Abstract
Celiac disease (CD) is an autoimmune-mediated enteropathy triggered by dietary gluten in genetically prone individuals. The current treatment for CD is a strict lifelong gluten-free diet. However, in some CD patients following a strict gluten-free diet, the symptoms do not remit. These cases may be refractory CD or due to gluten contamination; however, the lack of response could be related to other dietary ingredients, such as maize, which is one of the most common alternatives to wheat used in the gluten-free diet. In some CD patients, as a rare event, peptides from maize prolamins could induce a celiac-like immune response by similar or alternative pathogenic mechanisms to those used by wheat gluten peptides. This is supported by several shared features between wheat and maize prolamins and by some experimental results. Given that gluten peptides induce an immune response of the intestinal mucosa both in vivo and in vitro, peptides from maize prolamins could also be tested to determine whether they also induce a cellular immune response. Hypothetically, maize prolamins could be harmful for a very limited subgroup of CD patients, especially those that are non-responsive, and if it is confirmed, they should follow, in addition to a gluten-free, a maize-free diet.
Highlights
IntroductionCeliac disease (CD) is an immune-mediated enteropathy triggered by dietary wheat, rye and barley gluten (water-insoluble proteins) in genetically predisposed individuals [1]
Celiac disease (CD) is an immune-mediated enteropathy triggered by dietary wheat, rye and barley gluten in genetically predisposed individuals [1]
Intestinal mucosa damage in CD patients begins with an innate response that leads to a cellular immune response [3]
Summary
Celiac disease (CD) is an immune-mediated enteropathy triggered by dietary wheat, rye and barley gluten (water-insoluble proteins) in genetically predisposed individuals [1]. The damaged barrier allows the arrival of gliadin peptides to the lamina propria, where tissue transglutaminase (tTG) deamidates specific glutamine residues to confer an overall negative charge. These peptides are bound to the human leucocyte antigen (HLA) DQ2 or DQ8 molecules, in antigen presenting cells, which present them to T-cells to develop the full immune response required for CD [5]. CD symptoms disappear in the majority of patients after dietary gluten withdrawal; in some patients, the symptoms are still present even after they adopt a strict gluten-free diet [6] This is due to either refractory CD or to the presence of gluten as a contaminant or as a non-declared additive in foods [7]. In active CD, peptides derived from zeins could exacerbate the immune response in the intestinal mucosa, because they have sequence characteristics and/or electronegative residues that resemble gluten peptides
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