ATTENUATION OF CYTOMEGALOVIRUS-INDUCED ENDOTHELIAL INTERCELLULAR ADHESION MOLECULE-1 mRNA/PROTEIN EXPRESSION AND T LYMPHOCYTE ADHESION BY A 2′-O-METHOXYETHYL ANTISENSE OLIGONUCLEOTIDE1,2

2000 ◽  
Vol 69 (3) ◽  
pp. 417-426 ◽  
Author(s):  
Deborah A. Knight ◽  
Bruce R. Briggs ◽  
C. Frank Bennett ◽  
Nagaradona Harindranath ◽  
W. James Waldman ◽  
...  
1991 ◽  
Vol 34 (10) ◽  
pp. 1245-1253 ◽  
Author(s):  
Raymond F. Krzesicki ◽  
William E. Fleming ◽  
Greg E. Winterrowd ◽  
Cheryl A. Hatfield ◽  
Martin E. Sanders ◽  
...  

1988 ◽  
Vol 107 (1) ◽  
pp. 321-331 ◽  
Author(s):  
M L Dustin ◽  
T A Springer

Intercellular adhesion molecule-1 (ICAM-1) on the surface of cultured umbilical vein and saphenous vein endothelial cells was upregulated between 2.5- and 40-fold by rIL-1, rTNF, LPS and rIFN gamma corresponding to up to 5 X 10(6) sites/cell. Endothelial cell ICAM-1 was a single band of 90 kD in SDS-PAGE. Purified endothelial cell ICAM-1 reconstituted into liposomes and bound to plastic was an excellent substrate for both JY B lymphoblastoid cell and T lymphoblast adhesion. Adhesion to endothelial cell ICAM-1 in planar membranes was blocked completely by monoclonal antibodies to lymphocyte function associated antigen-1 (LFA-1) or ICAM-1. Adhesion to artificial membranes was most sensitive to ICAM-1 density within the physiological range found on resting and stimulated endothelial cells. Adhesion of JY B lymphoblastoid cells, normal and genetically LFA-1 deficient T lymphoblasts and resting peripheral blood lymphocytes to endothelial cell monolayers was also assayed. In summary, LFA-1 dependent (60-90% of total adhesion) and LFA-1-independent basal adhesion was observed and the use of both adhesion pathways by different interacting cell pairs was increased by monokine or lipopolysaccharide stimulation of endothelial cells. The LFA-1-dependent adhesion could be further subdivided into an LFA-1/ICAM-1-dependent component which was increased by cytokines and a basal LFA-1-dependent, ICAM-1-independent component which did not appear to be affected by cytokines. We conclude that ICAM-1 is a regulated ligand for lymphocyte-endothelial cell adhesion, but at least two other major adhesion pathways exist.


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