The causes of inflammatory bowel diseases, such as ulcerative colitis (UC) and 
Crohn's disease (CD), remain to be elucidated. However, characteristic 
inflammation of the gastrointestinal mucosa is caused by infiltration of T 
lymphocytes into the submucosal layer. Inhibiting this immune response is a 
promising therapeutic target. Integrins expressed on the cell surface mediate 
gut homing of T lymphocytes. Blockade of integrin-cell adhesion molecule 
interaction using antibodies against α₄-containing integrins, namely 
natalizumab, has shown clinical efficacy; however, this drug's lack of 
α₄-containing integrin specificity leads to systemic immunosuppression that 
caused progressive multifocal leukoencephalopathy and death in some patients 
resulting in its withdrawal from the market. Vedolizumab specifically targets 
the α₄β₇ integrin that is selectively expressed on gut-homing T lymphocytes. 
Vedolizumab successfully extended clinical remission in patients with UC or CD 
and reduced patient reliance on corticosteroid use. The drug is well tolerated 
and there have been no deaths or reports of progressive multifocal 
leukoencephalopathy infection in patients receiving vedolizumab. A phase III 
long-term 7-year safety study in patients with UC and CD is under way. 
Regulatory applications are under review in the U.S. and E.U. for its use in the 
treatment of patients with UC and CD, with decisions expected in mid-2014.