• 主题
高级搜索  >
历史搜索 清空历史
首页> 美国卫生研究院文献>The Journal of Immunology Author Choice >T Cell–Derived IL-10 Impairs Host Resistance to Mycobacterium tuberculosis Infection
【2h】

T Cell–Derived IL-10 Impairs Host Resistance to Mycobacterium tuberculosis Infection

机译：T细胞衍生的IL-10损害宿主对结核分枝杆菌感染的抵抗力

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。
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Tuberculosis (TB), caused by Mycobacterium tuberculosis infection, is a leading cause of mortality and morbidity, causing ∼1.5 million deaths annually. CD4+ T cells and several cytokines, such as the Th1 cytokine IFN-γ, are critical in the control of this infection. Conversely, the immunosuppressive cytokine IL-10 has been shown to dampen Th1 cell responses to M. tuberculosis infection impairing bacterial clearance. However, the critical cellular source of IL-10 during M. tuberculosis infection is still unknown. Using IL-10 reporter mice, we show in this article that during the first 14 d of M. tuberculosis infection, the predominant cells expressing IL-10 in the lung were Ly6C+ monocytes. However, after day 21 postinfection, IL-10–expressing T cells were also highly represented. Notably, mice deficient in T cell–derived IL-10, but not mice deficient in monocyte-derived IL-10, showed a significant reduction in lung bacterial loads during chronic M. tuberculosis infection compared with fully IL-10–competent mice, indicating a major role for T cell–derived IL-10 in TB susceptibility. IL-10–expressing cells were detected among both CD4+ and CD8+ T cells, expressed high levels of CD44 and Tbet, and were able to coproduce IFN-γ and IL-10 upon ex vivo stimulation. Furthermore, during M. tuberculosis infection, Il10 expression in CD4+ T cells was partially regulated by both IL-27 and type I IFN signaling. Together, our data reveal that, despite the multiple immune sources of IL-10 during M. tuberculosis infection, activated effector T cells are the major source accounting for IL-10–induced TB susceptibility.
机译：由结核分枝杆菌感染引起的结核病（TB）是致死率和发病率的主要原因，每年造成约150万人死亡。 CD4 + T细胞和几种细胞因子，例如Th1细胞因子IFN-γ，对于控制这种感染至关重要。相反，已显示免疫抑制性细胞因子IL-10可抑制Th1细胞对结核分枝杆菌感染损害细菌清除的反应。然而，结核分枝杆菌感染期间IL-10的关键细胞来源仍然未知。本文使用IL-10报告基因小鼠显示，在结核分枝杆菌感染的前14 d，肺中表达IL-10的主要细胞是Ly6C + 单核细胞。然而，在感染后第21天，表达IL-10的T细胞也得到了很高的代表。值得注意的是，与完全具备IL-10能力的小鼠相比，在慢性结核分枝杆菌感染期间，缺乏T细胞来源的IL-10的小鼠，但没有缺乏具有单核细胞来源的IL-10的小鼠，肺细菌负荷显着降低。 T细胞来源的IL-10在结核病易感性中起重要作用。在CD4 + 和CD8 + T细胞中均检测到表达IL-10的细胞，表达高水平的CD44和Tbet，并能够共同产生IFN-γ和IL在离体刺激下-10。此外，在结核分枝杆菌感染期间，CD4 + T细胞中的IL10表达受到IL-27和I型IFN信号转导的部分调节。总之，我们的数据表明，尽管在结核分枝杆菌感染期间存在多种IL-10免疫源，但激活的效应T细胞仍是导致IL-10引起的结核病易感性的主要来源。

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