Abstract
The peptic-tryptic-cotazym digest of a wheat gliadin was fractionated into ten primary fractions. Subfraction 2R of fraction 9 is known to be toxic to patients with coeliac disease. Fraction 9 and subfraction 2R also agglutinate K562(S) cells, previously shown to be a good indication of toxicity to in vitro intestinal bioptic specimens from coeliac patients. Subfraction 2R was still able to agglutinate K562(S) cells after digestion by morphologically normal small intestinal mucosa of coeliacs in remission, but was inactivated after digestion by normal mucosa. These results are consistent with the hypothesis that there is a mucosal defect in handling gliadin peptides in coeliac patients, and suggest that there is either a primary (or secondary) enzyme deficiency, or some other mechanism, operating in the intestinal mucosa of coeliac patients in remission.
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