Galectin-9 binds IgM-BCR to regulate B cell signaling

Anh Cao, Nouf Alluqmani, Fatima Hifza Mohammed Buhari, Laabiah Wasim, Logan K. Smith, Andrew T. Quaile, Michael Shannon, Zaki Hakim, Hossai Furmli, Dylan M. Owen, Alexei Savchenko and Bebhinn Treanor ()
Additional contact information
Anh Cao: University of Toronto
Nouf Alluqmani: University of Toronto
Fatima Hifza Mohammed Buhari: University of Toronto Scarborough
Laabiah Wasim: University of Toronto
Logan K. Smith: University of Toronto
Andrew T. Quaile: University of Toronto
Michael Shannon: King’s College London Guy’s Campus
Zaki Hakim: University of Toronto
Hossai Furmli: University of Toronto Scarborough
Dylan M. Owen: King’s College London Guy’s Campus
Alexei Savchenko: University of Toronto
Bebhinn Treanor: University of Toronto

Nature Communications, 2018, vol. 9, issue 1, 1-18

Abstract: Abstract The galectin family of secreted lectins have emerged as important regulators of immune cell function; however, their role in B-cell responses is poorly understood. Here we identify IgM-BCR as a ligand for galectin-9. Furthermore, we show enhanced BCR microcluster formation and signaling in galectin-9-deficient B cells. Notably, treatment with exogenous recombinant galectin-9 nearly completely abolishes BCR signaling. We investigated the molecular mechanism for galectin-9-mediated inhibition of BCR signaling using super-resolution imaging and single-particle tracking. We show that galectin-9 merges pre-existing nanoclusters of IgM-BCR, immobilizes IgM-BCR, and relocalizes IgM-BCR together with the inhibitory molecules CD45 and CD22. In resting naive cells, we use dual-color super-resolution imaging to demonstrate that galectin-9 mediates the close association of IgM and CD22, and propose that the loss of this association provides a mechanism for enhanced activation of galectin-9-deficient B cells.

Date: 2018
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DOI: 10.1038/s41467-018-05771-8

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