New research may help patients get diagnosed with celiac disease sooner, cutting down on the average time of 10 years to get an accurate diagnosis. A study published in the July 2008 issue of the journal Gastroenterology finds and identifies a key gluten receptor in the small intestine that opens the gateway through which gluten enters the body and triggers the immune response in celiac patients.
The study was conducted by researchers at the University of Maryland School of Medicine’s Center for Celiac Research and led by Dr. Alessio Fasano, professor of Pediatrics, Medicine and Physiology for the center.
According to the researchers, the study answers a “fundamental question relating to the cause of celiac disease and , possibly other autoimmune disorders such as Type 1 diabetes and multiple sclerosis.”
Dr. Fasano says that the identified receptor--known as CXCR3--is “critical to the early stages of the faulty immune response” and notes that its discovery could help physicians treat celiac disease more effectively.
According to the study, gliadin--the part of gluten that causes a problem for patients with celiac disease--binds to the CXCR3 receptor. The interaction between the two (gliadin and CXCR3) leads to the release of a protein called zonulin. This protein “opens the intestinal barrier to make it more permeable.”
For healthy patients the reaction is temporary and non-harmful, but for people with celiac disease the long-term damage can be detrimental.
Dr. Fasano says the same process may occur in patients with multiple sclerosis and type 1 diabetes. “For the first time, we have evidence of how the foreign antigen gains access to the body, causing the autoimmune response.
He notes that additional research is necessary, but adds that the findings could help prevent the immune response amongst patients with celiac and other diseases in the future.
In an article published in the Baltimore Sun, Dr. Peter Green, the director of the Celiac Disease Center at Columbia University and a spokesman for the American Gastroenterological Association commented on the study, saying it is “extensive and well-designed,” but notes that it remains “unclear how this research fits into scientists’ understanding of all the mechanisms of damage in celiac disease, because it involves various pathways.”