LETTER

Is gliadin really safe for non-coeliac individuals? Production of interleukin 15 in biopsy culture from non-coeliac individuals challenged with gliadin peptides

D Bernardo¹, J A Garrote², L Fernández-Salazar³, S Riestra⁴, E Arranz⁵

¹ Department of Paediatrics & Immunology, Mucosal Immunology Laboratory, IBGM-University of Valladolid, Valladolid, Spain
² Research Unit, Hospital Clínico Universitario, Valladolid, Spain
³ Depatment of Gastroenterology, Hospital Clínico Universitario, Valladolid, Spain
⁴ Digestive Service, Hospital Universitario Central de Asturias, Oviedo, Spain
⁵ Department of Paediatrics & Immunology, Mucosal Immunology Laboratory, IBGM-University of Valladolid, Valladolid, Spain

Correspondence to:
Correspondence to:
Dr E Arranz
Department of Paediatrics & Immunology, Mucosal Immunology Laboratory, IBGM-University of Valladolid, Spain. c/Ramón y Cajal, 7 47005, Valladolid, Spain; earranz@med.uva.es

The first 150 words of the full text of this article appear below.

Nowadays it is assumed that an innate immunity to gluten plays a key role in the development of coeliac disease (CD).¹ This innate response, mediated by interleukin (IL) 15 and elicited by "toxic peptides", like the 19-mer, through a DQ2-independent mechanism, induces epithelial stress and reprogrammes intraepithelial lymphocytes into natural killer (NK)-like cells² leading to enterocyte apoptosis and an increase in epithelium permeability. Thus, immunodominant peptides, like the 33-mer, can reach the lamina propria to trigger adaptive immunity. However, although an innate specific response in CD has been reported,³ no differential factors between patients with and without CD have been described controlling the innate immune response. Thus, since the toxic 19-mer elicits its harmful effect through a DQ2-independent mechanism, we hypothesise that the innate response is common in patients with and without CD, whereas the adaptive response is exclusive of susceptible patients with CD.

To test the hypothesis, biopsy cultures . . . [Full text of this article]

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