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Inflammatory bowel conditions (IBD) are chronic relapsing diseases. Crohn’s disease (CD) is characterised by transmural inflammation due to an imbalance between proand antiinflammatory molecules. Ulcerative colitis (UC) is only a mucosal disease, however one quarter of patients develop fulminating disease and 20% require surgery. Treatment objectives usually include steroid-free remission, decrease in hospitalization and surgery and sustained clinical remission and mucosal healing as well as reduction in the risk of dysplasia and cancer. The description of the cell signalling cascade over the past 20 years has led to a surge in potential treatments for IBD. It was initially thought that since CD is mediated through the T helper 1 cascade, using specific molecules to block it would be a reasonable approach to potential cure. A multitude of medications and trials later proved this theory to be true. In addition, UC which was thought to be mediated through a different inflammatory cascade (T helper 2) was soon discovered to respond to these newer molecules. In fact several trials showed T helper 1 cells to be prevalent in the serum, stool and mucosa of patients with active UC. The better knowledge of the inflammatory pathways in IBD lead to the development of new targeted therapies with a multitude of actions including inhibition of leukocytes trafficking, inhibition of T cell activation or polarization and inhibition of proinflammatory cytokines. Additionally a new technique called humanization was developed through advances in protein engineering and lead to the production of partially humanized and finally fully humanized antibodies.

Biologic Agents for Inflammatory Bowel Disease (The Current, the Future and the Controversy)