Findings Could Hold Significance for Other Autoimmune Disorders
A new study from researchers at the Center for Celiac Research at the University of Maryland School of Medicine answers a fundamental question relating to the cause of celiac disease and, possibly, other autoimmune disorders such as Type I diabetes and multiple sclerosis.
People with celiac disease must not eat foods containing gluten, a protein found in wheat. For them, gluten triggers an autoimmune response in which the immune system attacks the body, leading to a wide spectrum of serious health problems.
The new study, published in the July 2008 issue of the journal Gastroenterology, identifies the key gluten receptor in the intestine that opens the gateway through which gluten enters the body and triggers a faulty immune response in celiac patients.
The receptor, called CXCR3, is critical to the early stages of the faulty immune response. Pinpointing it could help doctors treat celiac disease more effectively, according to Alessio Fasano, M.D., professor of Pediatrics, Medicine and Physiology of the University of Maryland School of Medicine and medical director of the Center for Celiac Research.
“This is a scientific question that had never been answered before,” Dr. Fasano says. “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.”
There are three key components of celiac disease, according to Dr. Fasano. One is genes, and researchers have already identified a number of genes that seem common among celiac patients, but none that are consistently found in all patients.
The second component is the environmental trigger that leads to the autoimmune attack. Triggers have remained elusive for all autoimmune diseases except celiac disease, in which gluten is the undisputable trigger.
The third component is a leaky gut, wherein the barrier of the intestine becomes permeable enough to allow in the offending antigen — in this case, gluten, to come through.
Researchers at the Center for Celiac Research found that gliadin, the component of gluten that proves problematic for celiac patients, binds to the receptor called CXCR3.
This interaction between gliadin and CXCR3 triggers the release of a human protein called zonulin, which opens up the intestinal barrier to make it more permeable. In healthy patients, this effect is temporary. In celiac patients, the effect is long-term, and the results can be devastating.
The findings may be significant for other autoimmune disorders as well, Dr. Fasano says. The same process may occur in patients with Type I diabetes and multiple sclerosis, in which the intestines are the port of entry or the pathway through which the offending antigens in these and other autoimmune disorders get into the body, he explains.
“For the first time, we have evidence of how the foreign antigen gains access to the body, causing the autoimmune response,” according to Dr. 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.”
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