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Blood, Vol. 92 No. 11 (December 1), 1998:
pp. 4167-4177
Role of Tissue Factor in Adhesion of Mononuclear Phagocytes to and
Trafficking Through Endothelium In Vitro
Gwendalyn J. Randolph,
Thomas Luther,
Sybille Albrecht,
Viktor Magdolen, and
William A. Muller
From the Department of Pathology, Cornell University Medical College,
New York, NY; the Institute of Pathology, Technical University of
Dresden, Dresden; and the Department of Gynecology, Technical
University of Munich, Munich, Germany.
An in vitro model consisting of endothelium grown on
collagen was used to investigate how mononuclear phagocytes traverse endothelium in the basal-to-apical direction (reverse transmigration), a process that mimics their migration across vascular and/or
lymphatic endothelium during atherosclerosis and resolution of
inflammation, respectively. Monoclonal antibody (MoAb) VIC7 against
tissue factor (TF) inhibited reverse transmigration by 77%.
Recombinant tissue factor fragments containing at least six amino acids
C-terminal to residue 202 also strongly inhibited reverse
transmigration. TF was absent on resting monocytes but was induced on
these cells after initial apical-to-basal transendothelial migration.
Two additional observations suggest that TF is involved in adhesion between mononuclear phagocytes and endothelium: (1) when monocytes were
incubated with lipopolysaccharide (LPS) to stimulate expression of TF
before they were added to endothelium, VIC7 or soluble TF modestly
inhibited their adhesion to the apical endothelial surface, each by
about 35%; and (2) endothelial cells specifically bound to surfaces
coated with TF fragments containing amino acids 202-219. This binding
was blocked by anti-TF MoAb, suggesting that endothelial cells bear a
receptor for TF. These data suggest that mononuclear phagocytes use TF, perhaps as an adhesive protein, to exit sites of
inflammation.
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