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Selectins and other immune cell surface receptors comprise a diverse group of proteins that mediate the interaction between leukocytes and the vascular endothelium or other cells. The selectin family, including E-selectin (CD62E), L-selectin (CD62L), and P-selectin (CD62P), is essential for the initial capture and 'rolling' of leukocytes on the vessel wall during the inflammatory response [McEver, 2015; Mitroulis et al., 2015]. Other receptors in this category, such as integrins and various costimulatory molecules, further regulate leukocyte adhesion, extravasation, and activation [Ley et al., 2007]. These molecules play critical roles in the pathophysiology of inflammatory diseases, autoimmune disorders, and sickle cell disease, where they contribute to tissue damage and vaso-occlusion [Ataga et al., 2017; Mitroulis et al., 2015]. Therapeutic agents targeting these receptors, such as the P-selectin inhibitor crizanlizumab or integrin-targeting antibodies like vedolizumab, aim to disrupt these pathological interactions to alleviate disease symptoms [Ataga et al., 2017; Ley et al., 2007]. However, because these receptors are vital for normal immune surveillance, their inhibition can lead to safety concerns, including an increased risk of infections and rare but serious adverse events like progressive multifocal leukoencephalopathy [Ley et al., 2007; Mitroulis et al., 2015].
Inhibition of cell-cell adhesion and leukocyte recruitment by blocking receptor-ligand interactions on the surface of immune and endothelial cells.
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