{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Serr I"],"funding":["Kompetenznetz Diabetes mellitus","German Center for Diabetes Research","Deutsche Forschungsgemeinschaft","Juvenile Diabetes Research Foundation","National Research Foundation of Korea","National Institutes of Health","Clinical Research Unit 257 CEDER","German Federal Ministry of Education and Research"],"pagination":["eaag1782"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5828501"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(422)"],"pubmed_abstract":["Molecular checkpoints that trigger the onset of islet autoimmunity or progression to human type 1 diabetes (T1D) are incompletely understood. Using T cells from children at an early stage of islet autoimmunity without clinical T1D, we find that a microRNA181a (miRNA181a)-mediated increase in signal strength of stimulation and costimulation links nuclear factor of activated T cells 5 (NFAT5) with impaired tolerance induction and autoimmune activation. We show that enhancing miRNA181a activity increases NFAT5 expression while inhibiting FOXP3+ regulatory T cell (Treg) induction in vitro. Accordingly, Treg induction is improved using T cells from NFAT5 knockout (NFAT5ko) animals, whereas altering miRNA181a activity does not affect Treg induction in NFAT5ko T cells. Moreover, high costimulator"],"journal":["Science translational medicine"],"pubmed_title":["A miRNA181a/NFAT5 axis links impaired T cell tolerance induction with autoimmune type 1 diabetes."],"pmcid":["PMC5828501"],"funding_grant_id":["award309930","JDRF 17-2012-16","JDRF 2-SRA-2014-161-Q-R","award309935","award309924","award309936","award309937","UC4DK112217","award309938","award309931","award309932","award309933","2015R1A3A2032927","award309923","award309934","FKZ 01GI0805-07","WE 4656/2","award309929","JDRF 6-2012-20","FKZ 01GI0805","CRC1054 B11","CRC1811 B02"],"pubmed_authors":["Kuper C","Becker M","Loretz B","Waisman A","Scherm MG","Flynn VK","Spornraft M","Haase B","Gerlach K","Segars J","Kalin S","Hippich M","Kaestner KH","Ziegler AG","Palmisano R","Kim WU","Daniel C","Kirchner B","Zahm AM","Lehr CM","Achenbach P","Schug J","Nikolaev A","Liebsch N","Willis RA","Serr I","Weigmann B"],"additional_accession":[]},"is_claimable":false,"name":"A miRNA181a/NFAT5 axis links impaired T cell tolerance induction with autoimmune type 1 diabetes.","description":"Molecular checkpoints that trigger the onset of islet autoimmunity or progression to human type 1 diabetes (T1D) are incompletely understood. Using T cells from children at an early stage of islet autoimmunity without clinical T1D, we find that a microRNA181a (miRNA181a)-mediated increase in signal strength of stimulation and costimulation links nuclear factor of activated T cells 5 (NFAT5) with impaired tolerance induction and autoimmune activation. We show that enhancing miRNA181a activity increases NFAT5 expression while inhibiting FOXP3+ regulatory T cell (Treg) induction in vitro. Accordingly, Treg induction is improved using T cells from NFAT5 knockout (NFAT5ko) animals, whereas altering miRNA181a activity does not affect Treg induction in NFAT5ko T cells. Moreover, high costimulator","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Jan","modification":"2025-04-18T23:20:30.534Z","creation":"2019-03-26T23:04:02Z"},"accession":"S-EPMC5828501","cross_references":{"pubmed":["29298866"],"doi":["10.1126/scitranslmed.aag1782"]}}