July 24 (HealthDay News) -- Researchers believe they have finally answered a basic question about the cause of celiac disease -- where in the body does the wheat protein gluten enter one's system?

A study published in the July issue of Gastroenterology identifies the CXCR3 receptor in the intestine as a gluten gateway. When people with celiac disease eat gluten, the protein triggers their immune system to attack the body, causing a wide range of serious health problems.

"This is a scientific question that had never been answered before," Dr. Alessio Fasano, medical director of the Center for Celiac Research at the University of Maryland School of Medicine, said in an university news release. "It is not only significant in the basic science of autoimmune disorders such as celiac disease, but in therapeutic approaches for the future. This opens a new scientific paradigm for the study of immunity."

The research team found that gliadin, the part of gluten that causes the most trouble for those with celiac disease, binds to the CXCR3 receptor. This results in the release of zonulin, a human protein that lowers the intestinal barrier to make it more permeable. While this effect is temporary in most people, the barrier stays down for long periods of time in people with celiac disease, causing disruption in the body's system.

The finding may help in research on the cause and treatment for other autoimmune diseases, Fasano said. People with type 1 diabetes and multiple sclerosis may experience a similar condition in which offending antigens enter the body through this gateway in the intestines.

"For the first time, we have evidence of how the foreign antigen gains access to the body, causing the autoimmune response," said Fasano, who is also a pediatric gastroenterologist at the University of Maryland Medical Center. "Further study is needed, but this could allow us to intervene before the zonulin is either released or activated, preventing the immune response altogether."

SOURCE: University of Maryland School of Medicine, news release, July 21, 2008