It is believed that leukocyte deformation supports firm adhesion by increasing the zone of contact, thereby allowing formation of more adhesive bonds.
These P-selectin densities were selected to support the firm adhesion of neutrophils on the substrates.
Separately, sLeX/P-selectin interactions support rolling and aICAM-1/ICAM-1 interactions mediate firm adhesion.
Mac-1 (CD11b/CD18), the major subtype of integrins, is responsible for the firm adhesion of neutrophils to the endothelium.
Mac-1 (CD11b/CD18), the major subtype of integrins, is responsible for the firm adhesion of neutrophils to endothelium [40].
Selectin-ligand interactions, which mediate rolling, are believed to be important for facilitating firm adhesion, either by activating integrins or by facilitating the transition to firm adhesion by making it easier for integrins to bind.
Interplay between rolling and firm adhesion elucidated with a cell-free system engineered with two distinct receptor ligand pairs.
However, this firm adhesion was largely reduced in THP-1 cells with SIRPα overexpression.
EC transfected with VCAM-1 support monocyte rolling and firm adhesion [14].
ICAM-1 is an important surface receptor in the immunoglobulin family, which mediates firm adhesion of monocytes to endothelium.
This interaction would mediate firm adhesion of the leukocyte to the endothelium, aiding the inflammatory response post surgery.
