CD99 (E2) up-regulates α 4β 1-dependent T cell adhesion to inflamed vascular endothelium under flow conditions

作者：Ghislaine Bernard, Vincent P. Raimondi, Isabelle Alberti, Monique Pourtein, John Widjenes, Michel Ticchioni, Alain Bernard · 发表于：European Journal of Immunology · 年份：2000 · DOI：10.1002/1521-4141(200010)30:10<3061::aid-immu3061>3.0.co;2-m · 被引用次数：76 · 研究领域：Cell Adhesion Molecules Research、T-cell and B-cell Immunology、Inflammatory mediators and NSAID effects

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.