<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Tai N</submitter><funding>NCATS NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>Iacocca Family Foundation</funding><funding>Juvenile Diabetes Research Foundation</funding><funding>National Institutes of Health</funding><pagination>2129-46</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5030808</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>213(10)</volume><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</pubmed_abstract><journal>The Journal of experimental medicine</journal><pubmed_title>Microbial antigen mimics activate diabetogenic CD8 T cells in NOD mice.</pubmed_title><pmcid>PMC5030808</pmcid><funding_grant_id>DK100500</funding_grant_id><funding_grant_id>P30 DK045735</funding_grant_id><funding_grant_id>R01 DK092882</funding_grant_id><funding_grant_id>DK092882</funding_grant_id><funding_grant_id>R01 DK100500</funding_grant_id><funding_grant_id>DK088181</funding_grant_id><funding_grant_id>2015-136</funding_grant_id><funding_grant_id>P30 DK945735</funding_grant_id><funding_grant_id>UL1 TR001863</funding_grant_id><funding_grant_id>R01 DK088181</funding_grant_id><pubmed_authors>Hu Y</pubmed_authors><pubmed_authors>Wen L</pubmed_authors><pubmed_authors>Tai N</pubmed_authors><pubmed_authors>Zhang X</pubmed_authors><pubmed_authors>Chen L</pubmed_authors><pubmed_authors>Wong FS</pubmed_authors><pubmed_authors>Gulden E</pubmed_authors><pubmed_authors>Peng J</pubmed_authors><pubmed_authors>Liu F</pubmed_authors></additional><is_claimable>false</is_claimable><name>Microbial antigen mimics activate diabetogenic CD8 T cells in NOD mice.</name><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</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Sep</publication><modification>2025-04-20T00:36:22.155Z</modification><creation>2021-02-20T09:36:11Z</creation></dates><accession>S-EPMC5030808</accession><cross_references><pubmed>27621416</pubmed><doi>10.1084/jem.20160526</doi></cross_references></HashMap>