...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Hiv Infection-associated Immune Activation Occurs By Two Distinct Pathways That Differentially Affect Cd4 And Cd8 T Cells
【24h】

Hiv Infection-associated Immune Activation Occurs By Two Distinct Pathways That Differentially Affect Cd4 And Cd8 T Cells

机译：艾滋病毒感染相关的免疫激活是通过两种不同的途径差异影响Cd4和Cd8 T细胞而发生的。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

HIV infection is characterized by a brisk immune activation that plays an important role in the CD4 depletion and immune dysfunction of patients with AIDS. The mechanism underlying this activation is poorly understood. In the current study, we tested the hypothesis that this activation is the net product of two distinct pathways: the inflammatory response to HIV infection and the homeostatic response to CD4 T cell depletion. Using ex vivo BrdU incorporation of PBMCs from 284 patients with different stages of HIV infection, we found that CD4 proliferation was better predicted by the combination of CD4 depletion and HIV viral load (R~2 = 0.375, P < 0.001) than by either parameter alone (CD4 T cell counts, R~2 = 0.202, P < 0.001; HIV viremia, R~2 = 0.302, P < 0.001). Interestingly, CD8 T cell proliferation could be predicted by HIV RNA levels alone (R~2 = 0.334, P < 0.001) and this predictive value increased only slightly (R~2 = 0.346, P < 0.001) when CD4 T cell depletion was taken into account. Consistent with the hypothesis that CD4 T cell proliferation is driven by IL-7 as a homeostatic response to CD4 T cell depletion, levels of phosphorylated STAT-5 were found to be elevated in naive subsets of CD4 and CD8 T cells from patients with HIV infection and in the central memory subset of CD4 T cells. Taken together these data demonstrate that at least two different pathways lead to immune activation of T cells in patients with HIV infection and these pathways differentially influence CD4 and CD8 T cell subsets.
机译：HIV感染的特征在于轻快的免疫激活，在AIDS患者的CD4耗竭和免疫功能障碍中起着重要作用。激活的机制尚不清楚。在当前的研究中，我们测试了以下假设：这种激活是两种不同途径的净产物：对HIV感染的炎症反应和对CD4 T细胞耗竭的体内稳态反应。使用离体BrdU掺入284名不同阶段HIV感染患者的PBMC，我们发现CD4耗竭和HIV病毒载量的组合可以更好地预测CD4的增殖（R〜2 = 0.375，P <0.001），而不是任何一个参数单独使用（CD4 T细胞计数，R〜2 = 0.202，P <0.001； HIV病毒血症，R〜2 = 0.302，P <0.001）。有趣的是，仅通过HIV RNA水平就可以预测CD8 T细胞的增殖（R〜2 = 0.334，P <0.001），而当采用CD4 T细胞耗竭时，该预测值仅略有增加（R〜2 = 0.346，P <0.001）。考虑在内。与IL-7驱动CD4 T细胞增殖作为对CD4 T细胞耗竭的体内稳态反应的假设相一致，发现来自HIV感染患者的CD4和CD8 T细胞的幼稚亚型中磷酸化STAT-5的水平升高。和在CD4 T细胞的中央记忆子集中总之，这些数据表明，至少有两种不同的途径导致HIV感染患者T细胞的免疫活化，并且这些途径差异地影响CD4和CD8 T细胞亚群。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

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