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Regulation of B-cell development and tolerance by different members of the miR-17∼92 family microRNAs

Author

Listed:
  • Maoyi Lai

    (The Scripps Research Institute)

  • Alicia Gonzalez-Martin

    (The Scripps Research Institute)

  • Anthony B. Cooper

    (The Scripps Research Institute
    Present address: Adimab, 7 Lucent Drive, Lebanon, New Hampshire 03766, USA)

  • Hiroyo Oda

    (The Scripps Research Institute
    Present address: Department of Immunology and Pathology, Research Institute, National Center for Global Health and Medicine, 1-7-1, Konodai, Ichikawa-shi, Chiba 272-8516, Japan)

  • Hyun Yong Jin

    (The Scripps Research Institute
    Kellogg School of Science and Technology, The Scripps Research Institute)

  • Jovan Shepherd

    (The Scripps Research Institute)

  • Linling He

    (The Scripps Research Institute)

  • Jiang Zhu

    (The Scripps Research Institute)

  • David Nemazee

    (The Scripps Research Institute)

  • Changchun Xiao

    (The Scripps Research Institute)

Abstract

The molecular mechanisms that regulate B-cell development and tolerance remain incompletely understood. In this study, we identify a critical role for the miR-17∼92 microRNA cluster in regulating B-cell central tolerance and demonstrate that these miRNAs control early B-cell development in a cell-intrinsic manner. While the cluster member miR-19 suppresses the expression of Pten and plays a key role in regulating B-cell tolerance, miR-17 controls early B-cell development through other molecular pathways. These findings demonstrate differential control of two closely linked B-cell developmental stages by different members of a single microRNA cluster through distinct molecular pathways.

Suggested Citation

  • Maoyi Lai & Alicia Gonzalez-Martin & Anthony B. Cooper & Hiroyo Oda & Hyun Yong Jin & Jovan Shepherd & Linling He & Jiang Zhu & David Nemazee & Changchun Xiao, 2016. "Regulation of B-cell development and tolerance by different members of the miR-17∼92 family microRNAs," Nature Communications, Nature, vol. 7(1), pages 1-13, November.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12207
    DOI: 10.1038/ncomms12207
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