E-selectin, L-selectin, P-selectin (CD62E, CD62L, CD62P)

Selectins are a small family of calcium-dependent transmembrane cell adhesion molecules that mediate the initial tethering and rolling of leukocytes on activated endothelial cells and platelets during inflammation and immune surveillance. E-selectin is inducibly expressed on activated endothelial cells and mediates leukocyte adhesion primarily in response to inflammatory cytokines. P-selectin is stored in platelet α-granules and endothelial Weibel–Palade bodies, rapidly translocated to the cell surface during vascular injury or activation. L-selectin is constitutively expressed on all leukocytes and is crucial for lymphocyte homing to lymph nodes and initial steps of leukocyte extravasation. All selectins recognize sialylated, fucosylated glycans (primarily sLe^x) on their target ligands, with nuanced differences in glycan recognition. They are critical in acute and chronic inflammation, immune cell trafficking, thrombosis, and cancer metastasis. Therapeutically, selectin inhibition is pursued for diseases involving aberrant leukocyte recruitment (e.g., sickle cell crisis, inflammatory disorders, metastatic cancer) with multiple antagonists in clinical testing and some drugs approved targeting P-selectin for sickle cell disease

Other names

Selectins (family)CD62E (E-selectin)CD62L (L-selectin)CD62P (P-selectin)ELAM-1 (E-selectin)LECAM-1 (L-selectin)GMP-140, PADGEM (P-selectin)Endothelial-leukocyte adhesion molecule 1 (E-selectin)Leukocyte-endothelial cell adhesion molecule 1 (L-selectin)Platelet activation-dependent granule external membrane protein (P-selectin)

Blockade of leukocyte rolling and adhesion to endothelium; Inhibition of cell recruitment to sites of inflammation; Interference with selectin-ligand interaction, especially sialyl Lewis x (sLe^x) glycan; Disruption of tumor cell extravasation (anti-metastatic effect); Reduction of platelet-leukocyte aggregation