Modifying T-cell trafficking to the intestinal as a potential management for inflammatory bowel disease

The Inflammatory Bowel Diseases (IBDs) are life-long chronic relapsing incurable inflammatory conditions that usually appear in the first few decades of life. There have been marked advances in the management of these conditions, but none of the currently available therapies are a panacea as they are neither universally efficacious nor will their efficacy necessarily last. There is a desperate need for new therapies that target the immunological deficits within the immune system with low side effects and long-term efficacy.

Leukocyte trafficking into the intestinal mucosa is central to the inflammatory pathogenesis in both Crohn's disease (CD) and ulcerative colitis (UC) and modification of this trafficking has the ability to reduce the level of inflammation. The α4β7 integrin heterodimer is highly expressed on the CD4(+)CD45RA-memory T-cell subpopulation located within the intestine, and these play a critical part in the pathogenesis of IBD.

By modifying the integrin and chemokine interactions with their specific receptors, inhibition of α4(+) and α4β7(+) T-cell trafficking to the sites of intestinal inflammation is possible with promising outcomes in the management of IBD.