首页> 外文期刊>American Journal of Pathology >Both Th1 and Th2 Cells Require P-Selectin Glycoprotein Ligand-1 for Optimal Rolling on Inflamed Endothelium
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Both Th1 and Th2 Cells Require P-Selectin Glycoprotein Ligand-1 for Optimal Rolling on Inflamed Endothelium

机译:Th1和Th2细胞均需要P-选择蛋白糖蛋白配体1才能在炎症内皮上获得最佳滚动

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摘要

The acquisition of homing receptors that redirect lymphocyte trafficking to nonlymphoid tissues after antigen encounter is a fundamental aspect of effector T-cell development. Although a role for selectins and their ligands has been well characterized for trafficking of Th1 cells to nonlymphoid sites, mechanisms responsible for Th2 trafficking are not well understood. Using a flow chamber system in which the endothelial interactions of two distinct T-cell populations could be examined simultaneously, we directly compared the requirements for Th1 and Th2 cell tethering and rolling. We found that although Th2 cells expressed significantly lower levels of selectin ligands than Th1 cells, activation of the endothelium by Th2-derived factors induced rolling interactions that were comparable for both Th1 and Th2 populations. Further, in the absence of PSGL-1, no other adhesion molecule could effectively compensate for lack of PSGL-1 to mediate rolling of either Th1 or Th2 cells. Thus, both Th1 and Th2 populations express functional PSGL-1-based selectin ligands for tethering and rolling on activated endothelium, and both effector populations can use PSGL-1 as the dominant scaffold for functional selectin ligand expression.
机译:抗原接触后获得使淋巴细胞 向非淋巴组织转移的归巢受体的获得是 效应器T细胞发育的基本方面。尽管 对于选择素及其配体的作用已得到很好的表征 用于将Th1细胞运输到非淋巴位点,但负责Th2运输的机制 并不很好了解。使用 流动室系统,其中可以同时检查两个不同T细胞群的内皮相互作用 我们直接比较了Th1的要求和Th2细胞束缚 和滚动。我们发现,尽管Th2细胞表达的选择素配体水平明显低于Th1细胞,但Th2衍生因子对内皮的激活 引起滚动相互作用 这对于Th1和Th2人群而言是可比的。此外,在没有PSGL-1的情况下 ,没有其他粘附分子可以有效地 补偿PSGL-1的缺乏来介导Th1 的滚动或Th2细胞。因此,Th1和Th2群体均表达基于功能性 PSGL-1的选择素配体,用于在活化的 内皮上进行束缚和滚动,并且两个效应子群体均可以将PSGL-1用作 功能性选择素配体表达的主要支架。

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  • 来源
    《American Journal of Pathology》 |2005年第6期|1661-1675|共15页
  • 作者单位

    From the Departments of Pathology,University of Alabama at Birmingham, Birmingham, Alabama|Microbiology,University of Alabama at Birmingham, Birmingham, Alabama;

    and Genetics,University of Alabama at Birmingham, Birmingham, Alabama;

    From the Departments of Pathology,University of Alabama at Birmingham, Birmingham, Alabama;

    and the Department of Physiology and Biophysics,Immunology Research Group, University of Calgary, Calgary, Canada;

    and the Department of Physiology and Biophysics,Immunology Research Group, University of Calgary, Calgary, Canada;

    From the Departments of Pathology,University of Alabama at Birmingham, Birmingham, Alabama;

    and Genetics,University of Alabama at Birmingham, Birmingham, Alabama;

    From the Departments of Pathology,University of Alabama at Birmingham, Birmingham, Alabama|Microbiology,University of Alabama at Birmingham, Birmingham, Alabama;

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