首页> 美国卫生研究院文献>Immunology >Lycopene suppresses the lipopolysaccharide-induced phenotypic and functional maturation of murine dendritic cells through inhibition of mitogen-activated protein kinases and nuclear factor-κB
【2h】

Lycopene suppresses the lipopolysaccharide-induced phenotypic and functional maturation of murine dendritic cells through inhibition of mitogen-activated protein kinases and nuclear factor-κB

机译:番茄红素通过抑制有丝分裂原激活的蛋白激酶和核因子-κB抑制脂多糖诱导的小鼠树突状细胞的表型和功能成熟

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

Dendritic cells (DC) are the most potent of antigen-presenting cells. The most important function of DC is to initiate the immune response by presenting antigens to naïve T lymphocytes. Currently, little is known about the basic action of lycopene in murine bone marrow (BM)-derived DC. In the present study, we have revealed that lycopene significantly attenuates the phenotypic and functional maturation of murine BM-DC, especially in lipopolysaccharide-induced DC maturation. We found that lycopene down-regulates the expression of costimulatory molecules (CD80 and CD86) and major histocompatibility complex type II molecules. We also determined that lycopene-treated DC were poor stimulators of naïve allogeneic T-cell proliferation and induced lower levels of interleukin-2 in responding T cells. They also exhibited impaired interleukin-12 production. Additionally, lycopene was able to inhibit mitogen-activated protein kinases, such as ERK1/2, p38 and JNK, and the transcription factor, nuclear factor-κB. Assessment of the in vivo effects of lycopene may reveal an inability to induce a normal cell-mediated immune response, despite the ability of the cells to migrate to the spleen. This data provides new insight into the immunopharmacology of lycopene and suggests a novel approach to the manipulation of DC for therapeutic application.
机译:树突状细胞(DC)是最有效的抗原呈递细胞。 DC的最重要功能是通过向幼稚的T淋巴细胞呈递抗原来启动免疫反应。目前,关于番茄红素在鼠骨髓(BM)衍生的DC中的基本作用了解甚少。在本研究中,我们发现番茄红素显着减弱了小鼠BM-DC的表型和功能成熟,特别是在脂多糖诱导的DC成熟中。我们发现番茄红素下调共刺激分子(CD80和CD86)和主要的组织相容性复杂的II型分子的表达。我们还确定,番茄红素处理过的DC不能刺激幼稚的同种T细胞增殖,并在应答T细胞中诱导较低的白细胞介素2水平。他们还表现出受损的白介素12的生产。此外,番茄红素能够抑制促分裂原活化的蛋白激酶,例如ERK1 / 2,p38和JNK,以及转录因子核因子-κB。尽管细胞具有迁移到脾脏的能力,但对番茄红素的体内作用的评估可能显示无法诱导正常的细胞介导的免疫反应。该数据为番茄红素的免疫药理学提供了新的见识,并提出了一种治疗DC的新方法。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号