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

Research output: Contribution to journalArticlepeer-review


  • Anh Cao
  • Nouf Alluqmani
  • Fatima Hifza Mohammed Buhari
  • Laabiah Wasim
  • Logan K. Smith
  • Andrew T. Quaile
  • Michael Shannon
  • Zaki Hakim
  • Hossai Furmli
  • Alexei Savchenko
  • Bebhinn Treanor

Colleges, School and Institutes


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.


Original languageEnglish
Article number3288
Number of pages18
JournalNature Communications
Issue number1
Early online date17 Aug 2018
Publication statusPublished - 1 Dec 2018