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人白介素1β转换酶(ICE)elisa试剂盒

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  • 公司名称厦门仑昌硕生物科技有限公司
  • 品       牌其他品牌
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  • 所  在  地厦门市
  • 厂商性质生产厂家
  • 更新时间2020/4/26 16:45:59
  • 访问次数836
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厦门仑昌硕生物科技有限公司集研发、生产、销售、服务及品牌代理为一体的生物技术公司,目前可提供各种抗体、免疫学相关的检测试剂盒、胎牛血清,动物抗血清等高品质产品及服务,涵盖分子生物学、细胞生物学、免疫学等生命科学领域。
公司非常注重企业信息化的建设及企业平台的建设,我们内部采用了*的信息处理平台,保证客户的需求可以准确、高效处理。
公司成立之初,立足外贸,和部分欧美及亚非国家的客户建立了良好的合作,随着国内生物领域的蓬勃发展,逐步把重心转移到国内来,为每一位科研人员献上高品质的产品及服务是我们的使命。

集研发、生产、销售、服务及品牌代理为一体的生物技术公司,目前可提供各种抗体、免疫学相关的检测试剂盒、胎牛血清,动物抗血清等高品质产品及服务,涵盖分子生物学、细胞生物学、免疫学等生命科学领域。
产地 国产 级别 其他
Background Patients with rheumatoid arthritis (RA) have a systemic Th1 defect associated with inflammation. Objective To examine the hypothesis that interleukin 17 (IL-17) contributes to this defect.
人白介素1β转换酶(ICE)elisa试剂盒 产品信息

Background Patients with rheumatoid arthritis (RA) have a systemic Th1 defect associated with inflammation. Objective To examine the hypothesis that interleukin 17 (IL-17) contributes to this defect. Methods IL-17 effects on Th1 markers were examined on T-bet and interferon γ (IFNγ) expression in peripheral blood mononuclear cells (PBMCs) from patients with RA or healthy controls (HC). Receptor specificities were determined by analysis of the Th1-specific IL-12 receptor β2 (IL-12Rβ2), Th17-specific IL-23R and the common IL-12Rβ1 chain expression. Effects of IL-17 or IFNγ on IL-6, IL-1, IL-8, matrix metalloproteinase-8 (MMP-8) were measured by real-time RT-PCR in RA synovial cells. Results RA PBMCs were less responsive to IL-12-induced IFNγ than HC PBMCs. IL-12 hyporesponsiveness was increased by IL-17 treatment associated with a selective reduction in IL-12Rβ2, but not IL-23R, IL-12Rβ1 or T-bet, which was reversed with IL-17R inhibition. IL-17 inhibited IL-12Rβ2 expression in developing Th1 cells. In RA synovial cells, IL-17 induced IL-6, IL-1, IL-8 and MMP-8, whereas IFNγ haBackground Patients with rheumatoid arthritis (RA) have a systemic Th1 defect associated with inflammation. Objective To examine the hypothesis that interleukin 17 (IL-17) contributes to this defect. Methods IL-17 effects on Th1 markers were examined on T-bet and interferon γ (IFNγ) expression in peripheral blood mononuclear cells (PBMCs) from patients with RA or healthy controls (HC). Receptor specificities were determined by analysis of the Th1-specific IL-12 receptor β2 (IL-12Rβ2), Th17-specific IL-23R and the common IL-12Rβ1 chain expression. Effects of IL-17 or IFNγ on IL-6, IL-1, IL-8, matrix metalloproteinase-8 (MMP-8) were measured by real-time RT-PCR in RA synovial cells. Results RA PBMCs were less responsive to IL-12-induced IFNγ than HC PBMCs. IL-12 hyporesponsiveness was increased by IL-17 treatment associated with a selective reduction in IL-12Rβ2, but not IL-23R, IL-12Rβ1 or T-bet, which was reversed with IL-17R inhibition. IL-17 inhibited IL-12Rβ2 expression in developing Th1 cells. In RA synovial cells, IL-17 induced IL-6, IL-1, IL-8 and MMP-8, whereas IFNγ ha

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