Endothelial cell adhesion molecules (ECAMs) (ECAMs)

Endothelial cell adhesion molecules (ECAMs) are a diverse group of cell surface glycoproteins expressed on the vascular endothelium that mediate the recruitment and migration of circulating leukocytes into tissues (Ley et al., 2007, Nature Reviews Immunology). This category includes several distinct families, most notably the immunoglobulin superfamily (e.g., ICAM-1, VCAM-1), selectins (e.g., E-selectin, P-selectin), and certain integrins (Bui et al., 2020, Journal of Leukocyte Biology). Their primary biological function is to regulate the leukocyte adhesion cascade—a multi-step process involving rolling, activation, firm adhesion, and transmigration—which is essential for the immune response to injury and infection (Muller, 2013, Nature Reviews Immunology). However, the pathological overexpression of these molecules is a key driver in chronic inflammatory diseases, atherosclerosis, and the metastatic spread of cancer cells (Kong et al., 2018, Molecules). Therapeutic strategies targeting ECAMs involve monoclonal antibodies or small molecules designed to block the interaction between these receptors and their ligands on leukocytes (Polman et al., 2006, NEJM). For example, drugs like natalizumab and crizanlizumab target specific adhesion pathways to treat multiple sclerosis and sickle cell disease, respectively (Ataga et al., 2017, NEJM). While effective, inhibiting these molecules can lead to significant safety concerns, such as an increased risk of opportunistic infections like progressive multifocal leukoencephalopathy (PML) due to impaired immune surveillance (Polman et al., 2006, NEJM).

Other names

Endothelial and vascular adhesion moleculesCell adhesion moleculesECAMsVascular adhesion moleculesAdhesion receptors

Inhibition of leukocyte-endothelial cell adhesion and blockade of transendothelial migration by preventing ligand-receptor interactions between circulating cells and the vascular wall.