Abstract
The transition from rolling to firm adhesion is a phenomenon frequently observed when neutrophils are interacting with activated endothelium in vitroor in vivounder physiologically relevant shear stress. The mechanisms leading to this activation are poorly understood, though selectin-dependent tethering and CD18-integrin-dependent adhesion are known to be involved. This transition may involve a sequence of interactions that trigger sufficient integrin activation to allow cell arrest under flow. Recent evidence is reviewed in support of the concept that integrin (Mac-1 and LFA-1) activation results from signaling that occurs through selectin binding, chemotactic factor stimulation, and, possibly, LFA-1 binding. Microcirculation (2000) 7, 385–394.