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Leukocyte adhesion molecules are a heterogeneous group of cell surface receptors and ligands that orchestrate the movement of white blood cells from the bloodstream into peripheral tissues (StatPearls: Cell Adhesion Molecules [1]). This group includes three main families: selectins, which mediate initial rolling; integrins, which facilitate firm attachment; and members of the immunoglobulin superfamily, such as ICAM-1 and VCAM-1, which serve as ligands for integrins (Ley et al., Nature Reviews Immunology [2]). These molecules are essential for normal immune surveillance and the inflammatory response to injury or infection. However, their overactivation or overexpression is a hallmark of various inflammatory and autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, and inflammatory bowel disease (UniProt: ITGA4 [3]). Therapeutic strategies often involve monoclonal antibodies that block these interactions, thereby preventing the infiltration of pathogenic leukocytes into target organs (FDA: Tysabri [4], Entyvio [5]). While effective, these therapies carry risks such as impaired host defense and, in specific cases, serious opportunistic infections like progressive multifocal leukoencephalopathy.
Antagonism of cell-surface adhesion receptors to prevent leukocyte recruitment and extravasation into inflamed tissues.
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