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An important prerequisite for an inflammatory response to occur is the trafficking of blood-borne leukocytes from the blood to the site of inflammation. This process has been studied extensively, and many of the molecules responsible for leukocyte adhesion and concurrent extravasation have been elucidated (reviewed in ref. 1).
Leukocyte extravasation can be divided into three distinct stages(figure). The first stage, termed tethering and/or rolling, is mediated by a family of adhesion molecules called selectins. Selectins consist of three structurally homologous proteins that are expressed on leukocytes (L-selectin), platelets (P-selectin), and endothelial cells (E-selectin and P-selectin). In this first stage, a leukocyte that is flowing freely in the blood makes the initial contact with the inflamed vasculature at or near the site of the trauma and then rolls to a site close to where the leukocyte will ultimately leave the bloodstream in its journey to the lesion.
Figure. Depiction of a granulocyte going through the three stages of extravasation to traffic to an inflammatory lesion. The first stage is selectin-mediated rolling. The second, "adhesion strengthening stage," is mediated by the CD18 members LFA-1 and MAC-1 interacting with ICAM-1 and ICAM-2. The …
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