{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,14]],"date-time":"2026-08-14T12:37:28Z","timestamp":1786711048876,"version":"build-2736575974"},"reference-count":70,"publisher":"MDPI AG","issue":"16","license":[{"start":{"date-parts":[[2026,8,14]],"date-time":"2026-08-14T00:00:00Z","timestamp":1786665600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Nutrients"],"abstract":"<jats:p>Immune-mediated inflammatory diseases (IMIDs) arise from interactions among genetic susceptibility, epithelial barrier function, microbiota, diet, and other environmental exposures. Modern diets influence mucosal immunity not only through fibre intake, food processing, and microbiota composition, but also through a less explored exposure layer: plant-derived molecules with potential immune activity. Crop breeding, intensive agriculture, global trade, gluten-free substitutes, and plant-based food technologies have changed the spectrum, dose, concentration, and matrix in which plant defence proteins, antinutritional factors, endogenous toxicants, and novel plant antigens reach the intestinal surface. In this structured, hypothesis-generating narrative review, we propose dietary adjuvanticity as a mechanistic framework for considering how selected food-derived molecules may amplify mucosal immune responsiveness, modify antigen presentation, disturb barrier function, or lower tolerance thresholds without necessarily acting as classical autoantigens. The framework differs from general food-derived immunomodulation, nutritional exposomics, and diet-microbiota-host interaction models by focusing specifically on adjuvant-like immune amplification at the intestinal mucosa. The ASIA concept is used only in Shoenfeld\u2019s functional sense, as an analogy for exogenous immune amplification through innate activation, danger signalling, bystander activation, epitope spreading, and loss of tolerance in susceptible hosts; it is not applied as a dietary diagnosis. Wheat amylase-trypsin inhibitors, gluten epitopes, lectins, potato glycoalkaloids, saponins, quinoa prolamins, emerging legume proteins, L-canavanine, and tolerance-promoting plant substrates are discussed with explicit separation of established clinical evidence, strong mechanistic evidence, preclinical\/ex vivo evidence, and speculative disease-modifier hypotheses. Overall, plant-derived exposures are best interpreted as potential modifiers within the IMID exposome, not as primary causes of autoimmunity. Testing this model will require defined exposures, food-matrix and processing studies, biomarkers of barrier and immune activation, patient stratification, and controlled human studies.<\/jats:p>","DOI":"10.3390\/nu18162662","type":"journal-article","created":{"date-parts":[[2026,8,14]],"date-time":"2026-08-14T11:57:46Z","timestamp":1786708666000},"page":"2662","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Dietary Adjuvanticity in the Modern Plant Exposome: Implications for Immune-Mediated Inflammatory Diseases"],"prefix":"10.3390","volume":"18","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8200-6937","authenticated-orcid":false,"given":"Zsolt","family":"Barta","sequence":"first","affiliation":[{"name":"Department of Infectology, Faculty of Medicine, University of Debrecen, Bartok Bela U 2-26, 4031 Debrecen, Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0008-3355-492X","authenticated-orcid":false,"given":"Edit","family":"Posta","sequence":"additional","affiliation":[{"name":"Department of Infectology, Faculty of Medicine, University of Debrecen, Bartok Bela U 2-26, 4031 Debrecen, Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eva","family":"Gyarmati","sequence":"additional","affiliation":[{"name":"Department of Infectology, Faculty of Medicine, University of Debrecen, Bartok Bela U 2-26, 4031 Debrecen, Hungary"},{"name":"Doctoral School of Clinical Immunology and Allergology, Faculty of Medicine, University of Debrecen, Nagyerdei Krt. 98, 4032 Debrecen, Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Judit","family":"Baranyi","sequence":"additional","affiliation":[{"name":"Doctoral School of Health Sciences, University of Debrecen, Nagyerdei Krt. 98, 4032 Debrecen, Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-6204-815X","authenticated-orcid":false,"given":"Istvan","family":"Fekete","sequence":"additional","affiliation":[{"name":"Institute of Food Technology, Faculty of Agricultural and Food Sciences and Environmental Management, University of Debrecen, Boszormenyi Ut 138, 4032 Debrecen, Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eva","family":"Zold","sequence":"additional","affiliation":[{"name":"Department of Clinical Immunology, Institute of Internal Medicine, Faculty of Medicine, University of Debrecen, Moricz Zsigmond Krt. 22, 4032 Debrecen, Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2026,8,14]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"1878","DOI":"10.1016\/S0140-6736(23)00457-9","article-title":"Incidence, prevalence, and co-occurrence of autoimmune disorders over time and by age, sex, and socioeconomic status: A population-based cohort study of 22 million individuals in the UK","volume":"401","author":"Conrad","year":"2023","journal-title":"Lancet"},{"key":"ref_2","first-page":"132","article-title":"Global prevalence and incidence of inflammatory bowel disease: A systematic review and meta-analysis of population-based studies","volume":"18","author":"Heydari","year":"2025","journal-title":"Gastroenterol. 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