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For many years, physicians had only antitumour necrosis factor (anti-TNF) antibodies as biologicals for the treatment of IBD. With the regulatory approval of vedolizumab, a completely new mechanism of action was introduced into the therapeutic armamentarium of IBD specialists: vedolizumab is an ‘integrin antagonist’ binding to the α4β7 integrin expressed on the surface of mononuclear cells such as T-lymphocytes.1 Circulating blood T-cells require binding of α4β7 integrin to mucosal addressin cell adhesion molecule-1 (MAdCAM-1) expressed by the endothelial cells of the GI tract to be able to migrate into the mucosal layers.1 To prevent the migration of inflammatory mononuclear cells into the inflamed mucosa in patients with IBD, integrin antagonists have been developed. Several antagonists of integrin–adhesion molecule interactions are approved or under clinical development targeting either the α4β7 integrin heterodimer, the α4 integrin, the β7 integrin or MAdCAM-1 (such as etrolizumab, a β7 integrin antibody; and PF-00547659,17, an anti-MAdCAM-1 antibody).2 It is important to understand the mechanism of action of those therapies exactly to be able to adapt them to specific patient needs. …
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