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Integrin alpha-4 beta-7 (also known as LPAM-1) is a heterodimeric cell surface receptor composed of the alpha-4 (CD49d) and beta-7 subunits, primarily expressed on memory T-lymphocytes [UniProt: P13612, P26010]. Its primary biological function is to mediate the selective homing of these leukocytes to the gut-associated lymphoid tissue (GALT) by binding to the Mucosal Vascular Addressin Cell Adhesion Molecule-1 (MAdCAM-1) expressed on the intestinal endothelium [StatPearls: NBK541011]. In pathological conditions such as Ulcerative Colitis and Crohn's Disease, the dysregulated recruitment of alpha-4 beta-7-positive cells leads to chronic intestinal inflammation [PubMed: 24670407]. Vedolizumab is a therapeutic monoclonal antibody that specifically targets this integrin complex, inhibiting the interaction with MAdCAM-1 and thereby reducing the infiltration of pro-inflammatory cells into the gastrointestinal tract [FDA: Entyvio Label]. This mechanism provides a gut-selective therapeutic approach, distinguishing it from systemic immunosuppressants and reducing the risk of opportunistic infections in the central nervous system [NEJM: 369:689-710].
Vedolizumab is a humanized monoclonal antibody that specifically binds to the alpha-4 beta-7 integrin heterodimer. By binding to this receptor, it inhibits the interaction of alpha-4 beta-7 with mucosal vascular addressin cell adhesion molecule-1 (MAdCAM-1), which is primarily expressed on the vascular endothelium of the gastrointestinal tract. This blockade prevents the trafficking of pro-inflammatory T-lymphocytes into the intestinal mucosa, thereby reducing local inflammation without causing systemic immunosuppression.
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