Maize prolamins could induce a gluten-like cellular immune response in some celiac disease patients.

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.

Bovine milk caseins and transglutaminase-treated cereal prolamins are differentially recognized by IgA of celiac disease patients according to their age.

The prevalence of celiac disease (CD) has increased worldwide, which could be related to some dietary proteins in infant regimens and/or new food processes, affecting CD-predisposed infants and older children or adults differentially. IgA reactivity to human and bovine caseins, as well as yogurt caseins and prolamins from wheat or maize breads, microbial transglutaminase (mTG)-treated or not, was evaluated in three patient groups: G1, <2 years old; G2, approximately 3 years old; and G3 >8 years old. Human caseins were not recognized by IgA, whereas IgA reactivity of G2 and G3 was higher to bovine milk caseins. Immunoreactivity of G1 to yogurt caseins was lower and comparable to controls, with no effects due to mTG treatment. However, mTG treatment increased reactivity of G3 to wheat and maize prolamins. IgA immunoreactivity of CD patients to caseins and mTG-treated or not prolamins was age-dependent, which could reflect a differential manifestation of the effects of such proteins on the intestinal barrier.