Selectines

• L-Selectin
• E-selectin
• P-selectin.

Selectins initiate a complex cascade of adhesion events by locally concentrating flowing leukocytes from the capillary blood stream by mediating rolling deceleration along the vessel wall. This process occurs in a cascade of sequential molecular interactions.

First, selectins mediate "docking" and rolling of leukocytes on the endothelial surface. This leads to the slowing of leukocytes and allows contact with signaling substances on the endothelial surface, such as chemokines. These stimulate the activation of integrins on the leukocyte surface. Integrins then mediate the efficient binding of these cells to the endothelial surface.

Members of the immunoglobulin (Ig) superfamily act as ligands of integrins. The leukocytes, which are now stably adherent, are able to target and eventually actively migrate through the endothelial cell layer.

Of the three known selectins, one, L-selectin, is found on most leukocytes, whereas E-selectin is expressed exclusively by endothelial cells and P-selectin is found on endothelium and on platelets.

Leukocyte adhesion deficiency II (LAD II) is a genetic defect that leads to a primary immunodeficiency due to the absence of selectin ligands (recurrent severe infections with fever episodes, dramatic increase in leukocyte counts in the blood).