MiR-210 is induced by Oct-2, regulates B cells, and inhibits autoantibody production.

MiR-210 is induced by Oct-2, regulates B cells, and inhibits autoantibody production.
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DOI:
10.4049/jimmunol.1301289
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发表时间:
2013-09-15
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
通讯作者:
Smith KGC
Smith KGC
中科院分区:
其他
文献类型:
--
作者:
Mok Y;Schwierzeck V;Thomas DC;Vigorito E;Rayner TF;Jarvis LB;Prosser HM;Bradley A;Withers DR;Mårtensson IL;Corcoran LM;Blenkiron C;Miska EA;Lyons PA;Smith KGC

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MicroRNAs are small, non-coding RNAs that regulate gene expression post-transcriptionally. Here, 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 months of age. Overexpression of miR-210 in vivo resulted in cell autonomous expansion of the B1 lineage and impaired fitness of B2 cells. Mice over-expressing miR-210 exhibited impaired class-switched antibody responses, a finding confirmed in wild-type B-cells transfected with a miR-210 mimic. In vitro studies demonstrated a defect in cellular proliferation and cell-cycle entry, which was consistent with the transcriptomic analysis demonstrating down-regulation 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.
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