LAUSR

Wheat is the most important source of carbohydrate in the Western world with a constant increase in sales also in Eastern societies. Since gluten comprises 80% of the contemporary wheat proteins and is also heavily used as a food additive in the processed food industries, no doubt that its consumption is surging [1], in parallel to the increased prevalence in multiple autoimmune diseases (ADs), at list in recent decades [2]. Interestingly, an 8-fold increase in the wheat gluten content was observed, since it discovery around 15,000 years ago, in the Middle East Fertile Crescent. Owing to its evolutionary increased wheat content, its augmented immunogenicity and toxicity, and its multiple detrimental effects, gluten might be associated to some modern chronic disease development [1–3]. Being an ideal substrate for exand in-vivo enzymatic post translational modification of proteins, thus inducing physico-chemical and 3-dimensional changes, turning naive gluten to a neo-epitope peptide, the transformed gluten becomes a prime candidate to drive autoimunogenesis [1,3–6]. In fact, despite its popular use in food, gluten appears to have multiple side effects: increases intestinal permeability, changes composition and diversity of the microbiome/dysbiome ratio, increases oxidative stress, and changes epigenetic processes. Gluten was shown to be immunogenic, cytotoxic, proapoptotic, and proinflammatory. At the cellular level, it decreases cell differentiation and viability [3]. The above-mentioned background on wheat, gluten, and ADs sets the stage for the topic of the present editorial, trying to answer three important questions: