Then it reviews transcellular migration and makes a case that these 2 routes of transmigration may have more in common than originally thought. This review first focuses on some general types of molecules and mechanisms that have been implicated in paracellular TEM and tries to show how these observations may be related. The mechanisms behind transcellular migration are less well established.
Recently, there has been a flurry of interest in TEM through the endothelial cell body (transcellular migration). Most TEM takes place at endothelial borders (paracellular transmigration). All of the benefit from the inflammatory response and almost all of the collateral damage take place once leukocytes leave the blood vessels. Transendothelial migration (TEM), the step in the inflammatory response in which leukocytes actually cross the endothelial cells lining the blood vessels at the site of inflammation, is a critical point in the regulation of this response. Therefore, careful regulation of the inflammatory response is critical for our wellbeing.
Most pathology involves inflammation that persists too long, is self-directed, and/or is in the wrong place at the wrong time. 50, 69 The inflammatory response is a double-edged sword. In a sequence of adhesive steps, leukocytes attach to the vessel wall, locomote along the wall to the endothelial borders, traverse the endothelium and the subendothelial basement membrane, and migrate through the interstitial tissue.
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Getting leukocytes to the site of injury or infection is of prime importance, and an elaborate series of adhesion events between leukocytes and endothelium ensures that leukocytes leave the bloodstream only at the inflammatory site.
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