Intercellular Adhesion Molecule 1 (ICAM-1) and Vascular Cell Adhesion Molecule 1 (VCAM-1) (ICAM-1/VCAM-1)

Intercellular Adhesion Molecule 1 (ICAM-1) and Vascular Cell Adhesion Molecule 1 (VCAM-1) are transmembrane glycoproteins of the immunoglobulin superfamily that mediate the adhesion of leukocytes to the vascular endothelium (UniProt: P05362, P19320). ICAM-1 binds to the integrin LFA-1 (CD11a/CD18), while VCAM-1 interacts with VLA-4 (alpha4beta1 integrin), facilitating the recruitment and extravasation of immune cells into inflamed tissues (PubMed: 15121770). These interactions are central to the pathogenesis of various inflammatory and autoimmune diseases, including multiple sclerosis and dry eye disease, where leukocyte infiltration is excessive (StatPearls: Cell Adhesion Molecules). Therapeutic agents like Natalizumab and Lifitegrast target these pathways by blocking the binding of integrins to their respective adhesion molecule ligands, thereby reducing inflammation (FDA: Tysabri, Xiidra). However, disrupting these interfaces can lead to significant safety concerns, such as an increased risk of opportunistic infections like progressive multifocal leukoencephalopathy (PML) due to impaired immune surveillance (PubMed: 16510744). Additionally, these molecules play roles in cancer metastasis by facilitating the attachment of tumor cells to the endothelium (PubMed: 11544349).

Other names

CD54CD106Intercellular adhesion molecule 1Vascular cell adhesion molecule 1Antigen CD54Antigen CD106INCAM-100

Inhibition of leukocyte-endothelial cell adhesion by blocking the interaction between cell adhesion molecules (ICAM-1/VCAM-1) and their integrin counter-receptors (LFA-1/VLA-4).