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

Alan 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 and Michael R. Gold ()
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Valentin Jaumouillé: Program in Cell Biology, The Hospital for Sick Kids Research Institute
Kate Choi: University of British Columbia
Brian E. Hsu: University of British Columbia
Harikesh S. Wong: Program in Cell Biology, The Hospital for Sick Kids Research Institute
Libin Abraham: University of British Columbia
Marcia L. Graves: University of British Columbia
Daniel Coombs: 1984 Mathematics Road, University of British Columbia
Calvin D. Roskelley: 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

Nature Communications, 2015, vol. 6, issue 1, 1-17

Abstract: 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.

Date: 2015
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DOI: 10.1038/ncomms7168

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