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pubmed:abstractText |
The authors demonstrate that resting CD56+/CD3- NK cell adhesion to the endothelial VCAM-1 is over three-fold higher than CD56-/CD3+ T-cell adhesion. T-cell, but not NK-cell adhesion, to VCAM-1 is enhanced significantly by stimulation. The expression of VCAM-1 receptor subunits alpha 4 and beta 1 on both effector cells remains unchanged upon stimulation. A subpopulation of NK cells, as well as of T cells, was found to express beta 7, whose expression was not altered upon stimulation. The authors conclude that the adhesive properties of the same receptor structures on these distinct cell populations are regulated in a different manner, according to the specific functions of the effector cells of the immune system.
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