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The transition from rolling to firm adhesion is a phenomenon frequently observed when neutrophils are interacting with activated endothelium in vitro or in vivo under 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.
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C. Wayne Smith (2000) studied this question.
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