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IgD attenuates the IgM-induced anergy response in transitional and mature B cells

Author

Listed:
  • Zahra Sabouri

    (John Curtin School of Medical Research, The Australian National University)

  • Samuel Perotti

    (John Curtin School of Medical Research, The Australian National University)

  • Emily Spierings

    (John Curtin School of Medical Research, The Australian National University)

  • Peter Humburg

    (The Garvan Institute of Medical Research)

  • Mehmet Yabas

    (John Curtin School of Medical Research, The Australian National University
    Trakya University)

  • Hannes Bergmann

    (John Curtin School of Medical Research, The Australian National University)

  • Keisuke Horikawa

    (John Curtin School of Medical Research, The Australian National University)

  • Carla Roots

    (John Curtin School of Medical Research, The Australian National University)

  • Samantha Lambe

    (John Curtin School of Medical Research, The Australian National University)

  • Clara Young

    (John Curtin School of Medical Research, The Australian National University)

  • T. Dan Andrews

    (John Curtin School of Medical Research, The Australian National University)

  • Matthew Field

    (John Curtin School of Medical Research, The Australian National University)

  • Anselm Enders

    (John Curtin School of Medical Research, The Australian National University)

  • Joanne H. Reed

    (The Garvan Institute of Medical Research)

  • Christopher C. Goodnow

    (John Curtin School of Medical Research, The Australian National University
    The Garvan Institute of Medical Research
    St Vincent’s Clinical School, School of Medicine, University of New South Wales, Darlinghurst)

Abstract

Self-tolerance by clonal anergy of B cells is marked by an increase in IgD and decrease in IgM antigen receptor surface expression, yet the function of IgD on anergic cells is obscure. Here we define the RNA landscape of the in vivo anergy response, comprising 220 induced sequences including a core set of 97. Failure to co-express IgD with IgM decreases overall expression of receptors for self-antigen, but paradoxically increases the core anergy response, exemplified by increased Sdc1 encoding the cell surface marker syndecan-1. IgD expressed on its own is nevertheless competent to induce calcium signalling and the core anergy mRNA response. Syndecan-1 induction correlates with reduction of surface IgM and is exaggerated without surface IgD in many transitional and mature B cells. These results show that IgD attenuates the response to self-antigen in anergic cells and promotes their accumulation. In this way, IgD minimizes tolerance-induced holes in the pre-immune antibody repertoire.

Suggested Citation

  • Zahra Sabouri & Samuel Perotti & Emily Spierings & Peter Humburg & Mehmet Yabas & Hannes Bergmann & Keisuke Horikawa & Carla Roots & Samantha Lambe & Clara Young & T. Dan Andrews & Matthew Field & Ans, 2016. "IgD attenuates the IgM-induced anergy response in transitional and mature B cells," Nature Communications, Nature, vol. 7(1), pages 1-11, December.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms13381
    DOI: 10.1038/ncomms13381
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    Cited by:

    1. Yijiang Xu & Hang Zhou & Ginell Post & Hong Zan & Paolo Casali, 2022. "Rad52 mediates class-switch DNA recombination to IgD," Nature Communications, Nature, vol. 13(1), pages 1-18, December.
    2. Hiroyuki Satofuka & Satoshi Abe & Takashi Moriwaki & Akane Okada & Kanako Kazuki & Hiroshi Tanaka & Kyotaro Yamazaki & Genki Hichiwa & Kayoko Morimoto & Haruka Takayama & Yuji Nakayama & Shinya Hatano, 2022. "Efficient human-like antibody repertoire and hybridoma production in trans-chromosomic mice carrying megabase-sized human immunoglobulin loci," Nature Communications, Nature, vol. 13(1), pages 1-15, December.

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