首页> 美国卫生研究院文献>other >Cigarette Smoke Exposure Impairs Dendritic Cell Maturation and T Cell Proliferation in Thoracic Lymph Nodes of Mice
【2h】

Cigarette Smoke Exposure Impairs Dendritic Cell Maturation and T Cell Proliferation in Thoracic Lymph Nodes of Mice

机译:香烟烟雾暴露损害小鼠胸腔淋巴结中的树突状细胞成熟和T细胞增殖。

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

Respiratory tract dendritic cells (DCs) are juxtaposed to directly sample inhaled environmental particles. Processing and presentation of these airborne Ags could result in either the development of immunity or tolerance. The purpose of this study was to determine the consequences of cigarette smoke exposure on DC function in mice. We demonstrate that while cigarette smoke exposure decreased the number of DCs in the lungs, Ag-induced DC migration to the regional thoracic lymph nodes was unaffected. However, cigarette smoking suppressed DC maturation within the lymph nodes as demonstrated by reduced cell surface expression of MHC class II and the costimulatory molecules CD80 and CD86. Consequently, DCs from cigarette smoke-exposed animals had a diminished capacity to induce IL-2 production by T cells that was associated with diminished Ag-specific T cell proliferation in vivo. Smoke-induced defects in DC function leading to impaired CD4+ T cell function could inhibit tumor surveillance and predispose patients with chronic obstructive pulmonary disease to infections and exacerbations.
机译:并置呼吸道树突状细胞(DC)以直接采样吸入的环境颗粒。这些空气中的Ag的加工和展示可能导致免疫力或耐受性的发展。这项研究的目的是确定香烟烟雾对小鼠DC功能的影响。我们证明,尽管香烟烟雾暴露减少了肺中DC的数量,但Ag诱导的DC迁移到区域胸腔淋巴结并不受影响。但是,吸烟抑制了淋巴结内的DC成熟,这表现为MHC II类细胞和共刺激分子CD80和CD86的细胞表面表达降低。因此,接触香烟烟雾的动物的DC诱导T细胞诱导IL-2产生的能力降低,这与体内Ag特异性T细胞增殖的降低有关。烟雾引起的DC功能缺陷导致CD4 + T细胞功能受损,可能抑制肿瘤监测,并使慢性阻塞性肺疾病患者容易感染和加重病情。

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