Journal article

MiR-210 Is Induced by Oct-2, Regulates B Cells, and Inhibits Autoantibody Production

Yingting Mok, Vera Schwierzeck, David C Thomas, Elena Vigorito, Tim F Rayner, Lorna B Jarvis, Haydn M Prosser, Allan Bradley, David R Withers, Inga-Lill Martensson, Lynn M Corcoran, Cherie Blenkiron, Eric A Miska, Paul A Lyons, Kenneth GC Smith

JOURNAL OF IMMUNOLOGY | AMER ASSOC IMMUNOLOGISTS | Published : 2013

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 transcript..

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University of Melbourne Researchers

Grants

Awarded by Wellcome Trust


Awarded by Cancer Research UK


Awarded by National Institute for Health Research


Funding Acknowledgements

This work was supported by the Agency for Science, Technology and Research, Singapore (to Y.M.), the Biomedical Research Centre Clinical Research Fellowship (to V.S.), Wellcome Trust Programme Grant 06753AIA (to K.G.C.S.), the National Institute for Health Research Cambridge Biomedical Research Centre (to K.G.C.S.), the Biotechnology and Biological Sciences Research Council and the Medical Research Council (to E.V.), and Wellcome Trust Grant WT098051 (to A.B. and H.M.P).