Integrins and leukocyte adhesion molecules (LAMs) (LAMs)

Integrins and leukocyte adhesion molecules (LAMs) represent a broad class of cell surface receptors and ligands that mediate the critical process of leukocyte trafficking from the blood into peripheral tissues. This group encompasses several families, including the heterodimeric integrins (e.g., LFA-1, VLA-4), selectins (E-, P-, and L-selectin), and members of the immunoglobulin superfamily such as Intercellular Adhesion Molecule-1 (ICAM-1) and Vascular Cell Adhesion Molecule-1 (VCAM-1) [1][2]. Biologically, these molecules facilitate a multi-step adhesion cascade—comprising rolling, activation, firm adhesion, and transmigration—that allows immune cells to reach sites of infection or injury [3]. In various pathological states, such as multiple sclerosis, Crohn's disease, and rheumatoid arthritis, the over-activation or over-expression of these molecules leads to chronic, damaging inflammation [4]. Therapeutic strategies often involve monoclonal antibodies that bind to specific integrin subunits to block these interactions, effectively acting as trafficking inhibitors that prevent pathogenic cells from entering target organs [5]. However, because these molecules are vital for systemic immune surveillance, their inhibition can lead to significant safety concerns, most notably the risk of opportunistic infections like progressive multifocal leukoencephalopathy (PML) [6].

Other names

Cell adhesion moleculesCAMsLeukocyte-endothelial adhesion moleculesAdhesion receptors

These molecules function as targets for antagonists, primarily monoclonal antibodies or small molecules, which bind to the extracellular domains of integrins or their ligands to competitively inhibit leukocyte-endothelial interactions, thereby preventing leukocyte recruitment and extravasation into inflamed tissues [3][5].