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

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, Anselm Enders, Joanne H. Reed and Christopher C. Goodnow ()
Additional contact information
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
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

Nature Communications, 2016, vol. 7, issue 1, 1-11

Abstract: 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.

Date: 2016
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DOI: 10.1038/ncomms13381

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