CHARLOTTESVILLE, Va., Nov. 10 Researchers at the University of Virginia Health System have discovered that a protein expressed by the immune system, called TL1A, is linked to inflammatory bowel disease (IBD) in patients, especially Crohn's disease. This is the first time TL1A has been linked to Crohn's. In a study involving fifty patients at U.Va., published in the Nov. 1 issue of The Journal of Immunology, the research team found that TL1A was expressed in patients suffering from IBD, but not in control patients who are disease free. The finding could lead to new treatments for people who suffer from IBD, the general name for two diseases that cause inflammation in the intestines.

Ulcerative colitis causes inflammation and ulcers in the top layer of the intestinal lining, usually in the lower part of the large intestine, while in Crohn's, the inflammation extends deep into the lining, usually in the small intestine. Over one million adults and children in the U.S. suffer from inflammatory bowel disease, with about 30,000 new cases diagnosed each year, according to the Crohn's and Colitis Foundation of America. Adolescents and young adults are most susceptible to IBD and there is no cure.

"What we have discovered here at U.Va. is a cytokine, a key protein that regulates the immune response, that could be an important target for therapy in IBD patients who are not responding to current treatments for ulcerative colitis and Crohn's disease," said Dr. Fabio Cominelli, principal investigator of the study, professor of internal medicine and microbiology and director of the Digestive Health Center of Excellence at U.Va. "Blocking the interaction between TL1A and its receptor in the immune response, called DR3, could be beneficial to the thousands of people suffering from chronic intestinal inflammation."

TL1A is a newly discovered member of the tumor necrosis factor (TNF) family of proteins thought to be expressed primarily in the e
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Contact: Bob Beard
reb8e@virginia.edu
434-982-4490
University of Virginia Health System
10-Nov-2003

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