Leukocyte–endothelial adhesion molecule (CAM)

The leukocyte–endothelial adhesion interface is a complex, multi-step biological system that facilitates the recruitment of white blood cells from the bloodstream into peripheral tissues (Ley et al., Nature Reviews Immunology, 2007). This process, known as the leukocyte adhesion cascade, involves a series of molecular interactions: initial tethering and rolling mediated by selectins, chemokine-triggered activation, firm adhesion mediated by integrins such as LFA-1 and VLA-4, and finally, transendothelial migration through the vascular wall via interactions with ligands like ICAM-1 and VCAM-1 (Muller, Annual Review of Pathology, 2011). This interface is fundamental to normal immune surveillance and the acute inflammatory response to infection or injury. However, dysregulated or chronic activation of these adhesion pathways is a hallmark of various inflammatory and autoimmune disorders, including multiple sclerosis and inflammatory bowel disease (Vestweber, Nature Reviews Immunology, 2015). Therapeutic targeting of this interface involves the use of monoclonal antibodies or small molecules that block specific adhesion receptors or their ligands, thereby preventing the pathological infiltration of leukocytes into target tissues (Mitroulis et al., Trends in Pharmacological Sciences, 2015). While effective, these therapies can carry risks such as increased susceptibility to infections, notably progressive multifocal leukoencephalopathy, due to impaired immune cell trafficking (Bloomgren et al., New England Journal of Medicine, 2012).

Other names

Leukocyte–endothelial adhesion interfacesLeukocyte adhesion cascadeLeukocyte trafficking moleculeCell adhesion molecule

Antagonism of cell adhesion molecules to prevent leukocyte extravasation into tissues by blocking the interaction between leukocyte integrins and endothelial ligands.