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Toll-like receptor ligands sensitize B-cell receptor signalling by reducing actin-dependent spatial confinement of the receptor

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  • Spencer A. Freeman

    (University of British Columbia
    University of British Columbia
    Life Sciences Institute I3 and Cell Research Groups, University of British Columbia
    Program in Cell Biology, The Hospital for Sick Kids Research Institute)

  • Valentin Jaumouillé

    (Program in Cell Biology, The Hospital for Sick Kids Research Institute)

  • Kate Choi

    (University of British Columbia
    Life Sciences Institute I3 and Cell Research Groups, University of British Columbia)

  • Brian E. Hsu

    (University of British Columbia
    Life Sciences Institute I3 and Cell Research Groups, University of British Columbia)

  • Harikesh S. Wong

    (Program in Cell Biology, The Hospital for Sick Kids Research Institute)

  • Libin Abraham

    (University of British Columbia
    Life Sciences Institute I3 and Cell Research Groups, University of British Columbia
    1984 Mathematics Road, University of British Columbia)

  • Marcia L. Graves

    (University of British Columbia
    University of British Columbia
    Life Sciences Institute I3 and Cell Research Groups, University of British Columbia)

  • Daniel Coombs

    (1984 Mathematics Road, University of British Columbia)

  • Calvin D. Roskelley

    (University of British Columbia
    Life Sciences Institute I3 and Cell Research Groups, University of British Columbia)

  • Raibatak Das

    (University of Colorado Denver)

  • Sergio Grinstein

    (Program in Cell Biology, The Hospital for Sick Kids Research Institute)

  • Michael R. Gold

    (University of British Columbia
    Life Sciences Institute I3 and Cell Research Groups, University of British Columbia)

Abstract

Integrating signals from multiple receptors allows cells to interpret the physiological context in which a signal is received. Here we describe a mechanism for receptor crosstalk in which receptor-induced increases in actin dynamics lower the threshold for signalling by another receptor. We show that the Toll-like receptor ligands lipopolysaccharide and CpG DNA, which are conserved microbial molecules, enhance signalling by the B-cell antigen receptor (BCR) by activating the actin-severing protein cofilin. Single-particle tracking reveals that increased severing of actin filaments reduces the spatial confinement of the BCR within the plasma membrane and increases BCR mobility. This allows more frequent collisions between BCRs and greater signalling in response to low densities of membrane-bound antigen. These findings implicate actin dynamics as a means of tuning receptor signalling and as a mechanism by which B cells distinguish inert antigens from those that are accompanied by indicators of microbial infection.

Suggested Citation

  • Spencer A. Freeman & Valentin Jaumouillé & Kate Choi & Brian E. Hsu & Harikesh S. Wong & Libin Abraham & Marcia L. Graves & Daniel Coombs & Calvin D. Roskelley & Raibatak Das & Sergio Grinstein & Mich, 2015. "Toll-like receptor ligands sensitize B-cell receptor signalling by reducing actin-dependent spatial confinement of the receptor," Nature Communications, Nature, vol. 6(1), pages 1-17, May.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7168
    DOI: 10.1038/ncomms7168
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