{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["Xu X"],"funding":["Intramural NIH HHS","NEI NIH HHS"],"pubmed_abstract":["Commensals shape host physiology through molecular crosstalk with host receptors. Identifying specific microbial factors that causally influence host immunity is key to understanding homeostasis at the host-microbe interface and advancing microbial-based therapeutics. Here, we identify trehalose monocorynomycolate (TMCM) from <i>Corynebacterium mastitidis</i> (<i>C. mast</i>) as a potent stimulator of IL-17 production by γδ T cells at the ocular surface. Mechanistically, TMCM-driven IL-17 responses require both IL-1 signals and γδ TCR signaling, which also supports endogenous γδ T cell IL-1R1 expression. Notably, synthetic TMCM alone is sufficient to mimic the effect of <i>C. mast</i> in inducing γδ T cell immunity and protect against pathogenic corneal infection. Our findings establish TM"],"journal":["bioRxiv : the preprint server for biology"],"pagination":["2025.03.17.643820"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11956969"],"repository":["biostudies-literature"],"pubmed_title":["Commensal-derived Trehalose Monocorynomycolate Triggers γδ T Cell-driven Protective Ocular Barrier Immunity."],"pmcid":["PMC11956969"],"funding_grant_id":["U24 EY035102","P30 EY008098","T32 EY017271","Z01 EY000184","R01 EY032482"],"pubmed_authors":["Brandes NT","Gaud G","Schwarz B","Carr M","Shane J","Mattapallil MJ","Jiang T","Peng Z","Richards C","Gupta A","Caspi RR","Love PE","Guo J","Jittayasothorn Y","Xu B","Rigas YE","Magone MT","Xu X","Nagarajan V","St Leger AJ","Zhang A","Bohrnsen E"],"additional_accession":[]},"is_claimable":false,"name":"Commensal-derived Trehalose Monocorynomycolate Triggers γδ T Cell-driven Protective Ocular Barrier Immunity.","description":"Commensals shape host physiology through molecular crosstalk with host receptors. Identifying specific microbial factors that causally influence host immunity is key to understanding homeostasis at the host-microbe interface and advancing microbial-based therapeutics. Here, we identify trehalose monocorynomycolate (TMCM) from <i>Corynebacterium mastitidis</i> (<i>C. mast</i>) as a potent stimulator of IL-17 production by γδ T cells at the ocular surface. Mechanistically, TMCM-driven IL-17 responses require both IL-1 signals and γδ TCR signaling, which also supports endogenous γδ T cell IL-1R1 expression. Notably, synthetic TMCM alone is sufficient to mimic the effect of <i>C. mast</i> in inducing γδ T cell immunity and protect against pathogenic corneal infection. Our findings establish TM","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2026-04-14T03:24:34.677Z","creation":"2025-07-05T03:04:33.783Z"},"accession":"S-EPMC11956969","cross_references":{"pubmed":["40166223"],"doi":["10.1101/2025.03.17.643820"]}}