Digging Deeper into Gluten Intolerance:
Researchers have pinpointed the molecular cause of the immune reaction that triggers celiac disease, the digestive condition that makes people intolerant to the protein gluten, which is found in bread, cereal, pasta, cookies, beer, and many other foods containing wheat, barley or rye. The findings may help create ways to diagnose, prevent and treat celiac disease, especially in genetically susceptible people. In individuals with celiac disease, eating foods containing gluten causes an immune reaction that damages the villi—hair-like projections that line the small intestine and snatch up vitamins, minerals and other nutrients from food. After a while, the inability to absorb proper amounts of nutrients can cause vitamin deficiencies that affect the brain, nervous system, bones, liver and other organs of celiac disease patients. So far, the only way to manage the disease is lifelong exclusion of food containing gluten. Even then, recovery of the intestine is often compromised by trace gluten contamination. For example, about half of all adults with celiac disease still have intestinal damage five years after adopting a gluten-free diet.
Over the last sixty years since gluten was discovered to be the environmental cause of celiac disease, there has been a search for the toxic gluten peptide or peptides causing celiac disease. Now, Jason Tye-Din and colleagues have profiled the immune responses of over 200 volunteers with celiac disease, ten times more than in previous studies. The researchers developed a simple algorithm to screen thousands of peptides— molecules that make up the building blocks of proteins--in individual patients who ate wheat, barley or rye for three days to activate their immune response to gluten. They found that a formerly overlooked peptide is responsible for the shared toxicity of wheat, barley and rye. Equally important, they found that immune cells called T cells that are specific for just three gluten peptides are responsible for most of the immune response to gluten. The findings support the longstanding but unproven hypothesis that celiac disease is caused by pathogenic T-cells being highly focused on just a few master peptides.
Article: "Comprehensive, Quantitative Mapping of T Cell Epitopes in Gluten During Celiac Disease," by J.A. Tye-Din; J.A. Stewart; J.A. Dromey; T. Beissbarth; S.I. Mannering; R.P. Anderson at The Walter and Eliza Hall Institute of Medical Research in Parkville, VIC, Australia; J.A. Tye-Din; J. McCluskey at The University of Melbourne in Parkville, VIC, Australia; J.A. Tye-Din; R.P. Anderson at The Royal Melbourne Hospital in Parkville, VIC, Australia; D.A. van Heel at Queen Mary University of London in London, UK; A. Tatham at University of Wales Institute in Cardiff, UK; K. Henderson; J. Rossjohn at Monash University in Clayton, VIC, Australia; C. Gianfrani at Institute of Food Science-CNR (National Research Council) in Avellino, Italy; D.P. Jewell; A.V.S. Hill at University of Oxford in Oxford, UK.
Contact: Robert Anderson at +61-3-93-45-24-58 (phone), +61-4-15-38-83-54 (cell), or banderson@wehi.edu.au (email).
Visuals: Related visuals are available at http://www.eurekalert.org/jrnls/scitransmed/ and http://www.eurekalert.org/jrnls/sci/
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