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Dutch Researchers Discover Grain Protein Homology Responsible for Toxicity in Celiacs
In 1994 I was diagnosed with celiac disease, which led me to create Celiac.com in 1995. I created this site for a single purpose: To help as many people as possible with celiac disease get diagnosed so they can begin to live happy, healthy gluten-free lives. Celiac.com was the first site on the Internet dedicated solely to celiac disease. In 1998 I foundedÂ The Gluten-Free Mall, Your Special Diet Superstore!, and I am the co-author of the book Cereal Killers, and founder and publisher of Journal of Gluten Sensitivity.View all articles by Scott Adams
Gastroenterology, Oct 2003, Vol 125, No 4, p1105-13
Celiac.com 10/30/2003 – It has long been known that celiac disease is caused by T-cell responses to wheat gluten-derived peptides, but the toxicity of other widely consumed grains has not been well studied. The researchers who conducted this study were aimed at determining the toxic T-cell stimulatory properties of barley hordeins, rye secalins, and oat avenins. Except for one instance, they found that there were no identical T-cell stimulatory gluten peptide matches in these grains. There were, however, similar responses found in "11 homologous sequences in hordeins, secalins, and avenins located in regions similar to those in the original gluten proteins," and seven of the 11 peptides were recognized by gluten-specific T-cell lines and/or clones from patients with celiac disease. The team discovered that key amino acids can be substituted, which will either partially or totally stop the T-cell stimulation by the gluten peptides, and that "single nucleotide substitutions in gluten genes will suffice to induce these effects."
The researchers conclude: "These results show that the disease-inducing properties of barley and rye can in part be explained by T-cell cross-reactivity against gluten-, secalin-, and hordein-derived peptides. Moreover, the results provide a first step toward a rational strategy for gluten detoxification via targeted mutagenesis at the genetic level."
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