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首页> 外文学位 >Role of hematopoietic and stromal cell Toll-like receptor 4 signaling in the initiation of Th1 and Th2 adaptive immune responses.
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Role of hematopoietic and stromal cell Toll-like receptor 4 signaling in the initiation of Th1 and Th2 adaptive immune responses.

机译：造血细胞和基质细胞Toll样受体4信号在Th1和Th2适应性免疫反应的启动中的作用。

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摘要

Allergic asthma is an inflammatory lung disease driven by T helper cells type 2 (Th2). Airway epithelial cells are known to play a role in the exacerbation of previously established airway disease; however, their role in the early events that govern the establishment of allergic disease is not known. Here, using studies in chimeric and transgenic mice, we report for the first time that the airway epithelial cell is the critical Toll-like receptor 4 (TLR4) signaling cell that drives the development of Th2-mediated allergic airway disease to inhaled antigen containing LPS. Bone marrow chimeric mice lacking TLR4 in the stromal compartment of the lung fail to mount Th2 responses to inhaled ovalbumin. Furthermore, bone marrow chimeric mice only expressing TLR4 in the stromal cells of the lung and transgenic mice only expressing TLR4 in airway epithelial cells (AECs) sensitized with OVA and high levels of lipopolysaccharide (LPS) mount exaggerated Th2 responses following airway challenge with antigen. AECs upregulate thymic stromal lymphopoietin mRNA and protein expression and induce dendritic cells to undergo a program of maturation favoring the polarization of Th2 but not Th1 effector cells following exposure to LPS. These studies show that the AEC response to LPS, a microbial TLR ligand associated with common aeroallergens, is the critical factor driving the development of Th2 adaptive immune responses to aeroallergens.
机译：过敏性哮喘是由2型T辅助细胞（Th2）驱动的炎症性肺疾病。众所周知，气道上皮细胞在加剧先前建立的气道疾病中起重要作用。但是，它们在控制过敏性疾病发展的早期事件中的作用尚不清楚。在这里，通过在嵌合和转基因小鼠中的研究，我们首次报道气道上皮细胞是关键的Toll样受体4（TLR4）信号传导细胞，该信号驱动Th2介导的过敏性气道疾病向吸入的含LPS抗原发展。在肺间质隔室中缺乏TLR4的骨髓嵌合小鼠无法引起Th2对吸入卵白蛋白的反应。此外，骨髓嵌合小鼠仅在肺间质细胞中表达TLR4，而转基因小鼠仅在对OVA致敏的气道上皮细胞（AEC）中表达TLR4，高水平的脂多糖（LPS）会在抗原对气道发起攻击后夸大Th2反应。 AEC上调胸腺基质淋巴细胞生成素mRNA和蛋白表达，并诱导树突状细胞经历成熟程序，使其在暴露于LPS后有利于Th2而不是Th1效应细胞的极化。这些研究表明，AEC对LPS（一种与常见气变应原相关的微生物TLR配体）的反应，是驱动针对气变应原的Th2适应性免疫反应发展的关键因素。

著录项

  • 作者

    Tan, Anna Marie.;

  • 作者单位

    Yale University.;

  • 授予单位 Yale University.;
  • 学科 Biology Cell.;Biology Molecular.;Biology Microbiology.
  • 学位 Ph.D.
  • 年度 2008
  • 页码 178 p.
  • 总页数 178
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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