A key immune deficiency can spur the disease, researchers say
FRIDAY, Oct. 5 (HealthDay News) -- U.S. researchers say they've identified a specific immune deficiency that's the likely cause of ulcerative colitis -- at least in mice.
A team at the Harvard School of Public Health (HSPH) said the problem may lie in a deficiency of the T-bet protein in dendritic cells -- white blood cells that detect foreign microbes and activate the immune system.
The lack of T-bet allows harmful bacteria in the large intestine to breach the bowel's protective lining and trigger damaging inflammation, the researchers said. They also found that once the disease was established in mice, it could be passed from mothers to offspring and even between adults, a discovery that has potential implications for public health and prevention.
The study was published online Thursday in the journal Cell.
"We have identified a new molecular player, T-bet, and when it's missing, there is spontaneous onset of the disease in mice. The importance of this study is that we now have a novel model for ulcerative colitis; the disease appears in 100 percent of the animals (that lack T-bet) and looks just like the human disease," team leader Laurie Glimcher, a professor of immunology at HSPH and a professor of medicine at Harvard Medical School, said in a prepared statement.
About half a million Americans have ulcerative colitis, a chronic and sometimes severe inflammatory disease of the colon or large intestine.
Because this mouse model closely resembles human ulcerative colitis, it may prove important for testing new therapies and preventive measures, Glimcher said.
The U.S. National Institute of Diabetes and Digestive and Kidney Diseases has more about ulcerative colitis.
-- Robert Preidt
SOURCE: Harvard School of Public Health, news release, Oct. 4, 2007
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