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Integrin alpha E beta 7 (αEβ7), also known as CD103, is a heterodimeric cell surface receptor primarily expressed on intraepithelial lymphocytes (IELs) and certain dendritic cell subsets within mucosal tissues, such as the gastrointestinal tract, lungs, and skin [1, 8]. It consists of the alpha E (ITGAE) and beta 7 (ITGB7) subunits and specifically binds to E-cadherin expressed on the surface of epithelial cells [7, 11]. This interaction is crucial for the retention of T cells within the epithelial layer, facilitating localized immune surveillance and response [9, 14]. In inflammatory conditions like ulcerative colitis and Crohn's disease, αEβ7-expressing pro-inflammatory T cells accumulate in the gut mucosa, contributing to chronic inflammation and tissue damage [1, 17]. Therapeutic strategies, most notably the monoclonal antibody etrolizumab, target the beta 7 subunit to block both αEβ7 and α4β7 integrins, thereby inhibiting both the recruitment and retention of pathogenic lymphocytes in the gut [2, 5]. While targeting this pathway offers a gut-selective approach to treating inflammatory bowel disease, clinical development continues to evaluate its efficacy and safety compared to other biologics [15, 22].
Antagonism of the integrin alpha E beta 7 prevents its interaction with E-cadherin on epithelial cells, thereby inhibiting the retention of pro-inflammatory lymphocytes within mucosal tissues such as the gastrointestinal tract [1, 2, 5].
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