selectinbinding

Selectin binding refers to the interaction between selectins, a family of cell adhesion molecules, and their carbohydrate ligands. Selectins are calcium-dependent proteins that initiate the initial contact between circulating leukocytes and the vascular endothelium or platelets, a step essential for leukocyte trafficking during immune surveillance and inflammation. The three vertebrate selectins are L-selectin, found on leukocytes; E-selectin, induced on activated endothelial cells; and P-selectin, stored in platelets and endothelial We should avoid this; will fix.

Corrected version:

Selectin binding refers to the interaction between selectins, a family of cell adhesion molecules, and their carbohydrate ligands. Selectins are calcium-dependent proteins that initiate the initial contact between circulating leukocytes and the vascular endothelium or platelets, a step essential for leukocyte trafficking during immune surveillance and inflammation. The three vertebrate selectins are L-selectin on leukocytes, E-selectin on activated endothelium, and P-selectin on platelets and endothelium.

Ligands for selectins include various glycoproteins bearing specific carbohydrate motifs, notably sialylated and fucosylated structures such as sialyl Lewis X and sialyl Lewis A. PSGL-1 (P-selectin glycoprotein ligand-1) is a key leukocyte ligand for P- and E-selectin, and other ligands such as ESL-1 and CD44 can contribute to binding. L-selectin has ligands including GlyCAM-1 and PNAd on high endothelial venules.

In physiological flow, selectin–ligand interactions support capture and rolling of leukocytes along the vessel wall. These low-affinity, shear-dependent interactions allow leukocytes to survey endothelium and to respond to chemokine signals that induce integrin activation, leading to firm adhesion and transmigration. Dysregulation of selectin binding can contribute to inflammatory diseases and influence cancer metastasis. Therapeutic approaches aim to disrupt selectin–ligand interactions to reduce inappropriate leukocyte recruitment.