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 gammadelta(+) 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.