Scientists find major susceptibility gene for Crohn...( ting to tease out the specific downstre...)

ting to tease out the specific downstream effects of this protective polymorphism. Yet, because IL-23 plays an important role in activating inflammation, including in the organs of the digestive tract, it could be an extremely important target for improving the management of Crohn's disease and other IBDs.

"We identified multiple genetic signals in the IL-23 receptor gene that were strongly associated with Crohn's disease. In fact, the statistical significance for some IL-23 receptor SNPs was two orders of magnitude greater than that of other SNPs in other genes. So, we believe that blocking the activity of IL-23 or manipulating its pathway will be an effective way to manage IBD," said Dr. Duerr, who also is head of the Inflammatory Bowel Disease Genetics Program at the University of Pittsburgh School of Medicine and co-director of the Inflammatory Bowel Disease Center at the University of Pittsburgh Medical Center.

In a previous study by other investigators, an early stage clinical trial showed that IBD patients exhibit improvement when given a monoclonal antibody that blocks IL-23 and a related inflammatory mediator. Furthermore, recent studies in mice in which the gene for IL-23 is deleted demonstrated that IL-23 is essential for the development and maintenance of chronic intestinal inflammation. Such evidence, combined with the current discovery, suggests therapies that target the IL-23 pathway may lead to more individualized, better-directed therapies for IBDs, the authors say.

"This important discovery not only offers new hope for better therapies for patients with Crohn's disease, it also highlights the promise of the human genome project and subsequent investments by the NIH in large scale, collaborative research projects to unravel the causes of, and hopefully better treatments for complex, enigmatic diseases," said Stephen P. James, M.D., director of the Division of Digestive Diseases and Nutrition at the National Institutes o
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26-Oct-2006

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