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Blood, Vol. 93 No. 3 (February 1), 1999:
pp. 886-896
Activation of Peripheral Blood T Cells by Interaction and Migration
Through Endothelium: Role of Lymphocyte Function
Antigen-1/Intercellular Adhesion Molecule-1 and Interleukin-15
David Sancho,
María Yáñez-Mó,
Reyes Tejedor, and
Francisco Sánchez-Madrid
From the Servicio de Inmulogía, Hospital de la Princesa,
Universidad Autónoma de Madrid, Madrid, Spain.
Cell adhesion molecules have a key role in the migration of T cells
to inflammatory foci. However, the effect of the endothelial-lymphocyte interaction on the activation of the latter cells remains unresolved. We have studied the effect of resting and stimulated endothelial cells
(ECs) on the activation of peripheral blood T cells (PBTLs), as
assessed by the expression of CD69 and CD25 activation antigens. The
incubation of PBTLs with tumor necrosis factor- -activated EC
monolayers, either alive or fixed, induced the expression of CD69 but
not CD25, preferentially in the CD8+
CD45RO+ cell subset. Furthermore, it induced the
production of cytokines such as IFN- , but not that of interleukin-2
(IL-2) and IL-4. EC treated with other stimuli such as IL-1 ,
IFN-, or lipopolysaccharide also showed the same proactivatory
effect on T cells. Lymphocyte activation was almost completely
inhibited by blocking anti-CD18 and anti-intercellular adhesion
molecule-1 (anti-ICAM-1) monoclonal antibodies (MoAbs), but only
slightly affected by MoAbs against CD49d, vascular cell adhesion
molecule-1, and anti-IL-15. In addition, the interaction of PBTL with
immobilized ICAM-1 induced CD69 expression in the same memory T-cell
subset. IL-15 induced T-cell activation with expression of CD69 and
CD25, and production of IFN-, and its effect was additive with that
triggered by cell adhesion to either EC or immobilized ICAM-1. The
transmigration of PBTLs through either confluent EC monolayers or
ICAM-1-coated membranes also induced efficiently the expression of
CD69. When IL-15 was used as chemoattractant in these assays, a further
enhancement in CD69 expression was observed in migrated cells. Together
these results indicate that stimulated endothelium may have an
important role in T-cell activation, through the lymphocyte function
antigen-1/ICAM-1 pathway, and that IL-15 efficiently cooperates in this
phenomenon. These observations could account for the abundance of
CD69+ cells in the lymphocytic infiltrates of several
chronic inflammatory diseases.
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