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CD99(E2)在流动条件下上调α4β1依赖性T细胞与炎症血管内皮的黏附。

CD99 (E2) up-regulates alpha4beta1-dependent T cell adhesion to inflamed vascular endothelium under flow conditions.

作者信息

Bernard G, Raimondi V, Alberti I, Pourtein M, Widjenes J, Ticchioni M, Bernard A

机构信息

INSERM U343 et Laboratoire d'Immunologie, Université de Nice-Sophia Antipolis, Nice, France.

出版信息

Eur J Immunol. 2000 Oct;30(10):3061-5. doi: 10.1002/1521-4141(200010)30:10<3061::AID-IMMU3061>3.0.CO;2-M.

DOI:10.1002/1521-4141(200010)30:10<3061::AID-IMMU3061>3.0.CO;2-M
PMID:11069091
Abstract

CD99/E2 is an integral transmembrane protein which forms, together with Xga, a distinct family whose genes are located in the pseudoautosomal region. The number of T cells that firmly bound to vascular endothelial cells under physiological shear stress increased 2-14-fold upon CD99 stimulation, and bound cells became much more resistant to detachment forces and spread. T cell arrest occurred within 1 min and was dependent on the alpha4beta1-VCAM-1 pathway. In contrast, the alphaLbeta2-ICAM-1 pathway remained unactivated. This was observed with T cell lines and with activated peripheral blood lymphocytes, and was limited within the resting peripheral CD4+ T cells to the memory subset, while virgin cells were unaffected. This discloses a stepwise regulation of the T cell extravasation cascade.

摘要

CD99/E2是一种整合型跨膜蛋白,它与Xga一起构成一个独特的家族,其基因位于假常染色体区域。在生理剪切应力下,与血管内皮细胞紧密结合的T细胞数量在CD99刺激后增加了2至14倍,且结合的细胞对分离力的抵抗力增强并发生铺展。T细胞在1分钟内发生停滞,且依赖于α4β1-VCAM-1途径。相比之下,αLβ2-ICAM-1途径仍未被激活。这在T细胞系和活化的外周血淋巴细胞中均有观察到,并且在静息外周CD4+ T细胞中仅限于记忆亚群,而初始细胞未受影响。这揭示了T细胞外渗级联反应的逐步调节。

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