Vascular cell adhesion protein 1 (VCAM-1) (VCAM-1)

Vascular cell adhesion protein 1 (VCAM-1), also designated as CD106, is a member of the immunoglobulin superfamily and a type I transmembrane glycoprotein primarily expressed on the surface of vascular endothelial cells following stimulation by pro-inflammatory cytokines such as TNF-alpha [1, 2]. Its core biological function is to mediate the firm adhesion and transendothelial migration of leukocytes—specifically monocytes, lymphocytes, eosinophils, and basophils—by interacting with the integrin alpha-4 beta-1 (VLA-4) on the leukocyte surface [2, 3]. This interaction is fundamental to the leukocyte adhesion cascade, facilitating the recruitment of immune cells to sites of injury or infection. VCAM-1 expression is markedly upregulated in pathological states such as atherosclerosis, where it promotes the formation of fatty streaks, and in autoimmune conditions like multiple sclerosis and Crohn’s disease [2]. In oncology, VCAM-1 facilitates tumor cell-endothelial interactions, aiding in the metastatic spread of cancer cells [2]. Pharmacological targeting of the VCAM-1/VLA-4 axis, most notably with the monoclonal antibody natalizumab, has shown significant clinical efficacy in reducing neuroinflammation, although such therapies are associated with risks of progressive multifocal leukoencephalopathy (PML) due to restricted immune surveillance in the central nervous system [4].

Other names

CD106Vascular cell adhesion molecule 1INCAM-100

Inhibition of leukocyte-endothelial cell adhesion through competitive antagonism of the VLA-4/VCAM-1 interaction or transcriptional downregulation of VCAM-1 expression.