Activation-independent binding of human memory T cells to adhesion molecule ELAM-1.
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 endothelium. Here we show that a third pathway involving the rapidly inducible endothelial cell-surface adhesion molecule ELAM-1 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. 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.
Shimizu
Y
Y
Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.
Shaw
S
S
Graber
N
N
Gopal
T V
TV
Horgan
K J
KJ
Van Seventer
G A
GA
Newman
W
W
D015704:CD4 Antigens / Q000276:immunology; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000276:immunology* / Q000302:isolation & purification; D019040:E-Selectin; D005353:Fibronectins / Q000502:physiology; D006801:Humans; D007156:Immunologic Memory; D066298:In Vitro Techniques; D008213:Lymphocyte Activation; D013601:T-Lymphocytes / Q000276:immunology*
D015704:CD4 Antigens; D015815:Cell Adhesion Molecules; D019040:E-Selectin; D005353:Fibronectins