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In Vitro–Deranged Intestinal Immune Response to Gliadin in Type 1 Diabetes

¹ Department of Pediatrics and European Laboratory for the Investigation of Food-Induced Diseases, University "Federico II," Naples, Italy
² Department of Experimental Medicine, University "Federico II," Naples, Italy

Dietary gluten has been associated with an increased risk of type 1 diabetes. We have evaluated inflammation and the mucosal immune response to gliadin in the jejunum of patients with type 1 diabetes. Small intestinal biopsies from 17 children with type 1 diabetes without serological markers of celiac disease and from 50 age-matched control subjects were examined by immunohistochemistry. In addition, biopsies from 12 type 1 diabetic patients and 8 control subjects were cultured with gliadin or ovalbumin peptic-tryptic digest and examined for epithelial infiltration and lamina propria T-cell activation. The density of intraepithelial CD3⁺ and ⁺ cells and of lamina propria CD25⁺ mononuclear cells was higher in jejunal biopsies from type 1 diabetic patients versus control subjects. In the patients’ biopsies cultured with peptic-tryptic gliadin, there was epithelial infiltration by CD3⁺ cells, a significant increase in lamina propria CD25⁺ and CD80⁺ cells and enhanced expression of lamina propria CD54 and crypt HLA-DR. No such phenomena were observed in control subjects, even those with celiac disease–associated HLA haplotypes. In conclusion, signs of mucosal inflammation were present in jejunal biopsies from type 1 diabetic patients, and organ culture studies indicate a deranged mucosal immune response to gliadin.

Abbreviations: CD, celiac disease

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