Abstract
Leukocyte adhesion must be tightly controlled in order for leukocytes to patrol the body as nonadherent cells, yet stop and emigrate from the blood into tissues at sites of infection or inflammation. A key element in this process is activation of β2 integrins. While β2 integrin activation involves conformational changes that increase affinity for ligand, evidence is accumulating that rearrangement of integrins, resulting in increases in avidity, is at least as important in regulating binding capacity. Recent work has established the importance of diffusion and rearrangement of integrins to activation of leukocyte adhesion, and has begun to unravel the molecular basis of its regulation.

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