Crohn's: An Autoimmune or Bacterial-Related Disease?

In 1996 geneticist Gilles Thomas and colleagues at the INSERM, the French Institute for Health and Medical Research in Paris, reported that IBD1, a region on the long arm of chromosome 16, was a Crohn's disease susceptibility locus.1 Five years later, in a second study, they announced that they had pinpointed the exact gene. The researchers contended that the connection between Crohn's and NOD2, the implicated gene located in IBD1, provided evidence to support the hypothesis that the disease is

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Another group, led by pathologist Gabriel Nunez, University of Michigan and gastroenterologist Judy Cho, University of Chicago, came to the same conclusion.2,3 Both identified a mutant NOD2 gene as a risk factor, which increases susceptibility to Crohn's disease. They also found that this mutation accounts for the condition in about 15 percent of Crohn's patients. They discussed their findings at the recent 2001 Digestive Disease Week conference in Atlanta.

This research, while not uncovering the etiology of Crohn's, which affects between 500,000 and 1 million Americans, strengthens the argument that environmental factors play a larger role than scientists previously thought. However, other work is showing that the case for an autoimmune basis is still strong, and Thomas' discovery apparently has not discouraged that line of thinking. Crohn's, which normally affects the ileum and causes, among other problems, abdominal pain, diarrhea, and sometimes fistulas, continues to prove itself a complex disease.

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