{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tai N"],"funding":["NCATS NIH HHS","NIDDK NIH HHS","Iacocca Family Foundation","Juvenile Diabetes Research Foundation","National Institutes of Health"],"pagination":["2129-46"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5030808"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["213(10)"],"pubmed_abstract":["Both animal model and human studies indicate that commensal bacteria may modify type 1 diabetes (T1D) development. However, the underlying mechanisms by which gut microbes could trigger or protect from diabetes are not fully understood, especially the interaction of commensal bacteria with pathogenic CD8 T cells. In this study, using islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP)-reactive CD8 T cell receptor NY8.3 transgenic nonobese diabetic mice, we demonstrated that MyD88 strongly modulates CD8(+) T cell-mediated T1D development via the gut microbiota. Some microbial protein peptides share significant homology with IGRP. Both the microbial peptide mimic of Fusobacteria and the bacteria directly activate IGRP-specific NY8.3 T cells and promote diabetes deve"],"journal":["The Journal of experimental medicine"],"pubmed_title":["Microbial antigen mimics activate diabetogenic CD8 T cells in NOD mice."],"pmcid":["PMC5030808"],"funding_grant_id":["DK100500","P30 DK045735","R01 DK092882","DK092882","R01 DK100500","DK088181","2015-136","P30 DK945735","UL1 TR001863","R01 DK088181"],"pubmed_authors":["Hu Y","Wen L","Tai N","Zhang X","Chen L","Wong FS","Gulden E","Peng J","Liu F"],"additional_accession":[]},"is_claimable":false,"name":"Microbial antigen mimics activate diabetogenic CD8 T cells in NOD mice.","description":"Both animal model and human studies indicate that commensal bacteria may modify type 1 diabetes (T1D) development. However, the underlying mechanisms by which gut microbes could trigger or protect from diabetes are not fully understood, especially the interaction of commensal bacteria with pathogenic CD8 T cells. In this study, using islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP)-reactive CD8 T cell receptor NY8.3 transgenic nonobese diabetic mice, we demonstrated that MyD88 strongly modulates CD8(+) T cell-mediated T1D development via the gut microbiota. Some microbial protein peptides share significant homology with IGRP. Both the microbial peptide mimic of Fusobacteria and the bacteria directly activate IGRP-specific NY8.3 T cells and promote diabetes deve","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Sep","modification":"2025-04-20T00:36:22.155Z","creation":"2021-02-20T09:36:11Z"},"accession":"S-EPMC5030808","cross_references":{"pubmed":["27621416"],"doi":["10.1084/jem.20160526"]}}