Dysregulated recruitment of leukocytes into the intestine is a characteristic feature of IBD. Several families of
molecules regulate the influx of these cells into sites of inflammation within the gastrointestinal tract. Pharmacological
blockade of interactions between molecules that mediate the formation of stable bonds (integrins) and their endothelial
ligands has already shown clinical efficacy. Antibodies that target participant molecules have been approved by the US
Federal Drug Administration for use in Crohn’s, multiple sclerosis (MS) (i.e. natalizumab) and psoriasis (i.e. efalizumab).
A more recent additional family of drugs, which might also interfere with lymphocyte traffic (i.e. sphingosine-1-
phosphate receptor agonists: fingolimod) is in clinical use for MS and just recently entered the clinical trial stage for ulcerative
colitis. In the present review we discuss basic aspects of clinically relevant molecules and compile the clinical
studies that support the targeting of specific steps of the leukocyte adhesion cascade for therapeutic purposes in IBD.
Keywords: Adhesion molecules, chemokines, Crohn’s disease, integrins, sphingosine1-phosphate, ulcerative colitis.
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