MiR-210 Is Induced by Oct-2, Regulates B Cells, and Inhibits Autoantibody Production
- Author(s)
- Mok, YT; Schwierzeck, V; Thomas, DC; Vigorito, E; Rayner, TF; Jarvis, LB; Prosser, HM; Bradley, A; Withers, DR; Martensson, IL; Corcoran, LM; Blenkiron, C; Miska, EA; Lyons, PA; Smith, KGC;
- Details
- Publication Year 2013-09-15,Volume 191,Issue #6,Page 3037-3048
- Journal Title
- JOURNAL OF IMMUNOLOGY
- Publication Type
- Journal Article
- Abstract
- MicroRNAs (MiRs) are small, noncoding RNAs that regulate gene expression posttranscriptionally. In this study, we show that MiR-210 is induced by Oct-2, a key transcriptional mediator of B cell activation. Germline deletion of MiR-210 results in the development of autoantibodies from 5 mo of age. Overexpression of MiR-210 in vivo resulted in cell autonomous expansion of the B1 lineage and impaired fitness of B2 cells. Mice overexpressing MiR-210 exhibited impaired class-switched Ab responses, a finding confirmed in wild-type B cells transfected with a MiR-210 mimic. In vitro studies demonstrated defects in cellular proliferation and cell cycle entry, which were consistent with the transcriptomic analysis demonstrating downregulation of genes involved in cellular proliferation and B cell activation. These findings indicate that Oct-2 induction of MiR-210 provides a novel inhibitory mechanism for the control of B cells and autoantibody production.
- Publisher
- AMER ASSOC IMMUNOLOGISTS
- Keywords
- INDUCED CYTIDINE DEAMINASE; GENE-EXPRESSION; LYMPHOCYTE LINEAGE; MICROARRAY DATA; CD40 LIGAND; MICRORNAS; ACTIVATION; DIFFERENTIATION; TRANSCRIPTION; PROGRESSION
- Research Division(s)
- Molecular Immunology
- Link To PubMed Central Version
- http://www.ncbi.nlm.nih.gov.ezp.lib.unimelb.edu.au/pmc/articles/PMC4162006/
- Publisher's Version
- https://doi.org/10.4049/jimmunol.1301289
- Terms of Use/Rights Notice
- Copyright ©2014 by The American Association of Immunologists, Inc. All rights reserved
Creation Date: 2013-09-15 12:00:00