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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 were taken from at least three patients with CD who are on a gluten-free diet (GFD) and three patients without …
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