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

Anh Cao1, Nouf Alluqmani2, Fatima Hifza Mohammed Buhari3

  • 1Department of Immunology, University of Toronto, 1 King's College Circle, Toronto, ON, M5S 1A8, Canada.

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|August 19, 2018
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Summary
This summary is machine-generated.

Galectin-9 binds to IgM-BCR, regulating B-cell responses. Loss of galectin-9 enhances B-cell activation, while its presence inhibits signaling by immobilizing IgM-BCR.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Galectins are secreted lectins regulating immune cell function.
  • The specific role of galectin-9 in B-cell responses remains unclear.
  • B-cell receptor (BCR) signaling is crucial for B-cell activation and function.

Purpose of the Study:

  • To investigate the role of galectin-9 in B-cell responses.
  • To identify ligands for galectin-9 on B cells.
  • To elucidate the molecular mechanisms by which galectin-9 modulates BCR signaling.

Main Methods:

  • Identification of galectin-9 ligand using biochemical assays.
  • Analysis of B-cell activation and signaling in wild-type and galectin-9-deficient cells.
  • Super-resolution imaging and single-particle tracking to visualize molecular interactions.
  • Dual-color super-resolution imaging to study protein complex formation.

Main Results:

  • Immunoglobulin M B-cell receptor (IgM-BCR) was identified as a ligand for galectin-9.
  • Galectin-9-deficient B cells exhibited enhanced BCR microcluster formation and signaling.
  • Exogenous galectin-9 treatment significantly inhibited BCR signaling.
  • Galectin-9 was shown to merge IgM-BCR nanoclusters, immobilize IgM-BCR, and co-localize it with CD45 and CD22.
  • Galectin-9 mediates the association between IgM and CD22 in resting naive cells.

Conclusions:

  • Galectin-9 is a novel regulator of BCR signaling, acting through direct interaction with IgM-BCR.
  • The interaction of galectin-9 with IgM-BCR and inhibitory molecules (CD45, CD22) is critical for controlling B-cell activation.
  • Dysregulation of galectin-9-mediated inhibition can lead to enhanced B-cell responsiveness.