Difference in Th1 and Th17 lymphocyte adhesion to endothelium.

Difference in Th1 and Th17 lymphocyte adhesion to endothelium.
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Th1和Th17淋巴细胞粘附于内皮的差异。

DOI:
10.4049/jimmunol.1101647
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发表时间:
2012-02-01
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
通讯作者:
Lichtman AH
Lichtman AH
中科院分区:
其他
文献类型:
--
作者:
Alcaide P;Maganto-Garcia E;Newton G;Travers R;Croce KJ;Bu DX;Luscinskas FW;Lichtman AH

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T细胞亚群特异性迁移到炎症部位受到严格调控,并涉及T细胞与内皮的相互作用。辅助性T细胞17(Th 17)通常出现在与辅助性T细胞1(Th 1)不同的炎症部位,或者两个亚群出现在相同部位但在不同时间。T细胞亚群与内皮细胞粘附的差异可能导致亚群特异性迁移行为,但这种可能性尚未得到很好的研究。我们检测了小鼠Th 17细胞与内皮细胞粘附分子和内皮细胞在体外流动和体内微血管中的粘附,并通过流式细胞术和qRT-PCR表征其迁移表型。Th 17细胞比Th 1细胞更多地与E-选择素相互作用。与Th 1细胞相比,Th 17细胞较少与TNF-α激活的E-选择素缺陷型内皮细胞结合,活体显微镜研究表明,在野生型小鼠中,Th 17细胞与TNF-α处理的微血管比Th 1细胞参与更多的滚动相互作用,但在E-选择素缺陷型小鼠中并非如此。Th 17与ICAM-1的粘附依赖于CCL 20对整合素的激活,CCL 20是Th 17细胞高度表达的CCR 6的配体。在气囊炎症模型中,CCL 20触发了Th 17细胞的募集,但没有触发Th 1细胞的募集。这些数据提供证据表明,E-选择素和ICAM-1依赖的Th 17和Th 1细胞与内皮细胞的粘附是定量不同的。
T cell subset specific migration to inflammatory sites is tightly regulated and involves interaction of the T cells with the endothelium. T helper 17 (Th17) cells often appear at different inflammatory sites than T helper 1 (Th1) cells, or both subsets appear at the same sites but at different times. Differences in T cell subset adhesion to endothelium may contribute to subset-specific migratory behavior, but this possibility has not been well studied. We examined the adhesion of mouse Th17 cells to endothelial adhesion molecules and endothelium under flow in vitro and microvessels in vivo, and characterized their migratory phenotype by flow cytometry and qRT-PCR. More Th17 than Th1 cells interacted with E-selectin. Fewer Th17 than Th1 cells bound to TNF-α activated E-selectin deficient endothelial cells, and intravital microscopy studies demonstrated that Th17 cells engage in more rolling interactions with TNF-α treated microvessels than Th1 cells in wild type mice but not in E-selectin deficient mice. Th17 adhesion to ICAM-1 was dependent on integrin activation by CCL20, the ligand for CCR6, which is highly expressed by Th17 cells. In an air pouch model of inflammation, CCL20 triggered recruitment of Th17 but not Th1 cells. These data provide evidence that E-selectin and ICAM-1 dependent adhesion of Th17 and Th1 cells with endothelium are quantitatively different.
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