{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Stephen-Victor E"],"funding":["NIDDK NIH HHS","NIAID NIH HHS","NIGMS NIH HHS"],"pagination":["760-768"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11996044"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["638(8051)"],"pubmed_abstract":["Tolerance to dietary antigens is critical for avoiding deleterious type 2 immune responses resulting in food allergy (FA) and anaphylaxis<sup>1,2</sup>. However, the mechanisms resulting in both the maintenance and failure of tolerance to food antigens are poorly understood. Here we demonstrate that the goblet-cell-derived resistin-like molecule β (RELMβ)<sup>3,4</sup> is a critical regulator of oral tolerance. RELMβ is abundant in the sera of both patients with FA and mouse models of FA. Deletion of RELMβ protects mice from FA and the development of food-antigen-specific IgE and anaphylaxis. RELMβ disrupts food tolerance through the modulation of the gut microbiome and depletion of indole-metabolite-producing Lactobacilli and Alistipes. Tolerance is maintained by the local production of i"],"journal":["Nature"],"pubmed_title":["RELMβ sets the threshold for microbiome-dependent oral tolerance."],"pmcid":["PMC11996044"],"funding_grant_id":["R01 AI065617","R01 AI126915","U01 AI143514","R01 AI158814","R01 AI171100","DP2 GM136652","P30 DK034854","K23 AI155940","U01 AI160087"],"pubmed_authors":["Kuziel GA","Zeve D","Schmitz-Abe K","Farraj FA","Abdel-Gadir A","Fong J","Saint-Denis E","Chatila TA","Stephen-Victor E","Breault DT","Rakoff-Nahoum S","Martinez-Blanco M","Wang Z","Chang I","Zhang A","Chen Q","Lozano GL","Benamar M","Holder-Niles F","Nadeau KC","Jugder BE","Cui Y","Rachid R","Crestani E","Phipatanakul W"],"additional_accession":[]},"is_claimable":false,"name":"RELMβ sets the threshold for microbiome-dependent oral tolerance.","description":"Tolerance to dietary antigens is critical for avoiding deleterious type 2 immune responses resulting in food allergy (FA) and anaphylaxis<sup>1,2</sup>. However, the mechanisms resulting in both the maintenance and failure of tolerance to food antigens are poorly understood. Here we demonstrate that the goblet-cell-derived resistin-like molecule β (RELMβ)<sup>3,4</sup> is a critical regulator of oral tolerance. RELMβ is abundant in the sera of both patients with FA and mouse models of FA. Deletion of RELMβ protects mice from FA and the development of food-antigen-specific IgE and anaphylaxis. RELMβ disrupts food tolerance through the modulation of the gut microbiome and depletion of indole-metabolite-producing Lactobacilli and Alistipes. Tolerance is maintained by the local production of i","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Feb","modification":"2026-03-18T13:33:32.487Z","creation":"2025-08-18T09:54:05.856Z"},"accession":"S-EPMC11996044","cross_references":{"pubmed":["39843735"],"doi":["10.1038/s41586-024-08440-7"]}}