The Experts below are selected from a list of 71766 Experts worldwide ranked by ideXlab platform
Shizuo Akira - One of the best experts on this subject based on the ideXlab platform.
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antiviral protein viperin promotes Toll Like Receptor 7 and Toll Like Receptor 9 mediated type i interferon production in plasmacytoid dendritic cells
Immunity, 2011Co-Authors: Tatsuya Saitoh, Satoshi Uematsu, Osamu Takeuchi, Taro Kawai, Takashi Satoh, Naoki Yamamoto, Shizuo AkiraAbstract:Toll-Like Receptor 7 (TLR7) and TLR9 sense viral nucleic acids and induce production of type I interferon (IFN) by plasmacytoid dendritic cells (pDCs) to protect the host from virus infection. We showed that the IFN-inducible antiviral protein Viperin promoted TLR7- and TLR9-mediated production of type I IFN by pDCs. Viperin expression was potently induced after TLR7 or TLR9 stimulation and Viperin localized to the cytoplasmic lipid-enriched compartments, lipid bodies, in pDCs. Viperin interacted with the signal mediators IRAK1 and TRAF6 to recruit them to the lipid bodies and facilitated K63-linked ubiquitination of IRAK1 to induce the nuclear translocation of transcription factor IRF7. Loss of Viperin reduced TLR7- and TLR9-mediated production of type I IFN by pDCs. However, Viperin was dispensable for the production of type I IFN induced by intracellular nucleic acids. Thus, Viperin mediates its antiviral function via the regulation of the TLR7 and TLR9-IRAK1 signaling axis in pDCs.
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regulation of lipopolysaccharide induced translation of tumor necrosis factor alpha by the Toll Like Receptor 4 adaptor protein tram
Journal of Innate Immunity, 2011Co-Authors: Lijian Wang, Shizuo Akira, Katherine A Fitzgerald, Estela Trebicka, Lisa Waggoner, Jonathan C Kagan, Bobby J CherayilAbstract:Lipopolysaccharide (LPS)-induced production of tumor necrosis factor (TNF)-α requires the recruitment of two pairs of adaptors to the Toll-Like Receptor 4 cytoplasmic domain. The contribution of one p
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salmonella induced sipb independent cell death requires Toll Like Receptor 4 signalling via the adapter proteins tram and trif
Immunology, 2007Co-Authors: Pamela Cook, Masahiro Yamamoto, Shizuo Akira, Katherine A Fitzgerald, Sabine Totemeyer, Catherine Stevenson, Duncan J Maskell, Clare E BryantAbstract:Salmonella enterica serovar typhimurium (S. typhimurium) is an intracellular pathogen that causes macrophage cell death by at least two different mechanisms. Rapid cell death is dependent on the Salmonella pathogenicity island-1 protein SipB whereas delayed cell death is independent of SipB and occurs 18-24 hr post infection. Lipopolysaccharide (LPS) is essential for the delayed cell death. LPS is the main structural component of the outer membrane of Gram-negative bacteria and is recognized by Toll-Like Receptor 4, signalling via the adapter proteins Mal, MyD88, Tram and Trif. Here we show that S. typhimurium induces SipB-independent cell death through Toll-Like Receptor 4 signalling via the adapter proteins Tram and Trif. In contrast to wild type bone marrow derived macrophages (BMDM), Tram(-/-) and Trif(-/-) BMDM proliferate in response to Salmonella infection.
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a critical role of Toll Like Receptor 2 in nerve injury induced spinal cord glial cell activation and pain hypersensitivity
Journal of Biological Chemistry, 2007Co-Authors: Donghoon Kim, Seyoung Choi, Kyungpyo Park, Shizuo Akira, Myung Ah Kim, Ikhyun Cho, Misun Kim, Soojin Lee, Joong Soo Kim, Sung Joong LeeAbstract:The activation of spinal cord glial cells has been implicated in the development of neuropathic pain upon peripheral nerve injury. The molecular mechanisms underlying glial cell activation, however, have not been clearly elucidated. In this study, we found that damaged sensory neurons induce the expression of tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, and inducible nitric-oxide synthase genes in spinal cord glial cells, which is implicated in the development of neuropathic pain. Studies using primary glial cells isolated from Toll-Like Receptor 2 knock-out mice indicate that damaged sensory neurons activate glial cells via Toll-Like Receptor 2. In addition, behavioral studies using Toll-Like Receptor 2 knock-out mice demonstrate that the expression of Toll-Like Receptor 2 is required for the induction of mechanical allodynia and thermal hyperalgesia due to spinal nerve axotomy. The nerve injury-induced spinal cord microglia and astrocyte activation is reduced in the Toll-Like Receptor 2 knock-out mice. Similarly, the nerve injury-induced pro-inflammatory gene expression in the spinal cord is also reduced in the Toll-Like Receptor 2 knock-out mice. These data demonstrate that Toll-Like Receptor 2 contributes to the nerve injury-induced spinal cord glial cell activation and subsequent pain hypersensitivity.
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Toll-Like Receptor-mediated regulation of zinc homeostasis influences dendritic cell function.
Nature immunology, 2006Co-Authors: Hidemitsu Kitamura, Shizuo Akira, Tsuneyasu Kaisho, Hideyuki Morikawa, Hokuto Kamon, Megumi Iguchi, Shintaro Hojyo, Toshiyuki Fukada, Susumu Yamashita, Masaaki MurakamiAbstract:Zinc is a trace element that is essential for the function of many enzymes and transcription factors. Zinc deficiency results in defects in innate and acquired immune responses. However, little is known about the mechanism(s) by which zinc affects immune cell function. Here we show that stimulation with the Toll-Like Receptor 4 agonist lipopolysaccharide (LPS) altered the expression of zinc transporters in dendritic cells and thereby decreased intracellular free zinc. A zinc chelator mimicked the effects of LPS, whereas zinc supplementation or overexpression of the gene encoding Zip6, a zinc transporter whose expression was reduced by LPS, inhibited LPS-induced upregulation of major histocompatibility complex class II and costimulatory molecules. These results establish a link between Toll-Like Receptor signaling and zinc homeostasis.
Seog Bae Oh - One of the best experts on this subject based on the ideXlab platform.
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a critical role of Toll Like Receptor 2 in nerve injury induced spinal cord glial cell activation and pain hypersensitivity
Journal of Biological Chemistry, 2007Co-Authors: Eunkyeong Jo, Heung Sik Na, Seyoung Choi, Kyungpyo Park, Seog Bae OhAbstract:Abstract The activation of spinal cord glial cells has been implicated in the development of neuropathic pain upon peripheral nerve injury. The molecular mechanisms underlying glial cell activation, however, have not been clearly elucidated. In this study, we found that damaged sensory neurons induce the expression of tumor necrosis factor-α, interleukin-1β, interleukin-6, and inducible nitric-oxide synthase genes in spinal cord glial cells, which is implicated in the development of neuropathic pain. Studies using primary glial cells isolated from Toll-Like Receptor 2 knock-out mice indicate that damaged sensory neurons activate glial cells via Toll-Like Receptor 2. In addition, behavioral studies using Toll-Like Receptor 2 knock-out mice demonstrate that the expression of Toll-Like Receptor 2 is required for the induction of mechanical allodynia and thermal hyperalgesia due to spinal nerve axotomy. The nerve injury-induced spinal cord microglia and astrocyte activation is reduced in the Toll-Like Receptor 2 knock-out mice. Similarly, the nerve injury-induced pro-inflammatory gene expression in the spinal cord is also reduced in the Toll-Like Receptor 2 knock-out mice. These data demonstrate that Toll-Like Receptor 2 contributes to the nerve injury-induced spinal cord glial cell activation and subsequent pain hypersensitivity.
Sung Joong Lee - One of the best experts on this subject based on the ideXlab platform.
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a critical role of Toll Like Receptor 2 in nerve injury induced spinal cord glial cell activation and pain hypersensitivity
Journal of Biological Chemistry, 2007Co-Authors: Donghoon Kim, Seyoung Choi, Kyungpyo Park, Shizuo Akira, Myung Ah Kim, Ikhyun Cho, Misun Kim, Soojin Lee, Joong Soo Kim, Sung Joong LeeAbstract:The activation of spinal cord glial cells has been implicated in the development of neuropathic pain upon peripheral nerve injury. The molecular mechanisms underlying glial cell activation, however, have not been clearly elucidated. In this study, we found that damaged sensory neurons induce the expression of tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, and inducible nitric-oxide synthase genes in spinal cord glial cells, which is implicated in the development of neuropathic pain. Studies using primary glial cells isolated from Toll-Like Receptor 2 knock-out mice indicate that damaged sensory neurons activate glial cells via Toll-Like Receptor 2. In addition, behavioral studies using Toll-Like Receptor 2 knock-out mice demonstrate that the expression of Toll-Like Receptor 2 is required for the induction of mechanical allodynia and thermal hyperalgesia due to spinal nerve axotomy. The nerve injury-induced spinal cord microglia and astrocyte activation is reduced in the Toll-Like Receptor 2 knock-out mice. Similarly, the nerve injury-induced pro-inflammatory gene expression in the spinal cord is also reduced in the Toll-Like Receptor 2 knock-out mice. These data demonstrate that Toll-Like Receptor 2 contributes to the nerve injury-induced spinal cord glial cell activation and subsequent pain hypersensitivity.
Seyoung Choi - One of the best experts on this subject based on the ideXlab platform.
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a critical role of Toll Like Receptor 2 in nerve injury induced spinal cord glial cell activation and pain hypersensitivity
Journal of Biological Chemistry, 2007Co-Authors: Eunkyeong Jo, Heung Sik Na, Seyoung Choi, Kyungpyo Park, Seog Bae OhAbstract:Abstract The activation of spinal cord glial cells has been implicated in the development of neuropathic pain upon peripheral nerve injury. The molecular mechanisms underlying glial cell activation, however, have not been clearly elucidated. In this study, we found that damaged sensory neurons induce the expression of tumor necrosis factor-α, interleukin-1β, interleukin-6, and inducible nitric-oxide synthase genes in spinal cord glial cells, which is implicated in the development of neuropathic pain. Studies using primary glial cells isolated from Toll-Like Receptor 2 knock-out mice indicate that damaged sensory neurons activate glial cells via Toll-Like Receptor 2. In addition, behavioral studies using Toll-Like Receptor 2 knock-out mice demonstrate that the expression of Toll-Like Receptor 2 is required for the induction of mechanical allodynia and thermal hyperalgesia due to spinal nerve axotomy. The nerve injury-induced spinal cord microglia and astrocyte activation is reduced in the Toll-Like Receptor 2 knock-out mice. Similarly, the nerve injury-induced pro-inflammatory gene expression in the spinal cord is also reduced in the Toll-Like Receptor 2 knock-out mice. These data demonstrate that Toll-Like Receptor 2 contributes to the nerve injury-induced spinal cord glial cell activation and subsequent pain hypersensitivity.
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a critical role of Toll Like Receptor 2 in nerve injury induced spinal cord glial cell activation and pain hypersensitivity
Journal of Biological Chemistry, 2007Co-Authors: Donghoon Kim, Seyoung Choi, Kyungpyo Park, Shizuo Akira, Myung Ah Kim, Ikhyun Cho, Misun Kim, Soojin Lee, Joong Soo Kim, Sung Joong LeeAbstract:The activation of spinal cord glial cells has been implicated in the development of neuropathic pain upon peripheral nerve injury. The molecular mechanisms underlying glial cell activation, however, have not been clearly elucidated. In this study, we found that damaged sensory neurons induce the expression of tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, and inducible nitric-oxide synthase genes in spinal cord glial cells, which is implicated in the development of neuropathic pain. Studies using primary glial cells isolated from Toll-Like Receptor 2 knock-out mice indicate that damaged sensory neurons activate glial cells via Toll-Like Receptor 2. In addition, behavioral studies using Toll-Like Receptor 2 knock-out mice demonstrate that the expression of Toll-Like Receptor 2 is required for the induction of mechanical allodynia and thermal hyperalgesia due to spinal nerve axotomy. The nerve injury-induced spinal cord microglia and astrocyte activation is reduced in the Toll-Like Receptor 2 knock-out mice. Similarly, the nerve injury-induced pro-inflammatory gene expression in the spinal cord is also reduced in the Toll-Like Receptor 2 knock-out mice. These data demonstrate that Toll-Like Receptor 2 contributes to the nerve injury-induced spinal cord glial cell activation and subsequent pain hypersensitivity.
Kyungpyo Park - One of the best experts on this subject based on the ideXlab platform.
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a critical role of Toll Like Receptor 2 in nerve injury induced spinal cord glial cell activation and pain hypersensitivity
Journal of Biological Chemistry, 2007Co-Authors: Eunkyeong Jo, Heung Sik Na, Seyoung Choi, Kyungpyo Park, Seog Bae OhAbstract:Abstract The activation of spinal cord glial cells has been implicated in the development of neuropathic pain upon peripheral nerve injury. The molecular mechanisms underlying glial cell activation, however, have not been clearly elucidated. In this study, we found that damaged sensory neurons induce the expression of tumor necrosis factor-α, interleukin-1β, interleukin-6, and inducible nitric-oxide synthase genes in spinal cord glial cells, which is implicated in the development of neuropathic pain. Studies using primary glial cells isolated from Toll-Like Receptor 2 knock-out mice indicate that damaged sensory neurons activate glial cells via Toll-Like Receptor 2. In addition, behavioral studies using Toll-Like Receptor 2 knock-out mice demonstrate that the expression of Toll-Like Receptor 2 is required for the induction of mechanical allodynia and thermal hyperalgesia due to spinal nerve axotomy. The nerve injury-induced spinal cord microglia and astrocyte activation is reduced in the Toll-Like Receptor 2 knock-out mice. Similarly, the nerve injury-induced pro-inflammatory gene expression in the spinal cord is also reduced in the Toll-Like Receptor 2 knock-out mice. These data demonstrate that Toll-Like Receptor 2 contributes to the nerve injury-induced spinal cord glial cell activation and subsequent pain hypersensitivity.
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a critical role of Toll Like Receptor 2 in nerve injury induced spinal cord glial cell activation and pain hypersensitivity
Journal of Biological Chemistry, 2007Co-Authors: Donghoon Kim, Seyoung Choi, Kyungpyo Park, Shizuo Akira, Myung Ah Kim, Ikhyun Cho, Misun Kim, Soojin Lee, Joong Soo Kim, Sung Joong LeeAbstract:The activation of spinal cord glial cells has been implicated in the development of neuropathic pain upon peripheral nerve injury. The molecular mechanisms underlying glial cell activation, however, have not been clearly elucidated. In this study, we found that damaged sensory neurons induce the expression of tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, and inducible nitric-oxide synthase genes in spinal cord glial cells, which is implicated in the development of neuropathic pain. Studies using primary glial cells isolated from Toll-Like Receptor 2 knock-out mice indicate that damaged sensory neurons activate glial cells via Toll-Like Receptor 2. In addition, behavioral studies using Toll-Like Receptor 2 knock-out mice demonstrate that the expression of Toll-Like Receptor 2 is required for the induction of mechanical allodynia and thermal hyperalgesia due to spinal nerve axotomy. The nerve injury-induced spinal cord microglia and astrocyte activation is reduced in the Toll-Like Receptor 2 knock-out mice. Similarly, the nerve injury-induced pro-inflammatory gene expression in the spinal cord is also reduced in the Toll-Like Receptor 2 knock-out mice. These data demonstrate that Toll-Like Receptor 2 contributes to the nerve injury-induced spinal cord glial cell activation and subsequent pain hypersensitivity.
