 | 21424379 | The major alleles of coding SNPs in the TLR2 (rs3804100) and TLR4 (rs5030710) genes were associated with a dose-related increase (660 vs. 892 mIU/ml, p = 0.002) and a dose-related decrease (2,209 vs. 830 mIU/ml, p = 0.001) in measles-specific antibodies, respectively. |
| 1041 | 21424379 | We observed an additional 12 associations (p < 0.01) between coding (nonsynonymous and synonymous) polymorphisms within the TLRs (TLR2, 7, and 8), IKBKE, TICAM1, NFKBIA, IRAK2, and KIAA1542 genes and variations in measles-specific IL-2, IL-6, IFN-α, IFN-γ, IFNλ-1, and TNF-α secretion levels. |
| 1042 | 21499439 | The expression of CD1a, CD38, CD40, CD54, CD80, CD83, CD86, HLA-DR and CCR7 on URC-primed DC was enhanced. |
| 1043 | 21499439 | The production of IL-12p70 by URC-primed DC was inhibited by the anti-Toll-like receptor 4 (TLR4) monoclonal antibody (mAb), but partially abolished by anti-TLR2 mAb. mRNA coding for TLR2 and TLR4 was expressed in URC-primed DC. |
| 1044 | 21499439 | DC matured with URC had an intermediate migratory capacity towards CCL19 and CCL21. |
| 1045 | 21533081 | TLR2-dependent induction of IL-10 and Foxp3+ CD25+ CD4+ regulatory T cells prevents effective anti-tumor immunity induced by Pam2 lipopeptides in vivo. |
| 1046 | 21533081 | When we investigated the immune suppressive mechanisms, systemic injection of Pam2 lipopeptides induced IL-10 in a TLR2-dependent manner. |
| 1047 | 21533081 | The Pam2 lipopeptides increased the frequencies of Foxp3(+)CD4(+) regulatory T (T reg) cells in a TLR2- and IL-10- dependent manner. |
| 1048 | 21533081 | TLR2-dependent induction of IL-10 and Foxp3+ CD25+ CD4+ regulatory T cells prevents effective anti-tumor immunity induced by Pam2 lipopeptides in vivo. |
| 1049 | 21533081 | When we investigated the immune suppressive mechanisms, systemic injection of Pam2 lipopeptides induced IL-10 in a TLR2-dependent manner. |
| 1050 | 21533081 | The Pam2 lipopeptides increased the frequencies of Foxp3(+)CD4(+) regulatory T (T reg) cells in a TLR2- and IL-10- dependent manner. |
| 1051 | 21533081 | TLR2-dependent induction of IL-10 and Foxp3+ CD25+ CD4+ regulatory T cells prevents effective anti-tumor immunity induced by Pam2 lipopeptides in vivo. |
| 1052 | 21533081 | When we investigated the immune suppressive mechanisms, systemic injection of Pam2 lipopeptides induced IL-10 in a TLR2-dependent manner. |
| 1053 | 21533081 | The Pam2 lipopeptides increased the frequencies of Foxp3(+)CD4(+) regulatory T (T reg) cells in a TLR2- and IL-10- dependent manner. |
| 1054 | 21560483 | Increasing numbers of endogenous danger signals of host origin are being identified including, for example, uric acid and cholesterol crystals, high mobility group box1 (HMGB1) protein, oxidized LDL, vesicans, heat shock proteins (HSPs) and self DNA. |
| 1055 | 21560483 | Moreover, some PRRs (e.g., TLR2,TLR4 and NLRP3) and atypical PRRs can recognize both PAMPs and DAMPs, either as single entities or after forming complexes (e.g., immune complexes, or DNA- HMGB1 and DNA-LL37 complexes), so there must be a mechanism to selectively depress or alleviate the inflammatory response to DAMPs, while leaving that of PAMPs intact. |
| 1056 | 21560483 | For example, CD24 reacting with HMGB1 and HSPs has been implicated to function as negative regulator for RAGE. |
| 1057 | 21651945 | Now, we demonstrated a dose-response effect, with a concentration as low as 20μg/mL able to stimulate TLR2 and TLR4 transfected dendritic cells. |
| 1058 | 21651945 | These results favour a model whereby PVMA NPs adjuvant activate complement on site to attract immature antigen presenting cells that are activated through TLR2 and TLR4. |
| 1059 | 21651945 | Now, we demonstrated a dose-response effect, with a concentration as low as 20μg/mL able to stimulate TLR2 and TLR4 transfected dendritic cells. |
| 1060 | 21651945 | These results favour a model whereby PVMA NPs adjuvant activate complement on site to attract immature antigen presenting cells that are activated through TLR2 and TLR4. |
| 1061 | 21652516 | Priming of naive CD8 T cells by dendritic cells (DCs) entails both effective antigen presentation on MHC class I products and co-stimulatory signaling. |
| 1062 | 21652516 | To test whether it is possible to equip the resulting MHC-I complexes with an inherent ability to activate antigen-presenting cells, we engrafted the intracellular Toll/IL-1 receptor domain of mouse Toll-like receptor (TLR) 4 or TLR2 onto the peptide-β(2)m scaffold. |
| 1063 | 21674065 | We report an alternative approach, independent of BCR, for stimulating resting B (RB) cells, by involving TLR-2 and CD40--molecules crucial for innate and adaptive immunity. |
| 1064 | 21687418 | However, new important immune mediators have been revealed, including IL-17A, Toll-like receptor 2, and the inflammasome. |
| 1065 | 21687418 | CD4(+) and CD8(+) T cells are clearly important for control of primary infection and vaccine-induced protection, but new T cell subpopulations and the mechanisms employed by T cells are only beginning to be defined. |
| 1066 | 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). |
| 1067 | 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. |
| 1068 | 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. |
| 1069 | 21742006 | In conclusion, Pam(2)CSK(4) should be evaluated as a candidate adjuvant for a C. trachomatis vaccine. |
| 1070 | 21742967 | In this study, we show that electrostatic binding of synthetic branched cationic or anionic lipopeptides that contain the TLR-2 agonist Pam(2)Cys markedly enhance a protein's immunogenicity. |
| 1071 | 21742967 | The CD8(+) T cells elicited after vaccination with lipopeptide-protein Ag complexes produced proinflammatory cytokines, exhibited in vivo lytic activity, and protected mice from challenge with an infectious chimeric influenza virus containing a single OVA epitope as part of the influenza neuraminidase protein. |
| 1072 | 21746857 | A Salmonella vector vaccine expressing the saliva-binding region (SBR) of the adhesin AgI/II of Streptococcus mutans has been shown to induce a mixed Th1/Th2 anti-SBR immune response in mice and to require Toll-like receptor 2 (TLR2), TLR4, and MyD88 signaling for the induction of mucosal anti-SBR antibody responses. |
| 1073 | 21746857 | Bone marrow-derived DC from wild-type and TLR2, TLR4, and MyD88 knockout mice were stimulated with Salmonella vector BRD509, the SBR-expressing Salmonella vector vaccine BRD509(pSBRT7), or SBR protein, and the DC responses to different stimuli were compared by assessing costimulatory molecule expression, cytokine production, and signaling pathways. |
| 1074 | 21746857 | BRD509(pSBRT7) and BRD509 induced upregulation of CD80, CD86, CD40, and major histocompatibility complex class II (MHC II) expression. |
| 1075 | 21746857 | The low IL-12p40 and high IL-6 cytokine profile expressed by BRD509(pSBRT7)-stimulated DC may represent a shift toward a Th2 response, as suggested by the increased expression in Jagged-1. |
| 1076 | 21746857 | A Salmonella vector vaccine expressing the saliva-binding region (SBR) of the adhesin AgI/II of Streptococcus mutans has been shown to induce a mixed Th1/Th2 anti-SBR immune response in mice and to require Toll-like receptor 2 (TLR2), TLR4, and MyD88 signaling for the induction of mucosal anti-SBR antibody responses. |
| 1077 | 21746857 | Bone marrow-derived DC from wild-type and TLR2, TLR4, and MyD88 knockout mice were stimulated with Salmonella vector BRD509, the SBR-expressing Salmonella vector vaccine BRD509(pSBRT7), or SBR protein, and the DC responses to different stimuli were compared by assessing costimulatory molecule expression, cytokine production, and signaling pathways. |
| 1078 | 21746857 | BRD509(pSBRT7) and BRD509 induced upregulation of CD80, CD86, CD40, and major histocompatibility complex class II (MHC II) expression. |
| 1079 | 21746857 | The low IL-12p40 and high IL-6 cytokine profile expressed by BRD509(pSBRT7)-stimulated DC may represent a shift toward a Th2 response, as suggested by the increased expression in Jagged-1. |
| 1080 | 21901556 | Use of Lactobacillus species to combat UTI is now giving modern concept of modern genitourinary vaccine with the facts that it not only maintains low pH of the genital area, produces hydrogen peroxide and hinders the growth of E. coli but also activates Toll-like receptor-2 (TLR2), which produces interleukin-10 (IL-10) and myeloid differentiation factor 88 (MyD88). |
| 1081 | 21901556 | E. coli activates TLR4, which is responsible for the activation of IL-12, extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK). |
| 1082 | 21947769 | We also show that Hip1 dampens TLR2-independent activation of the inflammasome and limits secretion of interleukin-18 (IL-18). |
| 1083 | 22067741 | Yeast-surface expressed BVDV E2 protein induces a Th1/Th2 response in naïve T cells. |
| 1084 | 22067741 | S. cerevisiae activates the innate immune system by engaging pattern recognition receptors such as toll like receptor 2 (TLR2) and dectin-1. |
| 1085 | 22067741 | Additionally, bovine macrophages primed with S. cerevisiae expressing viral envelope proteins had a greater capacity for stimulating proliferation of CD4+ T-cells from BVDV-free animals compared to macrophages primed with envelope protein alone or S. cerevisiae without envelope protein expression. |
| 1086 | 22067741 | Additionally, heat-inactivation of recombinant S. cerevisiae induced less INFγ and IL-4 but equal amounts of IL-10 compared to live yeast T-cell cultures. |
| 1087 | 22102818 | These activities of ESAT-6 were dependent on TLR-2/MyD88 signalling and involved IL-6 and TGF-β production by dendritic cells. |
| 1088 | 22156342 | We previously demonstrated that intact heat-killed Streptococcus pneumoniae, a gram-positive bacterium, elicited a rapid primary pneumococcal capsular PS (PPS) response in mice that was dependent on CD4(+) T cells, B7-dependent costimulation, and CD40-CD40L interactions. |
| 1089 | 22156342 | However, this response was ICOS independent and failed to generate a boosted PPS-specific secondary IgG response. |
| 1090 | 22156342 | The secondary, but not primary, IgG anti-MCPS response to MenC was dependent on CD4(+) T cells, CD40L, CD28, and ICOS. |
| 1091 | 22156342 | The primary and secondary IgG anti-MCPS responses were lower in TLR4-defective (C3H/HeJ) but not TLR2(-/-) or MyD88(-/-) mice, but secondary boosting was still observed. |
| 1092 | 22253911 | In an attempt overcome this immunological non-responsiveness, we developed a self-adjuvanting vaccine candidate composed of three components: the B-cell epitope (J14), a universal helper T-cell epitope (P25) and a lipid moiety consisting of lipoamino acids (Laas) which target Toll-like receptor 2 (TLR2). |
| 1093 | 22415304 | Rv0577 recognizes Toll-like receptor 2 (TLR2) and functionally induces DC maturation by augmenting the expression of cell surface molecules (CD80, CD86, and MHC class I and II) and proinflammatory cytokine production (TNF-α, IL-1β, IL-6, and IL-12p70) in DCs on MyD88-dependent signaling, mitogen-activated protein kinases, and nuclear factor κB signaling pathways. |
| 1094 | 22415304 | In addition, Rv0577-treated DCs activated naive T cells, effectively polarized CD4(+) and CD8(+) T cells to secrete IFN-γ and IL-2, and induced T-cell proliferation, indicating that this protein possibly contributes to Th1-polarization of the immune response. |
| 1095 | 22415304 | More important, unlike LPS, Rv0577-treated DCs specifically induced the proliferation of memory CD4(+)/CD8(+)CD44(high)CD62L(low) T cells in the spleen of M. tuberculosis-infected mice in a TLR2-dependent manner. |
| 1096 | 22415304 | Rv0577 recognizes Toll-like receptor 2 (TLR2) and functionally induces DC maturation by augmenting the expression of cell surface molecules (CD80, CD86, and MHC class I and II) and proinflammatory cytokine production (TNF-α, IL-1β, IL-6, and IL-12p70) in DCs on MyD88-dependent signaling, mitogen-activated protein kinases, and nuclear factor κB signaling pathways. |
| 1097 | 22415304 | In addition, Rv0577-treated DCs activated naive T cells, effectively polarized CD4(+) and CD8(+) T cells to secrete IFN-γ and IL-2, and induced T-cell proliferation, indicating that this protein possibly contributes to Th1-polarization of the immune response. |
| 1098 | 22415304 | More important, unlike LPS, Rv0577-treated DCs specifically induced the proliferation of memory CD4(+)/CD8(+)CD44(high)CD62L(low) T cells in the spleen of M. tuberculosis-infected mice in a TLR2-dependent manner. |
| 1099 | 22426325 | At the injection site, 594 genes were differentially expressed, including up-regulation of the cytokines osteopontin (SPP1), IL-10 and IL-18 and the chemokines CCL2, CCL19 and CXCL16. |
| 1100 | 22426325 | Of the 362 genes differentially expressed in the lymph node, IL-1β and CXCL11 were up-regulated whereas IL18, CCL15 and CXCL12 were down-regulated. |
| 1101 | 22426325 | ISCOM-Matrix also modulated genes for pattern recognition receptors at the injection site (TLR2, TLR4, MRC1, PTX3, LGALS3) and in the lymph node (TLR4, RIG-I, MDA5, OAS1, EIF2AK2, LGALS3). |
| 1102 | 22441387 | Measurement of interleukin-8 (IL-8) produced by HEK293 cells transfected with Toll-like receptor (TLR) after stimulation with rlip-TbpB showed that the protein is a TLR2 agonist, which is in accordance with the structure of its lipid. |
| 1103 | 22473996 | We here demonstrate that M. bovis BCG triggers Toll-like receptor 2 (TLR2)-dependent microRNA-155 (miR-155) expression, which involves signaling cross talk among phosphatidylinositol 3-kinase (PI3K), protein kinase Cδ (PKCδ), and mitogen-activated protein kinases (MAPKs) and recruitment of NF-κB and c-ETS to miR-155 promoter. |
| 1104 | 22473996 | Genetic and signaling perturbations presented the evidence that miR-155 regulates PKA signaling by directly targeting a negative regulator of PKA, protein kinase inhibitor alpha (PKI-α). |
| 1105 | 22473996 | The miR-155-triggered activation of caspase-3, BAK1, and cytochrome c translocation involved signaling integration of MAPKs and epigenetic or posttranslational modification of histones or CREB. |
| 1106 | 22573738 | We demonstrated that direct exposure of porcine APCs to L. jensenii in the absence of inflammatory signals increased expression of interleukin-10 (IL-10) and transforming growth factor β in CD172a(+) APCs and caused them to display tolerogenic properties. |
| 1107 | 22573738 | In addition, pretreatment of CD172a(+) APCs with L. jensenii resulted in differential modulation of the production of pro- and anti-inflammatory cytokines in response to TLR4 activation. |
| 1108 | 22573738 | The immunomodulatory effect of strain TL2937 was not related to a downregulation of TLR4 but was related to an upregulation of the expression of three negative regulators of TLRs: single immunoglobulin IL-1-related receptor (SIGIRR), A20, and interleukin-1 receptor-associated kinase M (IRAK-M). |
| 1109 | 22573738 | Our results also indicated that TLR2 has an important role in the anti-inflammatory activity of L. jensenii TL2937, since anti-TLR2 antibodies blocked the upregulation of SIGIRR and IRAK-M in CD172a(+) APCs and the production of IL-10 in response to TLR4 activation. |
| 1110 | 22617845 | HLA class II genotype and suppression of transcript expression for TLR2, TLR4 and TLR8 in the nonresponder group may help explain the lack of vaccine response in this study group. |
| 1111 | 22623652 | FomA induces interleukin 8 (IL-8) secretion and NF-κB-dependent luciferase activity in HEK cells expressing TLR2, IL-6 secretion, and cell surface upregulation of CD86 and major histocompatibility complex (MHC) II in primary B cells from wild-type mice, but it fails to activate cells from TLR2 knockout mice. |
| 1112 | 22623652 | In a mouse model of immunization with ovalbumin (OVA), FomA induces enhanced production of OVA-specific IgM and IgG, including IgG1 and IgG2b antibodies, as well as enhanced secretion of IL-10 and IL-6, consistent with a Th2-type adjuvant effect. |
| 1113 | 22649499 | Depending on the ligands and cytokines studied, different age-related patterns were found: alum-induced IL-1β and CXCL8 responses were found to significantly decline with increasing age; inflammatory (IL-6, IL-1β, IFN-γ) responses to TLR2 and TLR3 agonists increased; and IL-10 responses remained constant or increased during infancy, while TNF-α responses either declined or remained the same. |
| 1114 | 22662179 | LOS activates the host immune response through a membrane bound CD14-TLR4 complex, while both heat killed and live M.cat require recognition by multiple toll like receptors such as TLR2, TLR4 and TLR9 without the requirement of CD14. |
| 1115 | 22662179 | We finally showed that TLR4 mutant C3H/HeJ mice produce significantly lower levels of pro-inflammatory cytokines TNF-α and IL-6 in vivo, An increased bacterial loads at 12 and 24 hours (P<0.001) in their lungs upon challenge with live M.cat in an aerosol chamber compared to wild-type (WT) control mice. |
| 1116 | 22677561 | ELL induced production of Type-1 cytokines such as IL-12 and TNF-α from bone marrow-derived dendritic cells (BMDCs) in TLR2- and TLR4-dependent manner and remarkably up-regulated the expression of MHC and co-stimulatory molecules. |
| 1117 | 22712385 | Meanwhile, gp96 has been shown to initiate innate immune responses through interaction with toll-like receptor 2 and toll-like receptor 4. |
| 1118 | 22778396 | Human TOLLIP regulates TLR2 and TLR4 signaling and its polymorphisms are associated with susceptibility to tuberculosis. |
| 1119 | 22778396 | Using short hairpin RNA knockdown of TOLLIP in peripheral blood human monocytes, we found that TOLLIP suppresses TNF and IL-6 production after stimulation with TLR2 and TLR4 ligands. |
| 1120 | 22778396 | In contrast, secretion of the anti-inflammatory cytokine IL-10 was induced by TOLLIP. |
| 1121 | 22778396 | Human TOLLIP regulates TLR2 and TLR4 signaling and its polymorphisms are associated with susceptibility to tuberculosis. |
| 1122 | 22778396 | Using short hairpin RNA knockdown of TOLLIP in peripheral blood human monocytes, we found that TOLLIP suppresses TNF and IL-6 production after stimulation with TLR2 and TLR4 ligands. |
| 1123 | 22778396 | In contrast, secretion of the anti-inflammatory cytokine IL-10 was induced by TOLLIP. |
| 1124 | 22796586 | Mycobacterium indicus pranii mediates macrophage activation through TLR2 and NOD2 in a MyD88 dependent manner. |
| 1125 | 22796586 | Treatment of macrophages with MIP caused upregulation of pro-inflammatory cytokines (like TNFα and IL-1β) which was mediated through both TLR2 and NOD2, as revealed by our knockdown and/or knockout studies. |
| 1126 | 22796586 | Mycobacterium indicus pranii mediates macrophage activation through TLR2 and NOD2 in a MyD88 dependent manner. |
| 1127 | 22796586 | Treatment of macrophages with MIP caused upregulation of pro-inflammatory cytokines (like TNFα and IL-1β) which was mediated through both TLR2 and NOD2, as revealed by our knockdown and/or knockout studies. |
| 1128 | 22908333 | ICOS-expressing CD4 T cells induced via TLR4 in the nasal mucosa are capable of inhibiting experimental allergic asthma. |
| 1129 | 22908333 | We investigated whether nasal rather than intrapulmonary application of Protollin, a mucosal adjuvant composed of TLR2 and TLR4 ligands, is sufficient to elicit protection against murine allergic lower airway disease. |
| 1130 | 22908333 | Inhibition was dependent on TLR4 and was associated with the induction of ICOS in cells of the nasal mucosa and on both CD4+Foxp3+ and CD4+Foxp3- T cells of the draining lymph nodes (LNs), as well as their recruitment to the lungs. |
| 1131 | 22908333 | Adoptive transfer of cervical LN CD4+ICOS+, but not CD4+ICOS-, cells inhibited BPEx-induced airway hyperresponsiveness and bronchoalveolar lavage eosinophilia. |
| 1132 | 22908333 | Thus, our data indicate that expansion of resident ICOS-expressing CD4+ T cells of the cervical LNs by nasal mucosal TLR4 stimulation may inhibit the development of allergic lower airway disease in mice. |
| 1133 | 22930672 | Control of adaptive immune responses by Staphylococcus aureus through IL-10, PD-L1, and TLR2. |
| 1134 | 22930672 | Herein we report that Staphylococcus aureus induces IL-10, Th17-inducing cytokines IL-6 and IL-23, chemokines, and regulates dendritic cell markers. |
| 1135 | 22930672 | S. aureus inhibits T-cell IL-2 responses through modulation of HLA-DR, CD86 and PD-L1. |
| 1136 | 22930672 | IFN-gamma, Src kinase inhibitors, or TLR2 antibodies prevented the down-modulation of HLA-DR by S. aureus. |
| 1137 | 22930672 | IL-10 and PD-L1 antagonists may boost immunity to vaccines for S. aureus and other microbes. |
| 1138 | 22934262 | In line with this notion, long-used preparations such as the Coley toxin (a mixture of killed Streptococcus pyogenes and Serratia marcescens bacteria) and the bacillus Calmette-Guérin (BCG, an attenuated strain of Mycobacterium bovis originally developed as a vaccine against tuberculosis), both of which have been associated with consistent anticancer responses, potently activate TLR2 and TLR4 signaling. |
| 1139 | 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. |
| 1140 | 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. |
| 1141 | 22953039 | By contrast, absent in melanoma 2 and retinoic acid-inducible gene I expression was lowest in aged animals. |
| 1142 | 22956655 | These synthetic mimics of antimicrobial peptides (SMAMPs) specifically reduced cytokine production in response to Staphylococcus aureus and the S. aureus component lipoteichoic acid (LTA), a TLR2 agonist. |
| 1143 | 22956655 | Anti-inflammatory SMAMPs prevented the induction of tumor necrosis factor (TNF), interleukin 6 (IL-6), and IL-10 in response to S. aureus or LTA, but no other TLR2 ligands. |
| 1144 | 22956655 | We show that these SMAMPs bind specifically to LTA in vitro and prevent its interaction with TLR2. |
| 1145 | 22956655 | Importantly, the SMAMP greatly reduced the induction of TNF and IL-6 in vivo in mice acutely infected with S. aureus while simultaneously reducing bacterial loads dramatically (4 log(10)). |
| 1146 | 22956655 | These synthetic mimics of antimicrobial peptides (SMAMPs) specifically reduced cytokine production in response to Staphylococcus aureus and the S. aureus component lipoteichoic acid (LTA), a TLR2 agonist. |
| 1147 | 22956655 | Anti-inflammatory SMAMPs prevented the induction of tumor necrosis factor (TNF), interleukin 6 (IL-6), and IL-10 in response to S. aureus or LTA, but no other TLR2 ligands. |
| 1148 | 22956655 | We show that these SMAMPs bind specifically to LTA in vitro and prevent its interaction with TLR2. |
| 1149 | 22956655 | Importantly, the SMAMP greatly reduced the induction of TNF and IL-6 in vivo in mice acutely infected with S. aureus while simultaneously reducing bacterial loads dramatically (4 log(10)). |
| 1150 | 22956655 | These synthetic mimics of antimicrobial peptides (SMAMPs) specifically reduced cytokine production in response to Staphylococcus aureus and the S. aureus component lipoteichoic acid (LTA), a TLR2 agonist. |
| 1151 | 22956655 | Anti-inflammatory SMAMPs prevented the induction of tumor necrosis factor (TNF), interleukin 6 (IL-6), and IL-10 in response to S. aureus or LTA, but no other TLR2 ligands. |
| 1152 | 22956655 | We show that these SMAMPs bind specifically to LTA in vitro and prevent its interaction with TLR2. |
| 1153 | 22956655 | Importantly, the SMAMP greatly reduced the induction of TNF and IL-6 in vivo in mice acutely infected with S. aureus while simultaneously reducing bacterial loads dramatically (4 log(10)). |
| 1154 | 23091628 | In this study, we have evaluated the use of an anionic self-adjuvanting lipopeptide containing the TLR2 agonist Pam(2)Cys (E(8)Pam(2)Cys) to enhance the immunogenicity of VLPs containing the HCV structural proteins (core, E1 and E2) of genotype 1a. |
| 1155 | 23091628 | Dramatically improved VLP and E2-specific antibody responses were observed in VLP+E(8)Pam(2)Cys vaccinated mice where up to 3 doses of non-adjuvanted or traditionally alum-adjuvanted VLPs was required to match the antibody titres obtained with a single dose of VLPs formulated with this lipopeptide. |
| 1156 | 23091628 | This result also correlated with significantly higher numbers of specific antibody secreting cells that was detected in the spleens of VLP+E(8)Pam(2)Cys vaccinated mice and greater ability of sera from these mice to neutralise the binding and uptake of VLPs by Huh7 cells. |
| 1157 | 23112821 | We conducted full-exon sequencing in samples obtained from Uganda (n = 48) and South Africa (n = 48), in four genes in the TLR pathway: TLR2, TLR4, TLR6, and TIRAP. |
| 1158 | 23112821 | We identified one novel TIRAP SNP (with minor allele frequency [MAF] 3.2%) and a novel TLR6 SNP (MAF 8%) in the Ugandan population, and a TLR6 SNP that is unique to the South African population (MAF 14%). |
| 1159 | 23132491 | Intracellular signaling pathways leading to host cell inflammation and innate immunity to Chlamydia include those mediated by Toll-like receptors (TLRs) and nucleotide binding oligomerization domain 1 (Nod1) protein. |
| 1160 | 23132491 | There is evidence that TLR3, TLR4, and, particularly, TLR2 are critical for Chlamydia-mediated host cell activation and pathology. |
| 1161 | 23132491 | Using MOMP formed in pure protein micelles (proteosomes), we show the induction of TLR2-dependent interleukin-8 (IL-8) and IL-6 secretion in vitro, the involvement of TLR1 as a TLR2 coreceptor, and the activation of both NF-κB and mitogen-activated protein (MAP) kinase intracellular pathways. |
| 1162 | 23132491 | Intracellular signaling pathways leading to host cell inflammation and innate immunity to Chlamydia include those mediated by Toll-like receptors (TLRs) and nucleotide binding oligomerization domain 1 (Nod1) protein. |
| 1163 | 23132491 | There is evidence that TLR3, TLR4, and, particularly, TLR2 are critical for Chlamydia-mediated host cell activation and pathology. |
| 1164 | 23132491 | Using MOMP formed in pure protein micelles (proteosomes), we show the induction of TLR2-dependent interleukin-8 (IL-8) and IL-6 secretion in vitro, the involvement of TLR1 as a TLR2 coreceptor, and the activation of both NF-κB and mitogen-activated protein (MAP) kinase intracellular pathways. |
| 1165 | 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. |
| 1166 | 23142133 | This DC subset expresses lipid sensors, TLR2 and TLR4, and nucleic acid sensors, TLR3, TLR9 and TLR13 and is specialized for antigen crosspresentation. |
| 1167 | 23166298 | Sonic hedgehog-dependent induction of microRNA 31 and microRNA 150 regulates Mycobacterium bovis BCG-driven toll-like receptor 2 signaling. |
| 1168 | 23166298 | Interestingly, sustained tumor necrosis factor alpha (TNF-α) secretion by macrophages was essential for robust SHH activation, as TNF-α(-/-) macrophages exhibited compromised ability to activate SHH signaling. |
| 1169 | 23166298 | Intriguingly, activated SHH signaling downregulated M. bovis BCG-mediated Toll-like receptor 2 (TLR2) signaling events to regulate a battery of genes associated with divergent functions of M1/M2 macrophages. |
| 1170 | 23166298 | Genome-wide expression profiling as well as conventional gain-of-function or loss-of-function analysis showed that SHH signaling-responsive microRNA 31 (miR-31) and miR-150 target MyD88, an adaptor protein of TLR2 signaling, thus leading to suppression of TLR2 responses. |
| 1171 | 23166298 | Sonic hedgehog-dependent induction of microRNA 31 and microRNA 150 regulates Mycobacterium bovis BCG-driven toll-like receptor 2 signaling. |
| 1172 | 23166298 | Interestingly, sustained tumor necrosis factor alpha (TNF-α) secretion by macrophages was essential for robust SHH activation, as TNF-α(-/-) macrophages exhibited compromised ability to activate SHH signaling. |
| 1173 | 23166298 | Intriguingly, activated SHH signaling downregulated M. bovis BCG-mediated Toll-like receptor 2 (TLR2) signaling events to regulate a battery of genes associated with divergent functions of M1/M2 macrophages. |
| 1174 | 23166298 | Genome-wide expression profiling as well as conventional gain-of-function or loss-of-function analysis showed that SHH signaling-responsive microRNA 31 (miR-31) and miR-150 target MyD88, an adaptor protein of TLR2 signaling, thus leading to suppression of TLR2 responses. |
| 1175 | 23166298 | Sonic hedgehog-dependent induction of microRNA 31 and microRNA 150 regulates Mycobacterium bovis BCG-driven toll-like receptor 2 signaling. |
| 1176 | 23166298 | Interestingly, sustained tumor necrosis factor alpha (TNF-α) secretion by macrophages was essential for robust SHH activation, as TNF-α(-/-) macrophages exhibited compromised ability to activate SHH signaling. |
| 1177 | 23166298 | Intriguingly, activated SHH signaling downregulated M. bovis BCG-mediated Toll-like receptor 2 (TLR2) signaling events to regulate a battery of genes associated with divergent functions of M1/M2 macrophages. |
| 1178 | 23166298 | Genome-wide expression profiling as well as conventional gain-of-function or loss-of-function analysis showed that SHH signaling-responsive microRNA 31 (miR-31) and miR-150 target MyD88, an adaptor protein of TLR2 signaling, thus leading to suppression of TLR2 responses. |
| 1179 | 23243590 | We found that Pam3Cys increases the proliferation of both CD4(+) effector T cells (Teffs) and Tregs co-cultured in vitro, but did not induce the proliferation of Tregs alone upon CD3 and CD28 stimulation. |
| 1180 | 23243590 | Teff from Pam3Cys-treated mice produced increased levels of Th1 and Th2-type cytokines and an interleukin (IL)-6-dependent secretion of IL-17 was observed in Teff:Treg co-cultures, suggesting that TLR2 stimulation had skewed the immune response toward a Th17 profile. |
| 1181 | 23345580 | After 24 h of incubation, production of tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), IL-6, and IL-10 was measured in supernatants by enzyme-linked immunosorbent assay (ELISA). |
| 1182 | 23345580 | The combinations of TLR2 and NOD2, TLR5 and NOD2, TLR5 and TLR3, and TLR5 and TLR9 acted as synergistic combinations. |
| 1183 | 23345580 | Surprisingly, inhibitory interactions between TLR4 and TLR2, TLR4 and Dectin-1, and TLR2 and TLR9 as well as TLR3 and TLR2 were observed. |
| 1184 | 23345580 | After 24 h of incubation, production of tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), IL-6, and IL-10 was measured in supernatants by enzyme-linked immunosorbent assay (ELISA). |
| 1185 | 23345580 | The combinations of TLR2 and NOD2, TLR5 and NOD2, TLR5 and TLR3, and TLR5 and TLR9 acted as synergistic combinations. |
| 1186 | 23345580 | Surprisingly, inhibitory interactions between TLR4 and TLR2, TLR4 and Dectin-1, and TLR2 and TLR9 as well as TLR3 and TLR2 were observed. |
| 1187 | 23432484 | We also found that OmpS1 is a Toll-like receptor 4 (TLR4) agonist, whereas OmpS2 is a TLR2 and TLR4 agonist. |
| 1188 | 23432484 | Both porins induced the production of tumour necrosis factor and interleukin-6, and OmpS2 was also able to induce interleukin-10 production. |
| 1189 | 23555011 | Combined TLR2- and TLR4-activated DC/tumor overcame immune-suppressive effect of TGF-β1 in comparison to those single activated or un-activated DC/tumor as demonstrated by: 1) up-regulation of MHC class II and CD86 expression on DC/tumor; 2) increased fusion efficiency; 3) increased production of fusions derived IL-12p70; 4) activation of CD4(+) and CD8(+) T cells that produce high levels of IFN-γ; 5) augmented induction of CTL activity specific for MUC1; and 6) superior efficacy in inhibiting CD4(+)CD25(+)Foxp3(+) T cell generation. |
| 1190 | 23593453 | Evaluation of an intranasal virosomal vaccine against respiratory syncytial virus in mice: effect of TLR2 and NOD2 ligands on induction of systemic and mucosal immune responses. |
| 1191 | 23595503 | Reduced frequency of a CD14+ CD16+ monocyte subset with high Toll-like receptor 4 expression in cord blood compared to adult blood contributes to lipopolysaccharide hyporesponsiveness in newborns. |
| 1192 | 23595503 | To better understand the mechanistic basis for this age-related difference in innate immunity, we compared tumor necrosis factor alpha (TNF-α) production by monocytes from cord blood (CB) and adult blood (AB) in response to LAM (lipoarabinomannan from Mycobacterium tuberculosis, a TLR2 ligand) and LPS (lipopolysaccharide from Escherichia coli, a TLR4 ligand). |
| 1193 | 23595503 | LPS or LAM-induced TNF-α production was 5 to 18 times higher in AB than in CB monocytes, whereas interleukin-1α (IL-1α) stimulated similar levels of TNF-α in both groups, suggesting that decreased responses to LPS or LAM in CB are unlikely to be due to differences in the MyD88-dependent signaling pathway. |
| 1194 | 23595503 | This impaired signaling was attributable, in part, to lower functional TLR4 expression, especially on CD14(+) CD16(+) monocytes, which are the primary cell subset for LPS-induced TNF-α production. |
| 1195 | 23595503 | Importantly, the frequency of CD14(+) CD16(+) monocytes in CB was 2.5-fold lower than in AB (P < 0.01). |
| 1196 | 23595503 | CB from Kenyan newborns sensitized to parasite antigens in utero had more CD14(+) CD16(+) monocytes (P = 0.02) and produced higher levels of TNF-α in response to LPS (P = 0.004) than CB from unsensitized Kenyan or North American newborns. |
| 1197 | 23595503 | Thus, a reduced CD14(+) CD16(+) activated/differentiated monocyte subset and a correspondingly lower level of functional TLR4 on monocytes contributes to the relatively low TNF-α response to LPS observed in immunologically naive newborns compared to the response in adults. |
| 1198 | 23595505 | Genetic variants in toll-like receptor 2 (TLR2), TLR4, TLR9, and FCγ receptor II are associated with antibody response to quadrivalent meningococcal conjugate vaccine in HIV-infected youth. |
| 1199 | 23595505 | Genetic variants associated with severity of meningococcal disease, including the IgG Fc receptor (FCγRII)-A484T, interleukin-10 (IL-10)-A1082G, -C819T, and -C627A, IL-4-C589T, mannose binding lectin-2 (MBL2)-A/O, -H/L, -P/Q, and -X/Y, toll-like receptor 2 (TLR2)-G2408A, TLR4-A12874G and -C13174T, and TLR9-T1237C and -T1486C were determined by real-time PCR (RT-PCR) for 271 HIV-infected subjects (median, 17 years). |
| 1200 | 23595505 | These findings suggest that for HIV-infected youth, the initial antibody response to MCV4 is associated with variants in TLR2 and TLR4 while the long-term response is associated with genetic polymorphisms in TLR9 and FcγRIIa. |
| 1201 | 23595505 | Genetic variants in toll-like receptor 2 (TLR2), TLR4, TLR9, and FCγ receptor II are associated with antibody response to quadrivalent meningococcal conjugate vaccine in HIV-infected youth. |
| 1202 | 23595505 | Genetic variants associated with severity of meningococcal disease, including the IgG Fc receptor (FCγRII)-A484T, interleukin-10 (IL-10)-A1082G, -C819T, and -C627A, IL-4-C589T, mannose binding lectin-2 (MBL2)-A/O, -H/L, -P/Q, and -X/Y, toll-like receptor 2 (TLR2)-G2408A, TLR4-A12874G and -C13174T, and TLR9-T1237C and -T1486C were determined by real-time PCR (RT-PCR) for 271 HIV-infected subjects (median, 17 years). |
| 1203 | 23595505 | These findings suggest that for HIV-infected youth, the initial antibody response to MCV4 is associated with variants in TLR2 and TLR4 while the long-term response is associated with genetic polymorphisms in TLR9 and FcγRIIa. |
| 1204 | 23595505 | Genetic variants in toll-like receptor 2 (TLR2), TLR4, TLR9, and FCγ receptor II are associated with antibody response to quadrivalent meningococcal conjugate vaccine in HIV-infected youth. |
| 1205 | 23595505 | Genetic variants associated with severity of meningococcal disease, including the IgG Fc receptor (FCγRII)-A484T, interleukin-10 (IL-10)-A1082G, -C819T, and -C627A, IL-4-C589T, mannose binding lectin-2 (MBL2)-A/O, -H/L, -P/Q, and -X/Y, toll-like receptor 2 (TLR2)-G2408A, TLR4-A12874G and -C13174T, and TLR9-T1237C and -T1486C were determined by real-time PCR (RT-PCR) for 271 HIV-infected subjects (median, 17 years). |
| 1206 | 23595505 | These findings suggest that for HIV-infected youth, the initial antibody response to MCV4 is associated with variants in TLR2 and TLR4 while the long-term response is associated with genetic polymorphisms in TLR9 and FcγRIIa. |
| 1207 | 23636320 | CD14 and TLR2 are also required for Eritoran-mediated protection, and CD14 directly binds Eritoran and inhibits ligand binding to MD2. |
| 1208 | 23781340 | In this study, IFN-gamma treatment of bone marrow-derived DC, followed by incubation with the TLR2, TLR4, or TLR9 agonists, enhanced DC activation compared to TLR ligation alone. |
| 1209 | 23781340 | Most notably, the upregulation of CD40 with LPS stimulation and CD86 with CpG stimulation was observed in in vitro cultures. |
| 1210 | 23781340 | Similarly, IFN-gamma coinjected with TLR ligands was able to promote DC activation in vivo, with DCs migrating from the site of immunization to the popliteal lymph nodes demonstrating increased expression of CD80 and CD86. |
| 1211 | 23797069 | We found that Vδ2 cells are indirectly activated by BCG in an interleukin (IL)-12p70-dependent manner, and that DC production of the IL-12p70 responsible for Vδ2 cell activation requires Toll-like receptor 2/4 ligands from BCG and interferon (IFN)-γ from memory CD4 T cells. |
| 1212 | 23797069 | Our data suggest that Vδ2 cell responses to BCG are dependent on the activation of IFN-γ-producing memory CD4 T cells, and provide novel insight into the complex interplay between cells of the innate and adaptive immune response. |
| 1213 | 23844129 | Separating volunteers into high and low responders on the basis of T cell responses to 85A peptides measured during the trial, an expansion of circulating CD4+ CD25+ Foxp3+ cells is seen in low but not high responders. |
| 1214 | 23844129 | In a classification model, combined expression levels of TLR1, TICAM2 and CD14 on day of vaccination and CTLA4 and IL2Rα two days post-vaccination can classify high and low responders with over 80% accuracy. |
| 1215 | 23844129 | Furthermore, administering MVA85A in mice with anti-TLR2 antibodies may abrogate high responses, and neutralising antibodies to TLRs 1, 2 or 6 or HMGB1 decrease CXCL2 production during in vitro stimulation with MVA85A. |
| 1216 | 23870458 | It has been demonstrated that recognition of chlamydial antigens is associated with TLR2, TLR4, and possibly, other PRRs. |
| 1217 | 23874845 | High-dose gp96 immunization elicited rapid and long-lasting protection of mice against concanavalin A (Con A)-and anti-CD137-induced liver injury, as evidenced by decreased alanine aminotransaminase (ALT) levels, hepatic necrosis, serum pro-inflammatory cytokines (IFN-γ, TNF-α, and IL-6), and number of IFN-γ (+) CD4(+) and IFN-γ (+) CD8(+) T cells in the spleen and liver. |
| 1218 | 23874845 | In contrast, CD4(+)CD25(+)Foxp3(+) Treg frequency and suppressive function were both increased, and the protective effect of gp96 could be generated by adoptive transfer of Treg cells from gp96-immunized mice. |
| 1219 | 23874845 | In vitro co-culture experiments demonstrated that gp96 stimulation enhanced Treg proliferation and suppressive function, and up-regulation of Foxp3, IL-10, and TGF-β1 induced by gp96 was dependent on TLR2- and TLR4-mediated NF-κB activation. |
| 1220 | 23901754 | Inhibition of toll-like receptor 2-mediated NF-kappaB activation in Vero cells with herpesvirus of turkeys. |
| 1221 | 23901754 | The results demonstrate the significant characteristics of HVT in activating TLR2 signaling. chTLR1 plays a key role in TLR2 subfamily-mediated NF-kappaB inhibition after HVT infection. |
| 1222 | 23901754 | Inhibition of toll-like receptor 2-mediated NF-kappaB activation in Vero cells with herpesvirus of turkeys. |
| 1223 | 23901754 | The results demonstrate the significant characteristics of HVT in activating TLR2 signaling. chTLR1 plays a key role in TLR2 subfamily-mediated NF-kappaB inhibition after HVT infection. |
| 1224 | 23925884 | We further show that lipid-mediated inhibition of inflammation is dependent on TLR2, MyD88, and the nuclear hormone and fatty acid receptor peroxisome proliferator-activated receptor α (PPARα). |
| 1225 | 23926349 | Secretion is accompanied by the stimulation of p38 and JNK mitogen-activated protein kinases (MAPKs) and nuclear factor NF-κB. |
| 1226 | 23926349 | NSP4 triggered the secretion of cytokines from murine macrophages derived from wild-type but not MyD88(-/-) or Toll-like receptor 2 (TLR2(-/-)) mice and induced secretion of interleukin-8 (IL-8) from human embryonic kidney cells transfected with TLR2 but not TLR4. |
| 1227 | 23933366 | Nasal vaccination with attenuated Salmonella expressing VapA: TLR2 activation is not essential for protection against R. equi infection. |
| 1228 | 23933366 | We have previously demonstrated that oral immunisation with attenuated Salmonella enterica Typhimurium strain expressing the antigen VapA (STM VapA+) induces specific and long-term humoral and cellular immunity against R. equi. |
| 1229 | 23933366 | It was shown that VapA activates Toll-like receptor 2 (TLR2) on macrophages by establishing an interaction that ultimately favours immunity against R. equi infection. |
| 1230 | 23933366 | The purpose of this study was to evaluate the immune response triggered by nasal immunisation with STM VapA+ and to determine whether TLR2 supports the vaccine effect. |
| 1231 | 23933366 | Nasal vaccination with STM VapA+ has also induced protection in Tlr2(-/-) mice and mice with non-functional TLR4. |
| 1232 | 23933366 | When similar experimental procedures were performed in TLR2 knockout mice, an increase in CD4(+) T cells with memory phenotype was not observed. |
| 1233 | 23933366 | Consequently, we conclude that nasal vaccination with attenuated Salmonella expressing the R. equi virulence factor VapA confers long-lasting protection against experimental rhodoccocosis and that TLR2 engagement was not crucial to induce this protection but may be required for a long-term immune response. |
| 1234 | 23933366 | Nasal vaccination with attenuated Salmonella expressing VapA: TLR2 activation is not essential for protection against R. equi infection. |
| 1235 | 23933366 | We have previously demonstrated that oral immunisation with attenuated Salmonella enterica Typhimurium strain expressing the antigen VapA (STM VapA+) induces specific and long-term humoral and cellular immunity against R. equi. |
| 1236 | 23933366 | It was shown that VapA activates Toll-like receptor 2 (TLR2) on macrophages by establishing an interaction that ultimately favours immunity against R. equi infection. |
| 1237 | 23933366 | The purpose of this study was to evaluate the immune response triggered by nasal immunisation with STM VapA+ and to determine whether TLR2 supports the vaccine effect. |
| 1238 | 23933366 | Nasal vaccination with STM VapA+ has also induced protection in Tlr2(-/-) mice and mice with non-functional TLR4. |
| 1239 | 23933366 | When similar experimental procedures were performed in TLR2 knockout mice, an increase in CD4(+) T cells with memory phenotype was not observed. |
| 1240 | 23933366 | Consequently, we conclude that nasal vaccination with attenuated Salmonella expressing the R. equi virulence factor VapA confers long-lasting protection against experimental rhodoccocosis and that TLR2 engagement was not crucial to induce this protection but may be required for a long-term immune response. |
| 1241 | 23933366 | Nasal vaccination with attenuated Salmonella expressing VapA: TLR2 activation is not essential for protection against R. equi infection. |
| 1242 | 23933366 | We have previously demonstrated that oral immunisation with attenuated Salmonella enterica Typhimurium strain expressing the antigen VapA (STM VapA+) induces specific and long-term humoral and cellular immunity against R. equi. |
| 1243 | 23933366 | It was shown that VapA activates Toll-like receptor 2 (TLR2) on macrophages by establishing an interaction that ultimately favours immunity against R. equi infection. |
| 1244 | 23933366 | The purpose of this study was to evaluate the immune response triggered by nasal immunisation with STM VapA+ and to determine whether TLR2 supports the vaccine effect. |
| 1245 | 23933366 | Nasal vaccination with STM VapA+ has also induced protection in Tlr2(-/-) mice and mice with non-functional TLR4. |
| 1246 | 23933366 | When similar experimental procedures were performed in TLR2 knockout mice, an increase in CD4(+) T cells with memory phenotype was not observed. |
| 1247 | 23933366 | Consequently, we conclude that nasal vaccination with attenuated Salmonella expressing the R. equi virulence factor VapA confers long-lasting protection against experimental rhodoccocosis and that TLR2 engagement was not crucial to induce this protection but may be required for a long-term immune response. |
| 1248 | 23933366 | Nasal vaccination with attenuated Salmonella expressing VapA: TLR2 activation is not essential for protection against R. equi infection. |
| 1249 | 23933366 | We have previously demonstrated that oral immunisation with attenuated Salmonella enterica Typhimurium strain expressing the antigen VapA (STM VapA+) induces specific and long-term humoral and cellular immunity against R. equi. |
| 1250 | 23933366 | It was shown that VapA activates Toll-like receptor 2 (TLR2) on macrophages by establishing an interaction that ultimately favours immunity against R. equi infection. |
| 1251 | 23933366 | The purpose of this study was to evaluate the immune response triggered by nasal immunisation with STM VapA+ and to determine whether TLR2 supports the vaccine effect. |
| 1252 | 23933366 | Nasal vaccination with STM VapA+ has also induced protection in Tlr2(-/-) mice and mice with non-functional TLR4. |
| 1253 | 23933366 | When similar experimental procedures were performed in TLR2 knockout mice, an increase in CD4(+) T cells with memory phenotype was not observed. |
| 1254 | 23933366 | Consequently, we conclude that nasal vaccination with attenuated Salmonella expressing the R. equi virulence factor VapA confers long-lasting protection against experimental rhodoccocosis and that TLR2 engagement was not crucial to induce this protection but may be required for a long-term immune response. |
| 1255 | 23933366 | Nasal vaccination with attenuated Salmonella expressing VapA: TLR2 activation is not essential for protection against R. equi infection. |
| 1256 | 23933366 | We have previously demonstrated that oral immunisation with attenuated Salmonella enterica Typhimurium strain expressing the antigen VapA (STM VapA+) induces specific and long-term humoral and cellular immunity against R. equi. |
| 1257 | 23933366 | It was shown that VapA activates Toll-like receptor 2 (TLR2) on macrophages by establishing an interaction that ultimately favours immunity against R. equi infection. |
| 1258 | 23933366 | The purpose of this study was to evaluate the immune response triggered by nasal immunisation with STM VapA+ and to determine whether TLR2 supports the vaccine effect. |
| 1259 | 23933366 | Nasal vaccination with STM VapA+ has also induced protection in Tlr2(-/-) mice and mice with non-functional TLR4. |
| 1260 | 23933366 | When similar experimental procedures were performed in TLR2 knockout mice, an increase in CD4(+) T cells with memory phenotype was not observed. |
| 1261 | 23933366 | Consequently, we conclude that nasal vaccination with attenuated Salmonella expressing the R. equi virulence factor VapA confers long-lasting protection against experimental rhodoccocosis and that TLR2 engagement was not crucial to induce this protection but may be required for a long-term immune response. |
| 1262 | 23933366 | Nasal vaccination with attenuated Salmonella expressing VapA: TLR2 activation is not essential for protection against R. equi infection. |
| 1263 | 23933366 | We have previously demonstrated that oral immunisation with attenuated Salmonella enterica Typhimurium strain expressing the antigen VapA (STM VapA+) induces specific and long-term humoral and cellular immunity against R. equi. |
| 1264 | 23933366 | It was shown that VapA activates Toll-like receptor 2 (TLR2) on macrophages by establishing an interaction that ultimately favours immunity against R. equi infection. |
| 1265 | 23933366 | The purpose of this study was to evaluate the immune response triggered by nasal immunisation with STM VapA+ and to determine whether TLR2 supports the vaccine effect. |
| 1266 | 23933366 | Nasal vaccination with STM VapA+ has also induced protection in Tlr2(-/-) mice and mice with non-functional TLR4. |
| 1267 | 23933366 | When similar experimental procedures were performed in TLR2 knockout mice, an increase in CD4(+) T cells with memory phenotype was not observed. |
| 1268 | 23933366 | Consequently, we conclude that nasal vaccination with attenuated Salmonella expressing the R. equi virulence factor VapA confers long-lasting protection against experimental rhodoccocosis and that TLR2 engagement was not crucial to induce this protection but may be required for a long-term immune response. |
| 1269 | 24019532 | Toll-like receptor 3-mediated necrosis via TRIF, RIP3, and MLKL. |
| 1270 | 24019532 | Toll-like receptor (TLR) signaling is triggered by pathogen-associated molecular patterns that mediate well established cytokine-driven pathways, activating NF-κB together with IRF3/IRF7. |
| 1271 | 24019532 | In addition, TLR3 drives caspase 8-regulated programmed cell death pathways reminiscent of TNF family death receptor signaling. |
| 1272 | 24019532 | We find that inhibition or elimination of caspase 8 during stimulation of TLR2, TLR3, TLR4, TLR5, or TLR9 results in receptor interacting protein (RIP) 3 kinase-dependent programmed necrosis that occurs through either TIR domain-containing adapter-inducing interferon-β (TRIF) or MyD88 signal transduction. |
| 1273 | 24019532 | TLR3 or TLR4 directly activates programmed necrosis through a RIP homotypic interaction motif-dependent association of TRIF with RIP3 kinase (also called RIPK3). |
| 1274 | 24019532 | In fibroblasts, this pathway proceeds independent of RIP1 or its kinase activity, but it remains dependent on mixed lineage kinase domain-like protein (MLKL) downstream of RIP3 kinase. |
| 1275 | 24019532 | Here, we describe two small molecule RIP3 kinase inhibitors and employ them to demonstrate the common requirement for RIP3 kinase in programmed necrosis induced by RIP1-RIP3, DAI-RIP3, and TRIF-RIP3 complexes. |
| 1276 | 24019532 | Cell fate decisions following TLR signaling parallel death receptor signaling and rely on caspase 8 to suppress RIP3-dependent programmed necrosis whether initiated directly by a TRIF-RIP3-MLKL pathway or indirectly via TNF activation and the RIP1-RIP3-MLKL necroptosis pathway. |
| 1277 | 24041710 | GP triggered the expression of pro-inflammatory cytokines IL-23p19, IL-8 and the β-glucan receptors dectin-1 and TLR2 by activated Caco-2 cells, and CCL20 in HT-29 cells. |
| 1278 | 24055352 | Our data demonstrate that neonatal mono-colonization with B. longum reduces allergic sensitization, likely by activation of regulatory responses via TLR2, MyD88, and MAPK signaling pathways. |
| 1279 | 24058377 | Therefore, since WE-CN did not induce maturation of DCs generated from mice with mutated TLR-4 or TLR-2, suggesting that TLR4 and TLR2 might function as membrane receptors for WE-CN. |
| 1280 | 24058377 | Moreover, the mechanism of action of WE-CN may be mediated by increased phosphorylation of ERK, p38, and JNK mitogen-activated protein kinase (MAPK) and increased NF- κ B p65 activity, which are important signaling molecules downstream of TLR-4 and TLR-2. |
| 1281 | 24058377 | Finally, coimmunization of mice with WE-CN and a HER-2/neu DNA vaccine induced a HER-2/neu-specific Th1 response that resulted in significant inhibition of HER-2/neu overexpressing mouse bladder tumor (MBT-2) growth. |
| 1282 | 24058377 | Therefore, since WE-CN did not induce maturation of DCs generated from mice with mutated TLR-4 or TLR-2, suggesting that TLR4 and TLR2 might function as membrane receptors for WE-CN. |
| 1283 | 24058377 | Moreover, the mechanism of action of WE-CN may be mediated by increased phosphorylation of ERK, p38, and JNK mitogen-activated protein kinase (MAPK) and increased NF- κ B p65 activity, which are important signaling molecules downstream of TLR-4 and TLR-2. |
| 1284 | 24058377 | Finally, coimmunization of mice with WE-CN and a HER-2/neu DNA vaccine induced a HER-2/neu-specific Th1 response that resulted in significant inhibition of HER-2/neu overexpressing mouse bladder tumor (MBT-2) growth. |
| 1285 | 24098572 | Colonization decreased frequencies of toll-like receptors (TLR) 2 and TLR4 expressing MNCs from vaccinated pigs (Pro+Vac) pre-challenge and increased frequencies of TLR3 expressing MNCs from Pro pigs post-challenge, suggesting that probiotics likely exert anti-inflammatory (TLR2 and 4 down-regulation) and antiviral (TLR3 up-regulation by HRV dsRNA) actions via TLR signaling. |
| 1286 | 24130733 | The addition of ESAT-6 or HspX alone to BCG-stimulated DC did not improve these processes, whereas their simultaneous addition enhanced BCG-dependent DC maturation and cytokine release, as well as the ability of BCG-treated DCs to stimulate IFN-γ release and CD69 expression by CD4(+) lymphocytes and NK cells. |
| 1287 | 24130733 | Our results indicate that ESAT-6 and HspX cooperation enables BCG-treated human DCs to induce T lymphocyte and NK cell-mediated immune responses through TLR2-dependent IL-12 secretion. |
| 1288 | 24252699 | Protollin (Prl)-based adjuvants (containing TLR2 and TLR4 ligands) are well-suited for nasal administration. |
| 1289 | 24252699 | This response was characterized by: (1) ≥four-fold increase of IgG2a levels compared to IgG1; and (2) high IL-2 (644pg/mL)/IFN-γ (228pg/mL) and low IL-5 (31pg/mL) secretion in MuV-restimulated splenocytes from animals receiving MuV-Prl formulations. |
| 1290 | 24291713 | A vaccine formulated with a combination of TLR-2 and TLR-9 adjuvants and the recombinant major outer membrane protein elicits a robust immune response and significant protection against a Chlamydia muridarum challenge. |
| 1291 | 24323452 | Protein-bound polysaccharide-K induces IL-1β via TLR2 and NLRP3 inflammasome activation. |
| 1292 | 24323452 | Using THP-1 cells, we have demonstrated that PSK induces both pro-IL-1β and mature IL-1β in THP-1 cells in a caspase 1- and NLRP3-dependent manner. |
| 1293 | 24323452 | PSK also induces IL-1β and IL-18 in human PBMC. |
| 1294 | 24323452 | Cathepsin B is required for PSK-induced inflammasome activation as CA-074-Me, a cathepsin B inhibitor, significantly decreased PSK-induced IL-1β. |
| 1295 | 24323452 | Comparison of PSK-induced IL-1β in bone marrow-derived macrophages from wild type C57BL/6 mice, TLR2(-/-), P2X7R(-/-) and NLRP3(-/-) mice demonstrated that PSK-induced IL-1β is dependent on both TLR2 and NLRP3. |
| 1296 | 24323452 | P2X7R is not required for PSK-induced inflammasome activation, but enhances PSK-induced caspase-1 activation and IL-1β induction. |
| 1297 | 24323452 | Altogether, these results demonstrated that PSK induces inflammasome activation and production of IL-1β in a TLR2- and NLRP3-dependent mechanism. |
| 1298 | 24323452 | Protein-bound polysaccharide-K induces IL-1β via TLR2 and NLRP3 inflammasome activation. |
| 1299 | 24323452 | Using THP-1 cells, we have demonstrated that PSK induces both pro-IL-1β and mature IL-1β in THP-1 cells in a caspase 1- and NLRP3-dependent manner. |
| 1300 | 24323452 | PSK also induces IL-1β and IL-18 in human PBMC. |
| 1301 | 24323452 | Cathepsin B is required for PSK-induced inflammasome activation as CA-074-Me, a cathepsin B inhibitor, significantly decreased PSK-induced IL-1β. |
| 1302 | 24323452 | Comparison of PSK-induced IL-1β in bone marrow-derived macrophages from wild type C57BL/6 mice, TLR2(-/-), P2X7R(-/-) and NLRP3(-/-) mice demonstrated that PSK-induced IL-1β is dependent on both TLR2 and NLRP3. |
| 1303 | 24323452 | P2X7R is not required for PSK-induced inflammasome activation, but enhances PSK-induced caspase-1 activation and IL-1β induction. |
| 1304 | 24323452 | Altogether, these results demonstrated that PSK induces inflammasome activation and production of IL-1β in a TLR2- and NLRP3-dependent mechanism. |
| 1305 | 24323452 | Protein-bound polysaccharide-K induces IL-1β via TLR2 and NLRP3 inflammasome activation. |
| 1306 | 24323452 | Using THP-1 cells, we have demonstrated that PSK induces both pro-IL-1β and mature IL-1β in THP-1 cells in a caspase 1- and NLRP3-dependent manner. |
| 1307 | 24323452 | PSK also induces IL-1β and IL-18 in human PBMC. |
| 1308 | 24323452 | Cathepsin B is required for PSK-induced inflammasome activation as CA-074-Me, a cathepsin B inhibitor, significantly decreased PSK-induced IL-1β. |
| 1309 | 24323452 | Comparison of PSK-induced IL-1β in bone marrow-derived macrophages from wild type C57BL/6 mice, TLR2(-/-), P2X7R(-/-) and NLRP3(-/-) mice demonstrated that PSK-induced IL-1β is dependent on both TLR2 and NLRP3. |
| 1310 | 24323452 | P2X7R is not required for PSK-induced inflammasome activation, but enhances PSK-induced caspase-1 activation and IL-1β induction. |
| 1311 | 24323452 | Altogether, these results demonstrated that PSK induces inflammasome activation and production of IL-1β in a TLR2- and NLRP3-dependent mechanism. |
| 1312 | 24349212 | Surface expression of activation markers on macrophages, including CD40, CD69, and CD86, was increased following PorB stimulation in vitro. |
| 1313 | 24349212 | Interestingly, some upregulation of CD54 and CD69 was still observed in macrophages obtained from TLR2 KO mice, indicating a possible non-TLR2 mediated activation pathway induced by PorB. |
| 1314 | 24422228 | We tested whether a Virulence Associated Protein A (VapA)/CpG vaccine against R. equi would impact the production of IL-10, IFN-γ and TNF-α in lung tissue and fluid samples, alter expression of TLR2 and TLR4 and alter their association with the lipid rafts in broncho-alveolar lavage (BAL) cells. |
| 1315 | 24422228 | We report adaptation of previous protocols to isolate plasma membrane fractions from BAL cells and identification of lipid raft fractions based on the presence of flotillin-1 and GM-1 and absence of transferrin receptor. |
| 1316 | 24422228 | TLR2 and TLR4 were restricted to plasma membrane fractions 7–9 of alveolar cells collected from vaccinated foals before and after the challenge. |
| 1317 | 24422228 | Taken together, we modified previous protocols to isolate plasma membrane fractions from BAL cells of foals and report that the vaccination with a VapA/CPG vaccine increases association of TLR2 and TLR4 with lipid raft fractions and alters expression of TNF-α and IL-10. |
| 1318 | 24422228 | The data point to a subtle effect of vaccination on the association of TLR2 and TLR4 with lipid rafts in BAL cells. |
| 1319 | 24422228 | We tested whether a Virulence Associated Protein A (VapA)/CpG vaccine against R. equi would impact the production of IL-10, IFN-γ and TNF-α in lung tissue and fluid samples, alter expression of TLR2 and TLR4 and alter their association with the lipid rafts in broncho-alveolar lavage (BAL) cells. |
| 1320 | 24422228 | We report adaptation of previous protocols to isolate plasma membrane fractions from BAL cells and identification of lipid raft fractions based on the presence of flotillin-1 and GM-1 and absence of transferrin receptor. |
| 1321 | 24422228 | TLR2 and TLR4 were restricted to plasma membrane fractions 7–9 of alveolar cells collected from vaccinated foals before and after the challenge. |
| 1322 | 24422228 | Taken together, we modified previous protocols to isolate plasma membrane fractions from BAL cells of foals and report that the vaccination with a VapA/CPG vaccine increases association of TLR2 and TLR4 with lipid raft fractions and alters expression of TNF-α and IL-10. |
| 1323 | 24422228 | The data point to a subtle effect of vaccination on the association of TLR2 and TLR4 with lipid rafts in BAL cells. |
| 1324 | 24422228 | We tested whether a Virulence Associated Protein A (VapA)/CpG vaccine against R. equi would impact the production of IL-10, IFN-γ and TNF-α in lung tissue and fluid samples, alter expression of TLR2 and TLR4 and alter their association with the lipid rafts in broncho-alveolar lavage (BAL) cells. |
| 1325 | 24422228 | We report adaptation of previous protocols to isolate plasma membrane fractions from BAL cells and identification of lipid raft fractions based on the presence of flotillin-1 and GM-1 and absence of transferrin receptor. |
| 1326 | 24422228 | TLR2 and TLR4 were restricted to plasma membrane fractions 7–9 of alveolar cells collected from vaccinated foals before and after the challenge. |
| 1327 | 24422228 | Taken together, we modified previous protocols to isolate plasma membrane fractions from BAL cells of foals and report that the vaccination with a VapA/CPG vaccine increases association of TLR2 and TLR4 with lipid raft fractions and alters expression of TNF-α and IL-10. |
| 1328 | 24422228 | The data point to a subtle effect of vaccination on the association of TLR2 and TLR4 with lipid rafts in BAL cells. |
| 1329 | 24422228 | We tested whether a Virulence Associated Protein A (VapA)/CpG vaccine against R. equi would impact the production of IL-10, IFN-γ and TNF-α in lung tissue and fluid samples, alter expression of TLR2 and TLR4 and alter their association with the lipid rafts in broncho-alveolar lavage (BAL) cells. |
| 1330 | 24422228 | We report adaptation of previous protocols to isolate plasma membrane fractions from BAL cells and identification of lipid raft fractions based on the presence of flotillin-1 and GM-1 and absence of transferrin receptor. |
| 1331 | 24422228 | TLR2 and TLR4 were restricted to plasma membrane fractions 7–9 of alveolar cells collected from vaccinated foals before and after the challenge. |
| 1332 | 24422228 | Taken together, we modified previous protocols to isolate plasma membrane fractions from BAL cells of foals and report that the vaccination with a VapA/CPG vaccine increases association of TLR2 and TLR4 with lipid raft fractions and alters expression of TNF-α and IL-10. |
| 1333 | 24422228 | The data point to a subtle effect of vaccination on the association of TLR2 and TLR4 with lipid rafts in BAL cells. |
| 1334 | 24467650 | Stimulation of THP-1 macrophages with recombinant PE35 and PPE68, singly or in combination, led to a dose-dependent increase in levels of the anti-inflammatory cytokine interleukin (IL)-10 and the chemokine monocyte chemoattractant protein-1, and caused a reciprocal decrease in levels of the proinflammatory cytokine IL-12. |
| 1335 | 24467650 | PE35/PPE68-stimulated production of IL-10 and monocyte chemoattractant protein-1 was observed to be dependent on toll-like receptor 2, as receptor blockade caused a significant reduction in their levels. |
| 1336 | 24475289 | Spores promoted activation of antigen presenting cells as demonstrated by the upregulation of MHC and CD40 molecules and enhanced secretion of pro-inflammatory cytokines by murine dendritic cells. |
| 1337 | 24475289 | In addition, in vivo studies indicated a direct role of the innate immunity on the immunomodulatory properties of B. subtilis spores, as demonstrated by the lack of adjuvant effects on MyD88 and TLR2 knockout mouse strains. |
| 1338 | 24532579 | In these studies, we demonstrate that W805EC NE adjuvant activates innate immunity, induces specific gene transcription, and modulates NF-κB activity via TLR2 and TLR4 by a mechanism that appears to be distinct from typical TLR agonists. |
| 1339 | 24532579 | Nasal immunization with NE-based vaccine showed that the TLR2, TLR4, and MyD88 pathways and IL-12 and IL-12Rβ1 expression are not required for an Ab response, but they are essential for the induction of balanced Th-1 polarization and Th-17 cellular immunity. |
| 1340 | 24532579 | NE adjuvant induces MHC class II, CD80, and CD86 costimulatory molecule expression and dendritic cell maturation. |
| 1341 | 24532579 | Further, upon immunization with NE, adjuvant mice deficient in the CD86 receptor had normal Ab responses but significantly reduced Th-1 cellular responses, whereas animals deficient in both CD80 and CD86 or lacking CD40 failed to produce either humoral or cellular immunity. |
| 1342 | 24532579 | Overall, our data show that intranasal administration of Ag with NE induces TLR2 and TLR4 activation along with a MyD88-independent Ab response and a MyD88-dependent Th-1 and Th-17 cell-mediated immune response. |
| 1343 | 24532579 | In these studies, we demonstrate that W805EC NE adjuvant activates innate immunity, induces specific gene transcription, and modulates NF-κB activity via TLR2 and TLR4 by a mechanism that appears to be distinct from typical TLR agonists. |
| 1344 | 24532579 | Nasal immunization with NE-based vaccine showed that the TLR2, TLR4, and MyD88 pathways and IL-12 and IL-12Rβ1 expression are not required for an Ab response, but they are essential for the induction of balanced Th-1 polarization and Th-17 cellular immunity. |
| 1345 | 24532579 | NE adjuvant induces MHC class II, CD80, and CD86 costimulatory molecule expression and dendritic cell maturation. |
| 1346 | 24532579 | Further, upon immunization with NE, adjuvant mice deficient in the CD86 receptor had normal Ab responses but significantly reduced Th-1 cellular responses, whereas animals deficient in both CD80 and CD86 or lacking CD40 failed to produce either humoral or cellular immunity. |
| 1347 | 24532579 | Overall, our data show that intranasal administration of Ag with NE induces TLR2 and TLR4 activation along with a MyD88-independent Ab response and a MyD88-dependent Th-1 and Th-17 cell-mediated immune response. |
| 1348 | 24532579 | In these studies, we demonstrate that W805EC NE adjuvant activates innate immunity, induces specific gene transcription, and modulates NF-κB activity via TLR2 and TLR4 by a mechanism that appears to be distinct from typical TLR agonists. |
| 1349 | 24532579 | Nasal immunization with NE-based vaccine showed that the TLR2, TLR4, and MyD88 pathways and IL-12 and IL-12Rβ1 expression are not required for an Ab response, but they are essential for the induction of balanced Th-1 polarization and Th-17 cellular immunity. |
| 1350 | 24532579 | NE adjuvant induces MHC class II, CD80, and CD86 costimulatory molecule expression and dendritic cell maturation. |
| 1351 | 24532579 | Further, upon immunization with NE, adjuvant mice deficient in the CD86 receptor had normal Ab responses but significantly reduced Th-1 cellular responses, whereas animals deficient in both CD80 and CD86 or lacking CD40 failed to produce either humoral or cellular immunity. |
| 1352 | 24532579 | Overall, our data show that intranasal administration of Ag with NE induces TLR2 and TLR4 activation along with a MyD88-independent Ab response and a MyD88-dependent Th-1 and Th-17 cell-mediated immune response. |
| 1353 | 24594065 | TLR2-mediated elimination of MTB involves multiple pathways such as promoting DCs maturation, generating biased Th1, Th2, Th17 type response, regulating the macrophage activation and cytokine secretion. |
| 1354 | 24595607 | We compared the influence of F. tularensis antigens (tularinum) in vitro on production of IL-1, IL-5, IL-6, IL-17, IFN-γ, and TNF-α by splenocytes obtained from intact mice and mice immunized with mutant F. tularensis 15∆23A and/or F. tularensis 15 NIIEG strains. |
| 1355 | 24595607 | We also compared expression of CD28, CD154, TLR-2, and CD69 markers on CD4 and CD8 T-cells after activation with tularinum in vitro. |
| 1356 | 24595607 | We found that tularinum-induced CD4(+) T-cells increased TNF-α and IFN-γ synthesis and expression of CD69 only in group mice with high degree of post immunization protection against F. tularensis Schu challenge. |
| 1357 | 24595607 | Estimation of CD69 expression on CD3(+)CD4(+) cells and IFN-γ, TNF-α synthesis by CD4(+) T-lymphocytes could be useful for determination protect ability of antitularemia immunity. |
| 1358 | 24602605 | Immunization of mice with encapsulated M278 elicited higher M278-specific T-cell cytokines [Th1 (IFN-γ, IL-2), Th17 (IL-17)] and antibodies [Th1 (IgG2a), Th2 (IgG1, IgG2b)] compared to bare M278. |
| 1359 | 24602605 | Encapsulated-M278 mouse serum inhibited Chlamydia infectivity of macrophages, with a concomitant transcriptional down-regulation of MOMP, its cognate TLR2 and CD80 co-stimulatory molecule. |
| 1360 | 24614655 | Interleukin-1 receptor but not Toll-like receptor 2 is essential for MyD88-dependent Th17 immunity to Coccidioides infection. |
| 1361 | 24614655 | Interleukin-17A (IL-17A)-producing CD4(+) T helper (Th17) cells have been shown to be essential for defense against pulmonary infection with Coccidioides species. |
| 1362 | 24614655 | Here, we report that both MyD88(-/-) and Card9(-/-) mice immunized with a live, attenuated vaccine also fail to acquire protective immunity to this respiratory disease. |
| 1363 | 24614655 | Like Card9(-/-) mice, vaccinated MyD88(-/-) mice revealed a significant reduction in numbers of both Th17 and Th1 cells in their lungs after Coccidioides infection. |
| 1364 | 24614655 | Both Toll-like receptor 2 (TLR2) and IL-1 receptor type 1 (IL-1r1) upstream of MyD88 have been implicated in Th17 cell differentiation. |
| 1365 | 24614655 | Surprisingly, vaccinated TLR2(-/-) and wild-type (WT) mice showed similar outcomes after pulmonary infection with Coccidioides, while vaccinated IL-1r1(-/-) mice revealed a significant reduction in the number of Th17 cells in their infected lungs compared to WT mice. |
| 1366 | 24614655 | Our data also reveal that the numbers of Th17 cells were reduced in IL-1r1(-/-) mice to a lesser extent than in MyD88(-/-) mice, raising the possibility that other TLRs are involved in MyD88-dependent Th17 immunity to coccidioidomycosis. |
| 1367 | 24614655 | Interleukin-1 receptor but not Toll-like receptor 2 is essential for MyD88-dependent Th17 immunity to Coccidioides infection. |
| 1368 | 24614655 | Interleukin-17A (IL-17A)-producing CD4(+) T helper (Th17) cells have been shown to be essential for defense against pulmonary infection with Coccidioides species. |
| 1369 | 24614655 | Here, we report that both MyD88(-/-) and Card9(-/-) mice immunized with a live, attenuated vaccine also fail to acquire protective immunity to this respiratory disease. |
| 1370 | 24614655 | Like Card9(-/-) mice, vaccinated MyD88(-/-) mice revealed a significant reduction in numbers of both Th17 and Th1 cells in their lungs after Coccidioides infection. |
| 1371 | 24614655 | Both Toll-like receptor 2 (TLR2) and IL-1 receptor type 1 (IL-1r1) upstream of MyD88 have been implicated in Th17 cell differentiation. |
| 1372 | 24614655 | Surprisingly, vaccinated TLR2(-/-) and wild-type (WT) mice showed similar outcomes after pulmonary infection with Coccidioides, while vaccinated IL-1r1(-/-) mice revealed a significant reduction in the number of Th17 cells in their infected lungs compared to WT mice. |
| 1373 | 24614655 | Our data also reveal that the numbers of Th17 cells were reduced in IL-1r1(-/-) mice to a lesser extent than in MyD88(-/-) mice, raising the possibility that other TLRs are involved in MyD88-dependent Th17 immunity to coccidioidomycosis. |
| 1374 | 24614655 | Interleukin-1 receptor but not Toll-like receptor 2 is essential for MyD88-dependent Th17 immunity to Coccidioides infection. |
| 1375 | 24614655 | Interleukin-17A (IL-17A)-producing CD4(+) T helper (Th17) cells have been shown to be essential for defense against pulmonary infection with Coccidioides species. |
| 1376 | 24614655 | Here, we report that both MyD88(-/-) and Card9(-/-) mice immunized with a live, attenuated vaccine also fail to acquire protective immunity to this respiratory disease. |
| 1377 | 24614655 | Like Card9(-/-) mice, vaccinated MyD88(-/-) mice revealed a significant reduction in numbers of both Th17 and Th1 cells in their lungs after Coccidioides infection. |
| 1378 | 24614655 | Both Toll-like receptor 2 (TLR2) and IL-1 receptor type 1 (IL-1r1) upstream of MyD88 have been implicated in Th17 cell differentiation. |
| 1379 | 24614655 | Surprisingly, vaccinated TLR2(-/-) and wild-type (WT) mice showed similar outcomes after pulmonary infection with Coccidioides, while vaccinated IL-1r1(-/-) mice revealed a significant reduction in the number of Th17 cells in their infected lungs compared to WT mice. |
| 1380 | 24614655 | Our data also reveal that the numbers of Th17 cells were reduced in IL-1r1(-/-) mice to a lesser extent than in MyD88(-/-) mice, raising the possibility that other TLRs are involved in MyD88-dependent Th17 immunity to coccidioidomycosis. |
| 1381 | 24614661 | Using proteomic screens, we recently identified several antigens that protected mice from pneumococcal colonization in a CD4(+) T cell- and interleukin-17A (IL-17A)-dependent manner. |
| 1382 | 24614661 | In contrast, immunization of Tlr2(-/-) mice elicited no detectable IL-17A response and no protection against pneumococcal colonization. |
| 1383 | 24632732 | In a PP cell culture system, b240 promoted the production of immunoglobulin A (IgA), interleukin (IL)-6, IL-10, interferon (IFN)-γ, and tumor necrosis factor, but not IL-4, IL-5, B-cell activating factors, IFN-α, IFN-β, and transforming growth factor-β1. |
| 1384 | 24632732 | The enhanced IgA production by b240 was attenuated by neutralizing IL-6, a potent IgA-enhancing cytokine. b240 stimulated DCs to produce an elevated amount of IL-6 in a Toll-like receptor (TLR) 2-, but not TLR4- or TLR9-dependent manner. |
| 1385 | 24632732 | Finally, we demonstrated that TLR2-mediated IL-6 production from PP DCs in response to b240 activated B cells to produce a large amount of IgA in a DC-B cell co-culture system. |
| 1386 | 24711582 | However, ZBTB20-deficient plasma cells expressed reduced levels of MCL1 relative to wild-type controls, and transgenic expression of BCL2 increased serum antibody titers. |
| 1387 | 24711582 | Strikingly, adjuvants that activate TLR2 and TLR4 restored long-term antibody production in ZBTB20-deficient chimeras through the induction of compensatory survival programs in plasma cells. |
| 1388 | 24743542 | Whole blood was stimulated for 24 hours and the pro-inflammatory tumor necrosis factor (TNF) and the anti-inflammatory/regulatory interleukin-10 (IL-10) cytokines in culture supernatant were measured by enzyme-linked immunosorbent assay (ELISA). |
| 1389 | 24743542 | Gabonese children had a lower pro-inflammatory response to poly(I:C) (TLR3 ligand), but a higher pro-inflammatory response to FSL-1 (TLR2/6 ligand), Pam3 (TLR2/1 ligand) and LPS (TLR4 ligand) compared to Dutch children. |
| 1390 | 24760892 | Here we show that TLR2/6 but not TLR1/2 heterodimers sense Junín virus glycoprotein and induce a cytokine response, which in turn upregulates the expression of the RNA helicases RIG-I and MDA5. |
| 1391 | 24760892 | NF-κB and Erk1/2 were important in the cytokine response, since both proteins were phosphorylated as a result of the interaction of virus with TLR2, and treatment with an Erk1/2-specific inhibitor blocked cytokine production. |
| 1392 | 24760892 | Here we show that TLR2/6 but not TLR1/2 heterodimers sense Junín virus glycoprotein and induce a cytokine response, which in turn upregulates the expression of the RNA helicases RIG-I and MDA5. |
| 1393 | 24760892 | NF-κB and Erk1/2 were important in the cytokine response, since both proteins were phosphorylated as a result of the interaction of virus with TLR2, and treatment with an Erk1/2-specific inhibitor blocked cytokine production. |
| 1394 | 24766519 | Prominent up-regulation of co-stimulatory molecules CD40, CD80 and CD86 was also observed in response to MIP. |
| 1395 | 24766519 | With the help of pharmacological inhibitors and Toll-like receptor (TLR) -deficient macrophages, we observed the role of TLR2, TLR4 and intracellular TLRs in MIP-mediated macrophage activation. |
| 1396 | 24797722 | The objective of the present study was to assess the adjuvant potential of TLR2 and TLR5 ligands flagellin and Pam3 respectively. |
| 1397 | 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. |
| 1398 | 24837764 | CD4(+) T-cell responses were optimally induced when using TLR9- and TLR3-ligand-adjuvants or CAF09. |
| 1399 | 24837764 | Rv2034-specific antibodies were observed following immunization with either TLR2-, TLR3-, TLR4-, TLR5-, TLR7- or TLR9-ligands or CAF09. |
| 1400 | 24842522 | Identification of the key differential transcriptional responses of human whole blood following TLR2 or TLR4 ligation in-vitro. |
| 1401 | 24842522 | Using the TLR2 ligand (Pam3CSK4) and the TLR4 ligand (LPS), human whole blood was stimulated for 0, 1, 3, 6, 12 or 24 hours at which times mRNA was isolated and a comparative microarray was undertaken. |
| 1402 | 24842522 | A common NFκB transcriptional programme was identified following both TLR2 and TLR4 ligation which peaked at between 3 to 6 hours including upregulation of many of the NFκB family members. |
| 1403 | 24842522 | In contrast an interferon transcriptional response was observed following TLR4 but not TLR2 ligation as early as 1 hour post stimulation and peaking at 6 hours. |
| 1404 | 24842522 | Our study demonstrates that a transcriptomic analysis of mRNA isolated from human whole blood can delineate both the temporal response and the key transcriptional differences following TLR2 and TLR4 ligation. |
| 1405 | 24842522 | Identification of the key differential transcriptional responses of human whole blood following TLR2 or TLR4 ligation in-vitro. |
| 1406 | 24842522 | Using the TLR2 ligand (Pam3CSK4) and the TLR4 ligand (LPS), human whole blood was stimulated for 0, 1, 3, 6, 12 or 24 hours at which times mRNA was isolated and a comparative microarray was undertaken. |
| 1407 | 24842522 | A common NFκB transcriptional programme was identified following both TLR2 and TLR4 ligation which peaked at between 3 to 6 hours including upregulation of many of the NFκB family members. |
| 1408 | 24842522 | In contrast an interferon transcriptional response was observed following TLR4 but not TLR2 ligation as early as 1 hour post stimulation and peaking at 6 hours. |
| 1409 | 24842522 | Our study demonstrates that a transcriptomic analysis of mRNA isolated from human whole blood can delineate both the temporal response and the key transcriptional differences following TLR2 and TLR4 ligation. |
| 1410 | 24842522 | Identification of the key differential transcriptional responses of human whole blood following TLR2 or TLR4 ligation in-vitro. |
| 1411 | 24842522 | Using the TLR2 ligand (Pam3CSK4) and the TLR4 ligand (LPS), human whole blood was stimulated for 0, 1, 3, 6, 12 or 24 hours at which times mRNA was isolated and a comparative microarray was undertaken. |
| 1412 | 24842522 | A common NFκB transcriptional programme was identified following both TLR2 and TLR4 ligation which peaked at between 3 to 6 hours including upregulation of many of the NFκB family members. |
| 1413 | 24842522 | In contrast an interferon transcriptional response was observed following TLR4 but not TLR2 ligation as early as 1 hour post stimulation and peaking at 6 hours. |
| 1414 | 24842522 | Our study demonstrates that a transcriptomic analysis of mRNA isolated from human whole blood can delineate both the temporal response and the key transcriptional differences following TLR2 and TLR4 ligation. |
| 1415 | 24842522 | Identification of the key differential transcriptional responses of human whole blood following TLR2 or TLR4 ligation in-vitro. |
| 1416 | 24842522 | Using the TLR2 ligand (Pam3CSK4) and the TLR4 ligand (LPS), human whole blood was stimulated for 0, 1, 3, 6, 12 or 24 hours at which times mRNA was isolated and a comparative microarray was undertaken. |
| 1417 | 24842522 | A common NFκB transcriptional programme was identified following both TLR2 and TLR4 ligation which peaked at between 3 to 6 hours including upregulation of many of the NFκB family members. |
| 1418 | 24842522 | In contrast an interferon transcriptional response was observed following TLR4 but not TLR2 ligation as early as 1 hour post stimulation and peaking at 6 hours. |
| 1419 | 24842522 | Our study demonstrates that a transcriptomic analysis of mRNA isolated from human whole blood can delineate both the temporal response and the key transcriptional differences following TLR2 and TLR4 ligation. |
| 1420 | 24842522 | Identification of the key differential transcriptional responses of human whole blood following TLR2 or TLR4 ligation in-vitro. |
| 1421 | 24842522 | Using the TLR2 ligand (Pam3CSK4) and the TLR4 ligand (LPS), human whole blood was stimulated for 0, 1, 3, 6, 12 or 24 hours at which times mRNA was isolated and a comparative microarray was undertaken. |
| 1422 | 24842522 | A common NFκB transcriptional programme was identified following both TLR2 and TLR4 ligation which peaked at between 3 to 6 hours including upregulation of many of the NFκB family members. |
| 1423 | 24842522 | In contrast an interferon transcriptional response was observed following TLR4 but not TLR2 ligation as early as 1 hour post stimulation and peaking at 6 hours. |
| 1424 | 24842522 | Our study demonstrates that a transcriptomic analysis of mRNA isolated from human whole blood can delineate both the temporal response and the key transcriptional differences following TLR2 and TLR4 ligation. |
| 1425 | 24890740 | Immune and anticancer responses elicited by fully synthetic aberrantly glycosylated MUC1 tripartite vaccines modified by a TLR2 or TLR9 agonist. |
| 1426 | 24912383 | We explored the changes in the expression of TLR2, TLR4 and the concentration of acute inflammatory cytokines, such as IL-2, IL-8, IL-12 and IFN-γ in Bama miniature pigs subjected to 21 consecutive days of heat stress, both in vitro and in vivo models. |
| 1427 | 24912383 | The results showed that heat stress induced the upregulation of cortisol in the plasma of pigs (P<0.05); TLR4 mRNA was elevated, but IL-2 was reduced in peripheral blood mononuclear cells (PBMC, P<0.05). |
| 1428 | 24912383 | In the in vitro model (PBMC heat shocked for 1 h followed by a 9 h recovery period), TLR2 and TLR4 mRNA expression also increased, as did the concentration of IL-12 in supernatants. |
| 1429 | 24912383 | We concluded that a consecutive heat stress period elevated the expression of TLR2 and TLR4 in PBMC and increased the plasma levels of inflammatory cytokines. |
| 1430 | 24912383 | We explored the changes in the expression of TLR2, TLR4 and the concentration of acute inflammatory cytokines, such as IL-2, IL-8, IL-12 and IFN-γ in Bama miniature pigs subjected to 21 consecutive days of heat stress, both in vitro and in vivo models. |
| 1431 | 24912383 | The results showed that heat stress induced the upregulation of cortisol in the plasma of pigs (P<0.05); TLR4 mRNA was elevated, but IL-2 was reduced in peripheral blood mononuclear cells (PBMC, P<0.05). |
| 1432 | 24912383 | In the in vitro model (PBMC heat shocked for 1 h followed by a 9 h recovery period), TLR2 and TLR4 mRNA expression also increased, as did the concentration of IL-12 in supernatants. |
| 1433 | 24912383 | We concluded that a consecutive heat stress period elevated the expression of TLR2 and TLR4 in PBMC and increased the plasma levels of inflammatory cytokines. |
| 1434 | 24912383 | We explored the changes in the expression of TLR2, TLR4 and the concentration of acute inflammatory cytokines, such as IL-2, IL-8, IL-12 and IFN-γ in Bama miniature pigs subjected to 21 consecutive days of heat stress, both in vitro and in vivo models. |
| 1435 | 24912383 | The results showed that heat stress induced the upregulation of cortisol in the plasma of pigs (P<0.05); TLR4 mRNA was elevated, but IL-2 was reduced in peripheral blood mononuclear cells (PBMC, P<0.05). |
| 1436 | 24912383 | In the in vitro model (PBMC heat shocked for 1 h followed by a 9 h recovery period), TLR2 and TLR4 mRNA expression also increased, as did the concentration of IL-12 in supernatants. |
| 1437 | 24912383 | We concluded that a consecutive heat stress period elevated the expression of TLR2 and TLR4 in PBMC and increased the plasma levels of inflammatory cytokines. |
| 1438 | 24995344 | We found that Tlr4 and Myd88 appeared to be required for an optimal immune response to the F1-V vaccine but not Tlr2 when compared to wild-type mice. |
| 1439 | 24995344 | However, there was a difference between the requirement for Tlr4 and MyD88 in vaccinated animals. |
| 1440 | 25019567 | Recombinant TB10.4 of Mycobacterium bovis induces cytokine production in RAW264.7 macrophages through activation of the MAPK and NF-κB pathways via TLR2. |
| 1441 | 25019567 | The TB10.4 antigen of Mycobacterium bovis/Mycobacterium tuberculosis induces a strong Th1 CD4+ T-cell response. |
| 1442 | 25019567 | Here, as stimulated RAW264.7 cells with recombinant TB10.4 (rTB10.4), derived from M. bovis, increased TNF-α, IL-6 and IL-12 p40 secretin in a dose-dependent manner. |
| 1443 | 25019567 | Blocking assays showed that TLR2-, but not TLR4-neutralizing antibody reduced expression of TNF-α, IL-6 and IL-12 p40 in RAW264.7 cells. rTB10.4 stimulation activated p38 kinase (p38) and extracellular-regulated kinase (ERK) was TLR2-dependent, whereas inhibition of p38 and ERK activity significantly reduced TNF-α, IL-6 and IL-12 p40 production. |
| 1444 | 25019567 | Furthermore, rTB10.4 stimulation of RAW264.7 cells resulted in TLR2-mediated activation of NF-κB and induced translocation of NF-κB p65 from the cytoplasm to the nucleus via IκBα degradation. rTB10.4-induced TNF-α, IL-6 and IL-12 p40 release was attenuated by the specific IκB phosphorylation inhibitor, BAY 11-7082. |
| 1445 | 25019567 | These findings indicate that the M. bovis-derived rTB10.4 induced production of TNF-α, IL-6 and IL-12 p40 involves p38, ERK and NF-κB via the TLR2 pathway. |
| 1446 | 25019567 | Recombinant TB10.4 of Mycobacterium bovis induces cytokine production in RAW264.7 macrophages through activation of the MAPK and NF-κB pathways via TLR2. |
| 1447 | 25019567 | The TB10.4 antigen of Mycobacterium bovis/Mycobacterium tuberculosis induces a strong Th1 CD4+ T-cell response. |
| 1448 | 25019567 | Here, as stimulated RAW264.7 cells with recombinant TB10.4 (rTB10.4), derived from M. bovis, increased TNF-α, IL-6 and IL-12 p40 secretin in a dose-dependent manner. |
| 1449 | 25019567 | Blocking assays showed that TLR2-, but not TLR4-neutralizing antibody reduced expression of TNF-α, IL-6 and IL-12 p40 in RAW264.7 cells. rTB10.4 stimulation activated p38 kinase (p38) and extracellular-regulated kinase (ERK) was TLR2-dependent, whereas inhibition of p38 and ERK activity significantly reduced TNF-α, IL-6 and IL-12 p40 production. |
| 1450 | 25019567 | Furthermore, rTB10.4 stimulation of RAW264.7 cells resulted in TLR2-mediated activation of NF-κB and induced translocation of NF-κB p65 from the cytoplasm to the nucleus via IκBα degradation. rTB10.4-induced TNF-α, IL-6 and IL-12 p40 release was attenuated by the specific IκB phosphorylation inhibitor, BAY 11-7082. |
| 1451 | 25019567 | These findings indicate that the M. bovis-derived rTB10.4 induced production of TNF-α, IL-6 and IL-12 p40 involves p38, ERK and NF-κB via the TLR2 pathway. |
| 1452 | 25019567 | Recombinant TB10.4 of Mycobacterium bovis induces cytokine production in RAW264.7 macrophages through activation of the MAPK and NF-κB pathways via TLR2. |
| 1453 | 25019567 | The TB10.4 antigen of Mycobacterium bovis/Mycobacterium tuberculosis induces a strong Th1 CD4+ T-cell response. |
| 1454 | 25019567 | Here, as stimulated RAW264.7 cells with recombinant TB10.4 (rTB10.4), derived from M. bovis, increased TNF-α, IL-6 and IL-12 p40 secretin in a dose-dependent manner. |
| 1455 | 25019567 | Blocking assays showed that TLR2-, but not TLR4-neutralizing antibody reduced expression of TNF-α, IL-6 and IL-12 p40 in RAW264.7 cells. rTB10.4 stimulation activated p38 kinase (p38) and extracellular-regulated kinase (ERK) was TLR2-dependent, whereas inhibition of p38 and ERK activity significantly reduced TNF-α, IL-6 and IL-12 p40 production. |
| 1456 | 25019567 | Furthermore, rTB10.4 stimulation of RAW264.7 cells resulted in TLR2-mediated activation of NF-κB and induced translocation of NF-κB p65 from the cytoplasm to the nucleus via IκBα degradation. rTB10.4-induced TNF-α, IL-6 and IL-12 p40 release was attenuated by the specific IκB phosphorylation inhibitor, BAY 11-7082. |
| 1457 | 25019567 | These findings indicate that the M. bovis-derived rTB10.4 induced production of TNF-α, IL-6 and IL-12 p40 involves p38, ERK and NF-κB via the TLR2 pathway. |
| 1458 | 25019567 | Recombinant TB10.4 of Mycobacterium bovis induces cytokine production in RAW264.7 macrophages through activation of the MAPK and NF-κB pathways via TLR2. |
| 1459 | 25019567 | The TB10.4 antigen of Mycobacterium bovis/Mycobacterium tuberculosis induces a strong Th1 CD4+ T-cell response. |
| 1460 | 25019567 | Here, as stimulated RAW264.7 cells with recombinant TB10.4 (rTB10.4), derived from M. bovis, increased TNF-α, IL-6 and IL-12 p40 secretin in a dose-dependent manner. |
| 1461 | 25019567 | Blocking assays showed that TLR2-, but not TLR4-neutralizing antibody reduced expression of TNF-α, IL-6 and IL-12 p40 in RAW264.7 cells. rTB10.4 stimulation activated p38 kinase (p38) and extracellular-regulated kinase (ERK) was TLR2-dependent, whereas inhibition of p38 and ERK activity significantly reduced TNF-α, IL-6 and IL-12 p40 production. |
| 1462 | 25019567 | Furthermore, rTB10.4 stimulation of RAW264.7 cells resulted in TLR2-mediated activation of NF-κB and induced translocation of NF-κB p65 from the cytoplasm to the nucleus via IκBα degradation. rTB10.4-induced TNF-α, IL-6 and IL-12 p40 release was attenuated by the specific IκB phosphorylation inhibitor, BAY 11-7082. |
| 1463 | 25019567 | These findings indicate that the M. bovis-derived rTB10.4 induced production of TNF-α, IL-6 and IL-12 p40 involves p38, ERK and NF-κB via the TLR2 pathway. |
| 1464 | 25023285 | Modulation of endotoxicity of Shigella generalized modules for membrane antigens (GMMA) by genetic lipid A modifications: relative activation of TLR4 and TLR2 pathways in different mutants. |
| 1465 | 25023285 | The results identify the relative contributions of TLR4 and TLR2 activation by GMMA, which need to be taken into consideration for GMMA vaccine development. |
| 1466 | 25023285 | Modulation of endotoxicity of Shigella generalized modules for membrane antigens (GMMA) by genetic lipid A modifications: relative activation of TLR4 and TLR2 pathways in different mutants. |
| 1467 | 25023285 | The results identify the relative contributions of TLR4 and TLR2 activation by GMMA, which need to be taken into consideration for GMMA vaccine development. |
| 1468 | 25024199 | We further find that this previously unappreciated function of Cas9 is critical during infection, as it promotes evasion of the host innate immune absent in melanoma 2/apoptosis associated speck-like protein containing a CARD (AIM2/ASC) inflammasome. |
| 1469 | 25024199 | Interestingly, the attenuation of the cas9 mutant is complemented only in mice lacking both the AIM2/ASC inflammasome and the bacterial lipoprotein sensor Toll-like receptor 2, but not in single knockout mice, demonstrating that Cas9 is essential for evasion of both pathways. |
| 1470 | 25114104 | In this article, we report that C57BL/6 mice lacking the adapter protein MyD88, which mediates signaling by TLRs and IL-1 family members, showed enhanced immunity to H. polygyrus infection. |
| 1471 | 25114104 | Alongside increased parasite expulsion, MyD88-deficient mice showed heightened IL-4 and IL-17A production from mesenteric lymph node CD4(+) cells. |
| 1472 | 25114104 | In addition, MyD88(-/-) mice developed substantial numbers of intestinal granulomas around the site of infection, which were not seen in MyD88-sufficient C57BL/6 mice, nor when signaling through the adapter protein TRIF (TIR domain-containing adapter-inducing IFN-β adapter protein) was also ablated. |
| 1473 | 25114104 | Mice deficient solely in TLR2, TLR4, TLR5, or TLR9 did not show enhanced parasite expulsion, suggesting that these TLRs signal redundantly to maintain H. polygyrus susceptibility in wild-type mice. |
| 1474 | 25114104 | Like IL-1R1(-/-) and MyD88(-/-) mice, animals lacking signaling through the type 1 IFN receptor (i.e., IFNAR1(-/-)) also developed intestinal granulomas. |
| 1475 | 25114104 | Hence, IL-1R1, MyD88, and type 1 IFN receptor signaling may provide pathways to impede granuloma formation in vivo, but additional MyD88-mediated signals are associated with inhibition of protective immunity in susceptible C57BL/6 mice. |
| 1476 | 25165025 | This study was conducted to evaluate the immunogenicity and protective efficacy of a DNA vaccine encoding Brucella abortus Cu,Zn superoxide dismutase (SOD) using the Toll-like receptor 2/6 agonist S-[2,3-bispalmitoyiloxy-(2R)-propyl]-R-cysteinyl-amido-monomethoxy polyethylene glycol (BPPcysMPEG) as an adjuvant. |
| 1477 | 25165025 | Humoral responses were characterized by the stimulation of IgG2a and IgG1 and by the presence of SOD-specific secretory IgA in nasal and bronchoalveolar lavage fluids. |
| 1478 | 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. |
| 1479 | 25248345 | The soluble forms of TLR-2, TLR-4, and TLR-7 were determined in serum samples by ELISA as well. |
| 1480 | 25250027 | TLR2 Signaling is Required for the Innate, but Not Adaptive Response to LVS clpB. |
| 1481 | 25250027 | We sought to determine whether TLR2 signaling was required during the immune response to LVS clpB. |
| 1482 | 25250027 | TLR2 knock-out (TLR2 KO) mice previously infected with LVS clpB are completely protected during a lethal challenge with LVS. |
| 1483 | 25250027 | Furthermore, the kinetics and magnitude of the primary T-cell response in B6 and TLR2 KO mice are similar indicating that TLR2 signaling is dispensable for the adaptive immune response to LVS clpB. |
| 1484 | 25250027 | TLR2 signaling was important, however, for the innate immune response to LVS clpB. |
| 1485 | 25250027 | IL-1α, IL-1β, IL-2, IL-17, MIP-1α, and TNF-α production depended on TLR2 signaling, while GM-CSF, IFN-γ, and VEGF production were completely independent of TLR2 signaling. |
| 1486 | 25250027 | IL-6, IL-12, IP-10, KC, and MIG production were partially dependent on TLR2 signaling. |
| 1487 | 25250027 | Together our data indicate that the innate immune response to LVS clpB requires TLR2 signaling for the maximal innate response, whereas TLR2 is not required for the adaptive immune response. |
| 1488 | 25250027 | TLR2 Signaling is Required for the Innate, but Not Adaptive Response to LVS clpB. |
| 1489 | 25250027 | We sought to determine whether TLR2 signaling was required during the immune response to LVS clpB. |
| 1490 | 25250027 | TLR2 knock-out (TLR2 KO) mice previously infected with LVS clpB are completely protected during a lethal challenge with LVS. |
| 1491 | 25250027 | Furthermore, the kinetics and magnitude of the primary T-cell response in B6 and TLR2 KO mice are similar indicating that TLR2 signaling is dispensable for the adaptive immune response to LVS clpB. |
| 1492 | 25250027 | TLR2 signaling was important, however, for the innate immune response to LVS clpB. |
| 1493 | 25250027 | IL-1α, IL-1β, IL-2, IL-17, MIP-1α, and TNF-α production depended on TLR2 signaling, while GM-CSF, IFN-γ, and VEGF production were completely independent of TLR2 signaling. |
| 1494 | 25250027 | IL-6, IL-12, IP-10, KC, and MIG production were partially dependent on TLR2 signaling. |
| 1495 | 25250027 | Together our data indicate that the innate immune response to LVS clpB requires TLR2 signaling for the maximal innate response, whereas TLR2 is not required for the adaptive immune response. |
| 1496 | 25250027 | TLR2 Signaling is Required for the Innate, but Not Adaptive Response to LVS clpB. |
| 1497 | 25250027 | We sought to determine whether TLR2 signaling was required during the immune response to LVS clpB. |
| 1498 | 25250027 | TLR2 knock-out (TLR2 KO) mice previously infected with LVS clpB are completely protected during a lethal challenge with LVS. |
| 1499 | 25250027 | Furthermore, the kinetics and magnitude of the primary T-cell response in B6 and TLR2 KO mice are similar indicating that TLR2 signaling is dispensable for the adaptive immune response to LVS clpB. |
| 1500 | 25250027 | TLR2 signaling was important, however, for the innate immune response to LVS clpB. |
| 1501 | 25250027 | IL-1α, IL-1β, IL-2, IL-17, MIP-1α, and TNF-α production depended on TLR2 signaling, while GM-CSF, IFN-γ, and VEGF production were completely independent of TLR2 signaling. |
| 1502 | 25250027 | IL-6, IL-12, IP-10, KC, and MIG production were partially dependent on TLR2 signaling. |
| 1503 | 25250027 | Together our data indicate that the innate immune response to LVS clpB requires TLR2 signaling for the maximal innate response, whereas TLR2 is not required for the adaptive immune response. |
| 1504 | 25250027 | TLR2 Signaling is Required for the Innate, but Not Adaptive Response to LVS clpB. |
| 1505 | 25250027 | We sought to determine whether TLR2 signaling was required during the immune response to LVS clpB. |
| 1506 | 25250027 | TLR2 knock-out (TLR2 KO) mice previously infected with LVS clpB are completely protected during a lethal challenge with LVS. |
| 1507 | 25250027 | Furthermore, the kinetics and magnitude of the primary T-cell response in B6 and TLR2 KO mice are similar indicating that TLR2 signaling is dispensable for the adaptive immune response to LVS clpB. |
| 1508 | 25250027 | TLR2 signaling was important, however, for the innate immune response to LVS clpB. |
| 1509 | 25250027 | IL-1α, IL-1β, IL-2, IL-17, MIP-1α, and TNF-α production depended on TLR2 signaling, while GM-CSF, IFN-γ, and VEGF production were completely independent of TLR2 signaling. |
| 1510 | 25250027 | IL-6, IL-12, IP-10, KC, and MIG production were partially dependent on TLR2 signaling. |
| 1511 | 25250027 | Together our data indicate that the innate immune response to LVS clpB requires TLR2 signaling for the maximal innate response, whereas TLR2 is not required for the adaptive immune response. |
| 1512 | 25250027 | TLR2 Signaling is Required for the Innate, but Not Adaptive Response to LVS clpB. |
| 1513 | 25250027 | We sought to determine whether TLR2 signaling was required during the immune response to LVS clpB. |
| 1514 | 25250027 | TLR2 knock-out (TLR2 KO) mice previously infected with LVS clpB are completely protected during a lethal challenge with LVS. |
| 1515 | 25250027 | Furthermore, the kinetics and magnitude of the primary T-cell response in B6 and TLR2 KO mice are similar indicating that TLR2 signaling is dispensable for the adaptive immune response to LVS clpB. |
| 1516 | 25250027 | TLR2 signaling was important, however, for the innate immune response to LVS clpB. |
| 1517 | 25250027 | IL-1α, IL-1β, IL-2, IL-17, MIP-1α, and TNF-α production depended on TLR2 signaling, while GM-CSF, IFN-γ, and VEGF production were completely independent of TLR2 signaling. |
| 1518 | 25250027 | IL-6, IL-12, IP-10, KC, and MIG production were partially dependent on TLR2 signaling. |
| 1519 | 25250027 | Together our data indicate that the innate immune response to LVS clpB requires TLR2 signaling for the maximal innate response, whereas TLR2 is not required for the adaptive immune response. |
| 1520 | 25250027 | TLR2 Signaling is Required for the Innate, but Not Adaptive Response to LVS clpB. |
| 1521 | 25250027 | We sought to determine whether TLR2 signaling was required during the immune response to LVS clpB. |
| 1522 | 25250027 | TLR2 knock-out (TLR2 KO) mice previously infected with LVS clpB are completely protected during a lethal challenge with LVS. |
| 1523 | 25250027 | Furthermore, the kinetics and magnitude of the primary T-cell response in B6 and TLR2 KO mice are similar indicating that TLR2 signaling is dispensable for the adaptive immune response to LVS clpB. |
| 1524 | 25250027 | TLR2 signaling was important, however, for the innate immune response to LVS clpB. |
| 1525 | 25250027 | IL-1α, IL-1β, IL-2, IL-17, MIP-1α, and TNF-α production depended on TLR2 signaling, while GM-CSF, IFN-γ, and VEGF production were completely independent of TLR2 signaling. |
| 1526 | 25250027 | IL-6, IL-12, IP-10, KC, and MIG production were partially dependent on TLR2 signaling. |
| 1527 | 25250027 | Together our data indicate that the innate immune response to LVS clpB requires TLR2 signaling for the maximal innate response, whereas TLR2 is not required for the adaptive immune response. |
| 1528 | 25250027 | TLR2 Signaling is Required for the Innate, but Not Adaptive Response to LVS clpB. |
| 1529 | 25250027 | We sought to determine whether TLR2 signaling was required during the immune response to LVS clpB. |
| 1530 | 25250027 | TLR2 knock-out (TLR2 KO) mice previously infected with LVS clpB are completely protected during a lethal challenge with LVS. |
| 1531 | 25250027 | Furthermore, the kinetics and magnitude of the primary T-cell response in B6 and TLR2 KO mice are similar indicating that TLR2 signaling is dispensable for the adaptive immune response to LVS clpB. |
| 1532 | 25250027 | TLR2 signaling was important, however, for the innate immune response to LVS clpB. |
| 1533 | 25250027 | IL-1α, IL-1β, IL-2, IL-17, MIP-1α, and TNF-α production depended on TLR2 signaling, while GM-CSF, IFN-γ, and VEGF production were completely independent of TLR2 signaling. |
| 1534 | 25250027 | IL-6, IL-12, IP-10, KC, and MIG production were partially dependent on TLR2 signaling. |
| 1535 | 25250027 | Together our data indicate that the innate immune response to LVS clpB requires TLR2 signaling for the maximal innate response, whereas TLR2 is not required for the adaptive immune response. |
| 1536 | 25250027 | TLR2 Signaling is Required for the Innate, but Not Adaptive Response to LVS clpB. |
| 1537 | 25250027 | We sought to determine whether TLR2 signaling was required during the immune response to LVS clpB. |
| 1538 | 25250027 | TLR2 knock-out (TLR2 KO) mice previously infected with LVS clpB are completely protected during a lethal challenge with LVS. |
| 1539 | 25250027 | Furthermore, the kinetics and magnitude of the primary T-cell response in B6 and TLR2 KO mice are similar indicating that TLR2 signaling is dispensable for the adaptive immune response to LVS clpB. |
| 1540 | 25250027 | TLR2 signaling was important, however, for the innate immune response to LVS clpB. |
| 1541 | 25250027 | IL-1α, IL-1β, IL-2, IL-17, MIP-1α, and TNF-α production depended on TLR2 signaling, while GM-CSF, IFN-γ, and VEGF production were completely independent of TLR2 signaling. |
| 1542 | 25250027 | IL-6, IL-12, IP-10, KC, and MIG production were partially dependent on TLR2 signaling. |
| 1543 | 25250027 | Together our data indicate that the innate immune response to LVS clpB requires TLR2 signaling for the maximal innate response, whereas TLR2 is not required for the adaptive immune response. |
| 1544 | 25286253 | We show that OmpA of S. flexneri 2a activates B cells to produce protective cytokines, IL-6 and IL-10 as well as facilitates their differentiation into antibody secreting cells (ASCs). |
| 1545 | 25286253 | We also report here that B cell activation by OmpA is mediated strictly through recognition by TLR2, resulting in initiation of cascades of signal transduction events, involving increased phosphorylation of protein tyrosine kinases (PTKs), ERK and IκBα, leading to nuclear translocation of NF-κB. |
| 1546 | 25312698 | Among the TLR family, TLR1, TLR2, TLR4, and TLR9 and their down-stream signaling proteins play critical roles in the initiation of the immune response in the pathogenesis of TB. |
| 1547 | 25312698 | The inflammasome pathway is associated with the coordinated release of cytokines such as IL-1β and IL-18 which also play a role in the pathogenesis of TB. |
| 1548 | 25348634 | Although incubation with high concentrations of these 3 strains resulted in significant activation of the MM6 cells, it was found to occur mainly through interaction with TLR2 and not through TLR4. |
| 1549 | 25353353 | Native FHA was found to strongly stimulate TLR2, but not TLR4 or TLR5 transfected cells. |
| 1550 | 25392526 | Cutting edge: New chimeric NOD2/TLR2 adjuvant drastically increases vaccine immunogenicity. |
| 1551 | 25392526 | In this study, we evaluated a new ligand that targets both TLR2 and NOD2 receptors. |
| 1552 | 25392526 | The chimeric NOD2/TLR2 ligand induced synergistic upregulation of dendritic cell maturation markers, costimulatory molecules, and secretion of proinflammatory cytokines compared with combinations of separate ligands. |
| 1553 | 25392526 | Cutting edge: New chimeric NOD2/TLR2 adjuvant drastically increases vaccine immunogenicity. |
| 1554 | 25392526 | In this study, we evaluated a new ligand that targets both TLR2 and NOD2 receptors. |
| 1555 | 25392526 | The chimeric NOD2/TLR2 ligand induced synergistic upregulation of dendritic cell maturation markers, costimulatory molecules, and secretion of proinflammatory cytokines compared with combinations of separate ligands. |
| 1556 | 25392526 | Cutting edge: New chimeric NOD2/TLR2 adjuvant drastically increases vaccine immunogenicity. |
| 1557 | 25392526 | In this study, we evaluated a new ligand that targets both TLR2 and NOD2 receptors. |
| 1558 | 25392526 | The chimeric NOD2/TLR2 ligand induced synergistic upregulation of dendritic cell maturation markers, costimulatory molecules, and secretion of proinflammatory cytokines compared with combinations of separate ligands. |
| 1559 | 25401327 | We hypothesized that the initial inflammatory events are initiated upon ligation of mycoplasma lipid associated membrane proteins (LAMP) to TLRs expressed on chicken tracheal epithelial cells (TEC). |
| 1560 | 25401327 | To test this hypothesis, live bacteria or LAMPs isolated from a virulent (R(low)) or a non-virulent (R(high)) strain were incubated with primary TECs or chicken tracheae ex vivo. |
| 1561 | 25401327 | Among the commonly up-regulated genes were IL-1β, IL-6, IL-8, IL-12p40, CCL-20, and NOS-2, all of which are important immune-modulators and/or chemo-attractants of leukocytes. |
| 1562 | 25401327 | Upon addition of a TLR-2 inhibitor, LAMP-mediated gene expression of IL-1β and CCL-20 was reduced by almost 5-fold while expression of IL-12p40, IL-6, IL-8 and NOS-2 mRNA was reduced by about 2-3 fold. |
| 1563 | 25401327 | Taken together we conclude that LAMPs isolated from both R(high) and R(low) induced rapid, TLR-2 dependent but transient up-regulation of inflammatory genes in primary TECs through an NF-κB dependent pathway. |
| 1564 | 25466255 | Activation of toll-like receptor-2 by endogenous matrix metalloproteinase-2 modulates dendritic-cell-mediated inflammatory responses. |
| 1565 | 25466255 | Significantly, MMP-2 polarizes T cells toward type 2 responses in vivo, in a TLR2-dependent manner. |
| 1566 | 25466255 | Activation of toll-like receptor-2 by endogenous matrix metalloproteinase-2 modulates dendritic-cell-mediated inflammatory responses. |
| 1567 | 25466255 | Significantly, MMP-2 polarizes T cells toward type 2 responses in vivo, in a TLR2-dependent manner. |
| 1568 | 25510899 | The ability of PSK to activate dendritic cells and T cells is dependent on its ability to stimulate Toll-like receptor 2 (TLR2), yet it remains unknown which structural component within PSK activates TLR2. |
| 1569 | 25510899 | The purpose of this study was to identify the TLR2 agonist within PSK and understand its role in the overall mechanism of PSK's immunogenic activity. |
| 1570 | 25510899 | TLR2 activity was eliminated by treatment with lipoprotein lipase but not by trypsin or lyticase. |
| 1571 | 25510899 | Rapid centrifugation of PSK can separate the fraction with TLR2 agonist activity from the soluble β-glucan fraction. |
| 1572 | 25510899 | Altogether, these results present evidence that PSK has two active components-the well-characterized protein-bound β-glucan and a previously unreported lipid-which work synergistically via the Dectin-1 and TLR2 receptors. |
| 1573 | 25510899 | The ability of PSK to activate dendritic cells and T cells is dependent on its ability to stimulate Toll-like receptor 2 (TLR2), yet it remains unknown which structural component within PSK activates TLR2. |
| 1574 | 25510899 | The purpose of this study was to identify the TLR2 agonist within PSK and understand its role in the overall mechanism of PSK's immunogenic activity. |
| 1575 | 25510899 | TLR2 activity was eliminated by treatment with lipoprotein lipase but not by trypsin or lyticase. |
| 1576 | 25510899 | Rapid centrifugation of PSK can separate the fraction with TLR2 agonist activity from the soluble β-glucan fraction. |
| 1577 | 25510899 | Altogether, these results present evidence that PSK has two active components-the well-characterized protein-bound β-glucan and a previously unreported lipid-which work synergistically via the Dectin-1 and TLR2 receptors. |
| 1578 | 25510899 | The ability of PSK to activate dendritic cells and T cells is dependent on its ability to stimulate Toll-like receptor 2 (TLR2), yet it remains unknown which structural component within PSK activates TLR2. |
| 1579 | 25510899 | The purpose of this study was to identify the TLR2 agonist within PSK and understand its role in the overall mechanism of PSK's immunogenic activity. |
| 1580 | 25510899 | TLR2 activity was eliminated by treatment with lipoprotein lipase but not by trypsin or lyticase. |
| 1581 | 25510899 | Rapid centrifugation of PSK can separate the fraction with TLR2 agonist activity from the soluble β-glucan fraction. |
| 1582 | 25510899 | Altogether, these results present evidence that PSK has two active components-the well-characterized protein-bound β-glucan and a previously unreported lipid-which work synergistically via the Dectin-1 and TLR2 receptors. |
| 1583 | 25510899 | The ability of PSK to activate dendritic cells and T cells is dependent on its ability to stimulate Toll-like receptor 2 (TLR2), yet it remains unknown which structural component within PSK activates TLR2. |
| 1584 | 25510899 | The purpose of this study was to identify the TLR2 agonist within PSK and understand its role in the overall mechanism of PSK's immunogenic activity. |
| 1585 | 25510899 | TLR2 activity was eliminated by treatment with lipoprotein lipase but not by trypsin or lyticase. |
| 1586 | 25510899 | Rapid centrifugation of PSK can separate the fraction with TLR2 agonist activity from the soluble β-glucan fraction. |
| 1587 | 25510899 | Altogether, these results present evidence that PSK has two active components-the well-characterized protein-bound β-glucan and a previously unreported lipid-which work synergistically via the Dectin-1 and TLR2 receptors. |
| 1588 | 25510899 | The ability of PSK to activate dendritic cells and T cells is dependent on its ability to stimulate Toll-like receptor 2 (TLR2), yet it remains unknown which structural component within PSK activates TLR2. |
| 1589 | 25510899 | The purpose of this study was to identify the TLR2 agonist within PSK and understand its role in the overall mechanism of PSK's immunogenic activity. |
| 1590 | 25510899 | TLR2 activity was eliminated by treatment with lipoprotein lipase but not by trypsin or lyticase. |
| 1591 | 25510899 | Rapid centrifugation of PSK can separate the fraction with TLR2 agonist activity from the soluble β-glucan fraction. |
| 1592 | 25510899 | Altogether, these results present evidence that PSK has two active components-the well-characterized protein-bound β-glucan and a previously unreported lipid-which work synergistically via the Dectin-1 and TLR2 receptors. |
| 1593 | 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. |
| 1594 | 25610736 | Aiming to increase the potency of synthetic long peptide (SLP)-based cancer vaccines, the Toll-like receptor 2 (TLR2) ligand Pam3CSK4 was conjugated in a chemically defined fashion to SLPs harbouring both cytotoxic T lymphocyte (CTL) and T helper epitopes. |
| 1595 | 25658110 | Although, Ara-LAM modulates TLR2 and MAPK signaling, it is not known whether Ara-LAM involves IFN-γ signaling for effective parasite clearance. |
| 1596 | 25658110 | Moreover, Ara-LAM reciprocally modulates IRF4 and IRF8 expression and reinstates anti-leishmanial Th1 response that eventuates in significantly reduced parasite load in spleen and liver of L. donovani-infected BALB/c mice. |
| 1597 | 25697665 | While Braun lipoprotein (Lpp) activates toll-like receptor-2 to initiate an inflammatory cascade, plasminogen activator (Pla) protease facilitates bacterial dissemination in the host. |
| 1598 | 25697665 | Importantly, the ability of the Δlpp Δpla double mutant to be phagocytized by macrophages, to stimulate production of tumor necrosis factor-α and interleukin-6, and to activate the nitric oxide killing pathways of the host cells remained unaltered when compared to the WT CO92-infected macrophages. |
| 1599 | 25723174 | Furthermore, we demonstrated that TLR2 and TLR4 are required for the stimulatory activity of AC hmwPSs on DCs. |
| 1600 | 25723174 | Thus, we conclude that hmwPSs are the major components of AC that stimulate DCs via the TLR2/TLR4 and NF-κB/MAPK signaling pathways. |
| 1601 | 25723174 | Furthermore, we demonstrated that TLR2 and TLR4 are required for the stimulatory activity of AC hmwPSs on DCs. |
| 1602 | 25723174 | Thus, we conclude that hmwPSs are the major components of AC that stimulate DCs via the TLR2/TLR4 and NF-κB/MAPK signaling pathways. |
| 1603 | 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. |
| 1604 | 25805409 | The Shimen strain infection resulted in a significant activation of IFN regulatory factor IRF7 and suppression of IRF3. |
| 1605 | 25934108 | Moreover, CVPS increased the expression of IL-2, IFN-γ, and IL-4 in CD4(+) T cells and IFN-γ expression in CD8(+) T cells. |
| 1606 | 25934108 | Additionally, CVPS enhanced CD40(+), CD80(+), and CD86(+) expression on DCs. |
| 1607 | 25934108 | In contrast, CVPS downregulated TGF-β mRNA expression and the frequency of CD4(+)CD25(+)Foxp3(+) Treg cells. |
| 1608 | 25934108 | Taken together, these results indicate that administering CVPS as an adjuvant enhances both cellular and humoral immune responses via the TLR-2 and TLR-4 signalling pathways, thereby promoting DC maturation and suppressing TGF-β expression and Treg frequency. |
| 1609 | 25955717 | Human Cytomegalovirus miR-UL112-3p Targets TLR2 and Modulates the TLR2/IRAK1/NFκB Signaling Pathway. |
| 1610 | 25955717 | Consistent with this observation, miR-UL112-3p transfection significantly reduced the expression of multiple cytokines (IL-1β, IL-6 and IL-8) upon stimulation with a TLR2 agonist. |
| 1611 | 25955717 | Finally, miR-UL112-3p transfection significantly inhibited the TLR2-induced post-translational activation of IRAK1, a kinase located in the upstream section of the TLR2/NFκB signaling axis. |
| 1612 | 25955717 | Human Cytomegalovirus miR-UL112-3p Targets TLR2 and Modulates the TLR2/IRAK1/NFκB Signaling Pathway. |
| 1613 | 25955717 | Consistent with this observation, miR-UL112-3p transfection significantly reduced the expression of multiple cytokines (IL-1β, IL-6 and IL-8) upon stimulation with a TLR2 agonist. |
| 1614 | 25955717 | Finally, miR-UL112-3p transfection significantly inhibited the TLR2-induced post-translational activation of IRAK1, a kinase located in the upstream section of the TLR2/NFκB signaling axis. |
| 1615 | 25955717 | Human Cytomegalovirus miR-UL112-3p Targets TLR2 and Modulates the TLR2/IRAK1/NFκB Signaling Pathway. |
| 1616 | 25955717 | Consistent with this observation, miR-UL112-3p transfection significantly reduced the expression of multiple cytokines (IL-1β, IL-6 and IL-8) upon stimulation with a TLR2 agonist. |
| 1617 | 25955717 | Finally, miR-UL112-3p transfection significantly inhibited the TLR2-induced post-translational activation of IRAK1, a kinase located in the upstream section of the TLR2/NFκB signaling axis. |
| 1618 | 26041040 | Here we investigated the roles of TLR2 and lipidation of proteins in WCV-induced interleukin-17A (IL-17A) responses and protection against NP carriage. |
| 1619 | 26041040 | Immunization of Tlr2(-/-) mice with WCV conferred significantly lower IL-17A levels and reduced protection against NP carriage, compared to wild-type (WT) mice, suggesting that host TLR2 engagement is required for effective immunity and protection elicited by WCV immunization. |
| 1620 | 26041040 | Here we investigated the roles of TLR2 and lipidation of proteins in WCV-induced interleukin-17A (IL-17A) responses and protection against NP carriage. |
| 1621 | 26041040 | Immunization of Tlr2(-/-) mice with WCV conferred significantly lower IL-17A levels and reduced protection against NP carriage, compared to wild-type (WT) mice, suggesting that host TLR2 engagement is required for effective immunity and protection elicited by WCV immunization. |
| 1622 | 26078314 | Unlike typical Gram-negative bacteria stimulating TLR2 and TLR4, KVC activated TLR2 but hardly TLR4. |
| 1623 | 26101787 | By binding to both TLR1 and TLR2, CU-T12-9 facilitates the TLR1/2 heterodimeric complex formation, which in turn activates the downstream signaling. |
| 1624 | 26101787 | Fluorescence anisotropy assays revealed competitive binding to the TLR1/2 complex between CU-T12-9 and Pam3CSK4 with a half-maximal inhibitory concentration (IC50) of 54.4 nM. |
| 1625 | 26101787 | Finally, we showed that CU-T12-9 signals through nuclear factor κB (NF-κB) and invokes an elevation of the downstream effectors tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), and inducible nitric oxide synthase (iNOS). |
| 1626 | 26141411 | ECTV interfered with p65 NF-κB nuclear translocation induced by TLR ligands such as lipopolysaccharide (LPS) (TLR4), polyinosinic-polycytidylic acid (poly(I:C)) (TLR3) and diacylated lipopeptide Pam2CSK4 (TLR2/6). |
| 1627 | 26148331 | We observed that at d 3-4 post vaccination, 6 genes were down-regulated, namely APC, CD3G, FASLG, IL7, CD8A and TLR1. |
| 1628 | 26148331 | Meanwhile at 6-7 days post vaccination, 9 genes were significantly up-regulated, including RIPK2, TGFB1, MICB, SOCS1, IL2RA, MS4A1, PTPRC, IL2 and IL8. |
| 1629 | 26148331 | By days 12-15 the genes RIPK2, IL4, IL12B and TLR2 were overexpressed. |
| 1630 | 26174952 | Here, we show porin differentially regulated splenic marginal zone (MZ) and follicular zone (FO) B cell responses in contrast to other classical TLR2-ligands FSL-1 and Pam3CSK4. |
| 1631 | 26174952 | The protein up-regulated TLR2 and TLR6 and stimulated the activation and costimulatory molecules on FO B cells skewing the cells toward TLR-dependent type-1 cytokine response. |
| 1632 | 26174952 | These cells responded to porin by expressing toll-interacting protein (TOLLIP), the TLR2 and -4 signaling inhibitor along with stimulation of the intracellular pathogen recognition receptor NLR caspase recruitment domain containing protein 5 (NLRC5). |
| 1633 | 26174952 | The CD1d(hi) MZ B cells released IL-10 unequivocally demonstrating regulatory B cell feature. |
| 1634 | 26174952 | Immunization with porin also resulted in transient IL-10 expression by the CD19(+)CD21(hi) B cells prior to plasma cell formation. |
| 1635 | 26174952 | Here, we show porin differentially regulated splenic marginal zone (MZ) and follicular zone (FO) B cell responses in contrast to other classical TLR2-ligands FSL-1 and Pam3CSK4. |
| 1636 | 26174952 | The protein up-regulated TLR2 and TLR6 and stimulated the activation and costimulatory molecules on FO B cells skewing the cells toward TLR-dependent type-1 cytokine response. |
| 1637 | 26174952 | These cells responded to porin by expressing toll-interacting protein (TOLLIP), the TLR2 and -4 signaling inhibitor along with stimulation of the intracellular pathogen recognition receptor NLR caspase recruitment domain containing protein 5 (NLRC5). |
| 1638 | 26174952 | The CD1d(hi) MZ B cells released IL-10 unequivocally demonstrating regulatory B cell feature. |
| 1639 | 26174952 | Immunization with porin also resulted in transient IL-10 expression by the CD19(+)CD21(hi) B cells prior to plasma cell formation. |
| 1640 | 26174952 | Here, we show porin differentially regulated splenic marginal zone (MZ) and follicular zone (FO) B cell responses in contrast to other classical TLR2-ligands FSL-1 and Pam3CSK4. |
| 1641 | 26174952 | The protein up-regulated TLR2 and TLR6 and stimulated the activation and costimulatory molecules on FO B cells skewing the cells toward TLR-dependent type-1 cytokine response. |
| 1642 | 26174952 | These cells responded to porin by expressing toll-interacting protein (TOLLIP), the TLR2 and -4 signaling inhibitor along with stimulation of the intracellular pathogen recognition receptor NLR caspase recruitment domain containing protein 5 (NLRC5). |
| 1643 | 26174952 | The CD1d(hi) MZ B cells released IL-10 unequivocally demonstrating regulatory B cell feature. |
| 1644 | 26174952 | Immunization with porin also resulted in transient IL-10 expression by the CD19(+)CD21(hi) B cells prior to plasma cell formation. |
| 1645 | 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. |
| 1646 | 26182986 | Stimulation of the mononuclear cells with agonists to these TLRs increased the expression of downstream TLR signaling products (IL1α, IL6, IL12A and IFNβ). |
| 1647 | 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. |
| 1648 | 26188153 | TLR2, TLR4, TLR7 and NLRP3-inflammasome signaling were not required for induction of this inflammatory response. |
| 1649 | 26188153 | In addition, Coa-ASC16 revealed an intrinsic adjuvant activity which was affected by MyD88 and IL-6 absence. |
| 1650 | 26214513 | Characterization of mechanisms involved in PspA induced expression of PD-L1 indicate the involvement of Toll-Like Receptor 2 (TLR2) and calcium homeostasis. |
| 1651 | 26214513 | Increase in PD-L1 expression, when costimulated with PspA and through TLR2 was higher than when stimulated with PspA or through TLR2. |
| 1652 | 26214513 | Further, knockdown of TLR2 and the intermediates in the TLR signaling machinery pointed towards the involvement of a MyD88 dependent pathway in PspA induced PD-L1 expression. |
| 1653 | 26214513 | Characterization of mechanisms involved in PspA induced expression of PD-L1 indicate the involvement of Toll-Like Receptor 2 (TLR2) and calcium homeostasis. |
| 1654 | 26214513 | Increase in PD-L1 expression, when costimulated with PspA and through TLR2 was higher than when stimulated with PspA or through TLR2. |
| 1655 | 26214513 | Further, knockdown of TLR2 and the intermediates in the TLR signaling machinery pointed towards the involvement of a MyD88 dependent pathway in PspA induced PD-L1 expression. |
| 1656 | 26214513 | Characterization of mechanisms involved in PspA induced expression of PD-L1 indicate the involvement of Toll-Like Receptor 2 (TLR2) and calcium homeostasis. |
| 1657 | 26214513 | Increase in PD-L1 expression, when costimulated with PspA and through TLR2 was higher than when stimulated with PspA or through TLR2. |
| 1658 | 26214513 | Further, knockdown of TLR2 and the intermediates in the TLR signaling machinery pointed towards the involvement of a MyD88 dependent pathway in PspA induced PD-L1 expression. |
| 1659 | 26277072 | Immunization of rabbits with a single TM yeast glycoprotein (Gp38 or Pst1), when conjugated to a promiscuous T-cell epitope peptide and coadministered with a Toll-like receptor 2 agonist, induced glycan-specific HIV-1 Env cross-reactive antibodies. |
| 1660 | 26286603 | We assayed the activation ex vivo and the responsiveness to TLR2 and TLR4 agonists in vitro in the three subsets and assessed the intracellular production of IL1-alpha (α), IL1-beta (β), IL-6, IL-8, TNF-α, and IL-10 of elderly adults (median 83 [67-90] years old;n= 20) compared with young controls (median 35 [27-40] years old;n= 20). |
| 1661 | 26286603 | Ex vivo, the elderly adults showed a higher percentage of classical monocytes that expressed intracellular IL1-α (p= .001), IL1-β (p= .001), IL-6 (p= .002), and IL-8 (p= .007). |
| 1662 | 26303218 | We have recently reported that Vi can generate inflammatory responses through activation of the TLR2/TLR1 complex. |
| 1663 | 26339315 | One mechanism employed by monocytes for sensing foreign antigens is via toll-like receptors (TLRs)-transmembrane proteins that distinguish classes of foreign pathogens, for example, bacteria (TLR4, 5, and 9) vs. fungi (TLR2) vs. viruses (TLR3, 7, and 8). |
| 1664 | 26339315 | Three cytokines, tumor necrosis factor-α, interleukin (IL)-6, and IL-10, were detected using anti-cytokine antibody arrays integrated into each of the six chambers. |
| 1665 | 26347747 | HIV-1 Structural Proteins Serve as PAMPs for TLR2 Heterodimers Significantly Increasing Infection and Innate Immune Activation. |
| 1666 | 26347747 | Importantly, we show that HIV-1 structural proteins, p17, p24, and gp41, act as viral PAMPs signaling through TLR2 and its heterodimers leading to significantly increased immune activation via the NFκB signaling pathway. |
| 1667 | 26347747 | Using co-immunoprecipitation and a dot blot method, we demonstrated direct protein interactions between these viral PAMPs and TLR2, while only p17 and gp41 bound to TLR1. |
| 1668 | 26347747 | Specifically, TLR2/1 heterodimer recognized p17 and gp41, while p24 lead to immune activation through TLR2/6. |
| 1669 | 26347747 | Interestingly, our results show in the absence of TLR6, p24 bound to TLR2 and blocked p17 and gp41-induced activation, thus providing a novel mechanism by which HIV-1 can manipulate innate sensing. |
| 1670 | 26347747 | HIV-1 Structural Proteins Serve as PAMPs for TLR2 Heterodimers Significantly Increasing Infection and Innate Immune Activation. |
| 1671 | 26347747 | Importantly, we show that HIV-1 structural proteins, p17, p24, and gp41, act as viral PAMPs signaling through TLR2 and its heterodimers leading to significantly increased immune activation via the NFκB signaling pathway. |
| 1672 | 26347747 | Using co-immunoprecipitation and a dot blot method, we demonstrated direct protein interactions between these viral PAMPs and TLR2, while only p17 and gp41 bound to TLR1. |
| 1673 | 26347747 | Specifically, TLR2/1 heterodimer recognized p17 and gp41, while p24 lead to immune activation through TLR2/6. |
| 1674 | 26347747 | Interestingly, our results show in the absence of TLR6, p24 bound to TLR2 and blocked p17 and gp41-induced activation, thus providing a novel mechanism by which HIV-1 can manipulate innate sensing. |
| 1675 | 26367276 | We previously demonstrated that vaccine-induced IL-17A+ CD8+ T cells (Tc17) are required for resistance against lethal fungal pneumonia in CD4+ T cell-deficient hosts, whereas the individual type I cytokines IFN-γ, TNF-α and GM-CSF, are dispensable. |
| 1676 | 26367276 | The poor accumulation of MyD88-deficient Tc17 cells was not linked to an early onset of contraction, nor to accelerated cell death or diminished expression of anti-apoptotic molecules Bcl-2 or Bcl-xL. |
| 1677 | 26367276 | Moreover, intrinsic IL-1R and TLR2, but not IL-18R, were required for MyD88 dependent Tc17 responses. |
| 1678 | 26391398 | Ac2PIM-responsive miR-150 and miR-143 target receptor-interacting protein kinase 2 and transforming growth factor beta-activated kinase 1 to suppress NOD2-induced immunomodulators. |
| 1679 | 26391398 | While Ac2PIM treatment of macrophages compromised their ability to induce NOD2-dependent immunomodulators like cyclooxygenase (COX)-2, suppressor of cytokine signaling (SOCS)-3, and matrix metalloproteinase (MMP)-9, no change in the NOD2-responsive NO, TNF-α, VEGF-A, and IL-12 levels was observed. |
| 1680 | 26391398 | Further, genome-wide microRNA expression profiling identified Ac2PIM-responsive miR-150 and miR-143 to target NOD2 signaling adaptors, RIP2 and TAK1, respectively. |
| 1681 | 26391398 | Interestingly, Ac2PIM was found to activate the SRC-FAK-PYK2-CREB cascade via TLR2 to recruit CBP/P300 at the promoters of miR-150 and miR-143 and epigenetically induce their expression. |
| 1682 | 26391398 | Loss-of-function studies utilizing specific miRNA inhibitors establish that Ac2PIM, via the miRNAs, abrogate NOD2-induced PI3K-PKCδ-MAPK pathway to suppress β-catenin-mediated expression of COX-2, SOCS-3, and MMP-9. |
| 1683 | 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. |
| 1684 | 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. |
| 1685 | 26395101 | In contrast, TLR2 and TLR3 are similarly expressed in both human and mouse Ag-presenting DCs. |
| 1686 | 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. |
| 1687 | 26395101 | We herein summarize the history and perspectives of TLR2 and TLR3 agonists in vaccine-adjuvant immunotherapy for cancer. |
| 1688 | 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. |
| 1689 | 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. |
| 1690 | 26395101 | In contrast, TLR2 and TLR3 are similarly expressed in both human and mouse Ag-presenting DCs. |
| 1691 | 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. |
| 1692 | 26395101 | We herein summarize the history and perspectives of TLR2 and TLR3 agonists in vaccine-adjuvant immunotherapy for cancer. |
| 1693 | 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. |
| 1694 | 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. |
| 1695 | 26395101 | In contrast, TLR2 and TLR3 are similarly expressed in both human and mouse Ag-presenting DCs. |
| 1696 | 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. |
| 1697 | 26395101 | We herein summarize the history and perspectives of TLR2 and TLR3 agonists in vaccine-adjuvant immunotherapy for cancer. |
| 1698 | 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. |
| 1699 | 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. |
| 1700 | 26395101 | In contrast, TLR2 and TLR3 are similarly expressed in both human and mouse Ag-presenting DCs. |
| 1701 | 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. |
| 1702 | 26395101 | We herein summarize the history and perspectives of TLR2 and TLR3 agonists in vaccine-adjuvant immunotherapy for cancer. |
| 1703 | 26431338 | However, microarray and qPCR validation results did not highlight pro-inflammatory molecules (such as TNFα, TLR2, IL-12B and IL-6), whereas inflammation is one of the most characteristic traits of acute CBPP. |