Thus, the interaction between α4-integrin and VCAM-1 was the main mechanism for binding (capture and firm adhesion) of flowing lymphocytes, although E-selectin might also have contributed in the capture phase.
During later stages of cell spreading, soluble skelemin either converts into insoluble skelemin, or dissociates from integrins, being replaced by talin or other actin-binding proteins and firm adhesion occurs.
Additionally, recombinant TNF-binding protein decreases rolling adhesion and firm adhesion of leukocytes to the hepatic interstitium after hemorrhage [ 24, 39].
'Adhesion dynamic modelling' predicts synergistic roles for selectins and integrins with transition between rolling and firm adhesion dependent on binding affinities and relative concentrations of receptor ligand interactions [23,24].
Computed models of adhesion molecule dynamics predict synergistic roles for selectins and integrins with transition between rolling and firm adhesion dependent on the binding affinities and relative concentrations of receptor-ligand interactions [56,57].
Adhesion is a complex sequential process of capture, rolling and firm adhesion, mainly mediated by the P- and E-selectin on the endothelial cells and their binding proteins, such as PSGL-1, CD18, CD11a and Mac-1, on the leukocyte membrane.
Thus, we conclude that sulfation of tyrosine 14 enhances the function of CX(3 CR1 in cell capture and firm adhesion.
EC transfected with VCAM-1 support monocyte rolling and firm adhesion [14].
Additionally, in an in vitro fluid shear flow model, exogenously added sL-selectin inhibited leukocyte rolling and firm adhesion to the endothelium in a dose-dependent manner, presumably by competing with cell surface L-selectin for binding of endothelial ligands [ 23].
This prolonged contact with the endothelium may be necessary to promote leukocyte activation and trigger integrin-mediated arrest and firm adhesion.
