Activation-independent binding of human memory T cells to adhesion molecule ELAM-1

Activation-independent binding of human memory T cells to adhesion molecule ELAM-1
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人类记忆 T 细胞与粘附分子 ELAM-1 的激活独立结合

DOI:
10.1038/349799a0
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发表时间:
1991
期刊:
影响因子:
64.8
通讯作者:
W. Newman
W. Newman
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Y. Shimizu;S. Shaw;N. Graber;T. V. Gopal;Kevin Morgan;G. Seventer;W. Newman

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炎性细胞因子诱导内皮细胞上粘附分子的集合可能对T淋巴细胞亚群向炎性部位的差异迁移至关重要。已知涉及VLA-4和LFA-1整联蛋白的两种分子途径介导T细胞粘附至活化的内皮1 -4。在这里,我们表明,涉及快速诱导的内皮细胞表面粘附分子ELAM-1(参考文献5,6)的第三种途径有助于静息CD 4 + T细胞与IL-1诱导的人内皮细胞的结合。所有三种途径都有助于记忆T细胞比初始T细胞更大地粘附于内皮。T细胞与纯化的ELAM-1的粘附有两个独特的特征:首先,ELAM-1专门介导记忆T细胞的粘附;其次,记忆T细胞与ELAM-1的结合不依赖于调节整联蛋白介导的粘附的急性激活事件7,8。因此,ELAM-1可能是最重要的记忆T细胞在体内发炎的内皮细胞的初始附着和记忆T细胞的优先迁移到组织和炎症部位。
THE induction of an ensemble of adhesion molecules on endothelial cells by inflammatory cytokines is likely to be crucial to the differential migration of T-lymphocyte subsets into inflammatory sites. Two molecular pathways involving the VLA-4 and LFA-1 integrins are known to mediate T-cell adhesion to activated endothelium1–4. Here we show that a third pathway involving the rapidly inducible endothelial cell-surface adhesion molecule ELAM-1 (refs 5,6) contributes to the binding of resting CD4+ T cells to IL-1 -induced human endothelial cells. All three pathways contribute to the greater adhesion to endothelium of memory T cells than naive T cells. There are two unique features of T-cell adhesion to purified ELAM-1: first, ELAM-1 exclusively mediates adhesion of memory T cells; second, memory T-cell binding to ELAM-1 is independent of acute activation events that regulate integrin-mediated adhesion 7,8. Thus, ELAM-1 may be of primary importance in the initial attachment of memory T cells to inflamed endothelium in vivo and to the preferential migration of memory T cells into tissue and inflammatory sites.
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