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Vascular endothelial adhesion molecules are a functional class of cell surface glycoproteins expressed by endothelial cells that facilitate the recruitment of leukocytes from the blood into tissues (Muller, 2011 [PubMed: 21346730]). This group includes members of the immunoglobulin superfamily, such as Intercellular Adhesion Molecule-1 (ICAM-1) and Vascular Cell Adhesion Molecule-1 (VCAM-1), as well as selectins like E-selectin and P-selectin (Kong et al., 2018 [PubMed: 29657554]). These molecules are typically upregulated in response to inflammatory cytokines like TNF-alpha and IL-1 beta, playing a pivotal role in the leukocyte adhesion cascade involving rolling, activation, firm adhesion, and diapedesis (Ley et al., 2007 [PubMed: 17717539]). Pathologically, their over-expression is linked to chronic inflammatory conditions, atherosclerosis, and autoimmune diseases by promoting excessive leukocyte infiltration (Blankenberg et al., 2003 [PubMed: 12742991]). In oncology, they contribute to tumor-associated angiogenesis and provide a mechanism for circulating tumor cells to extravasate and form metastases (Okegawa et al., 2004 [PubMed: 15138468]). Therapeutic targeting of these molecules or their leukocyte ligands has led to the development of drugs like Natalizumab and Crizanlizumab, which aim to disrupt these interactions to treat conditions such as multiple sclerosis and sickle cell disease (Ataga et al., 2017 [PubMed: 27911611]).
Inhibition of leukocyte-endothelial interactions by blocking the binding of endothelial adhesion molecules (e.g., VCAM-1, P-selectin) to their respective ligands on leukocytes (e.g., VLA-4, PSGL-1).
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