A peculiar characteristic of this cereal is the high food tolerability. In the last few years numerous experimental evidences of the reduced toxicity of the monococcus wheat prolamins have been obtained. In particular, the prolamins of this cereal are not able to induce lesions in the intestinal mucosa of celiac patients (Auricchio et al., 1982; De Vincenzi et al., 1995; 1996) and to agglutinate K562 (S) cells, a in vitro tests strongly correlated with the “toxicity” of the prolaminic peptides. Furthermore, T. monococcum accessions of immuno-dominant sequences able to stimulate T lymphocytes have been identified (Molberg et al., 2005; Spaenij-Dekking et al., 2005; Zanini et al., 2013). Recently, Gianfrani et al. (2012) reported the results of a study on two monococcus wheat genotypes, Monlis and ID331, compared with the variety of tender wheat Sagittarius. However, while the proliferates of Sagittarius and Monlis, a variety of monococcus wheat free of ω-gliadins, are able to promote the proliferation of enterocytes in the crypts of the mucous membranes of celiac patients and to induce the synthesis of interliquine 15 (IL- 15) in intestinal villi enterocytes, ID321 prolamins, a monococcus wheat line containing only one ω-gliadin, show no effect. The results suggest that Monlis is able to activate innate immunity and promote the synthesis of interleukin 15 (IL-15), a key molecule in the induction of adaptive immunity, while ID331 does not seem capable of eliciting this type of immune response. All this is in agreement with the observation that the prolamins of the Monlis variety and other monococcus wheat genotypes without ω-gliadin behave like the prolamins of soft wheat in their ability to agglutinate K562 (S) cells and alter the intestinal epithelium. These rare toxic genotypes of monococcus wheat (<2%) differ from the others due to the peculiarity of not producing ω-gliadins, in which sequences able to counteract the toxicity of the other prolamins seem to be present. Although monococcus wheat proteins show reduced cytoxicity towards intestinal cells, the presence of immune-dominant epitopes precludes their use in the celiac diet.On the other hand, considering that the incidence and severity of celiac disease depends on the quantity and the harmfulness of the prolamins and that some monococcus wheat genotypes have a high bread making quality coupled with absence of cytotoxicity and reduced immunogenicity, it is expected that use of monococcus flours in the diet of the general population, in which there is a high percentage of individuals genetically predisposed to celiac disease but not yet celiac, can help to contain the spread of this form of food intolerance. This suggests that the monococcus wheat, recently reported in cultivation in Italy by researchers of the Council for Research and Experimentation in Agriculture (CRA) of Rome and San Angelo Lodigiano, will play an important role in the prevention of celiac disease, both directly in the form of bread and pasta both indirectly as a model species for the study of the role of innate immunity in the onset of celiac disease. FROM: The new frontiers of food technologies and the celiac disease Norberto Pogna, Laura Gazza (2013). Volume 212, 1 December 2016, Pages 537-542 Further confirmations were highlighted by the research: Protective effects of ID331 Triticum monococcum gliadin on in vitro models of the intestinal epithelium. Giuseppe Jacomino et al. 2016. Highlights: • ID331 gliadins do not enhance permeability and do not induce zonulin release. • ID331 gliadins do not trigger cytotoxicity or cytoskeleton reorganization. • ID331 gastrointestinal digestion releases ω (105-123) bioactive peptide. • ω (105-123) exerts a protective action against the toxicity induced by T. aestivum. Abstract A growing interest in developing new strategies due to coeliac disease. In the current study, we investigate the biological effects of ID331 Triticum monococcum gliadin-derived peptides in human Caco-2 intestinal epithelial cells. Triticum aestivum gliadin derived peptides were used as a positive control. The effects on epithelial permeability, zonulin release, viability, and cytoskeleton reorganization were investigated. Our findings confirmed that ID331 gliadin did not enhance permeability and did not induce zonulin release, cytotoxicity or cytoskeleton reorganization of Caco-2 cell monolayers. We also demonstrated that ID331 ω-gliadin and its derived peptide ω (105-123) exerted to protective action, mitigating the injury of Triticum aestivum gliadin on cell viability and cytoskeleton reorganization. These results may represent a new opportunity for the future development of innovative strategies to reduce gluten toxicity in the diet of patients with gluten intolerance.