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Updated: Jul 6, 2026

An Efficient and High Yield Method for Isolation of Mouse Dendritic Cell Subsets
09:09

An Efficient and High Yield Method for Isolation of Mouse Dendritic Cell Subsets

Published on: April 18, 2016

Dendritic cell-dependent inhibition of B cell proliferation requires CD22

Lorna Santos1, Kevin E Draves, Mark Boton

  • 1Department of Immunology, University of Washington, Seattle, WA 98195, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|March 21, 2008
PubMed

Insights

Immature dendritic cells (DCs) inhibit B cell proliferation via CD22, a process reversed by BAFF. A distinct DC-associated CD22 ligand, independent of ST6Gal-I, is crucial for maintaining long-lived B cells in bone marrow.

Area of Science:

  • Immunology
  • Cell Biology
  • Glycobiology

Background:

  • Dendritic cells (DCs) are known regulators of B cell function.
  • The B cell receptor (BCR) coreceptor CD22 plays a role in B cell signaling and development.
  • ST6Gal-I sialyltransferase modifies glycoproteins with alpha2,6-sialic acids, influencing cellular interactions.

Purpose of the Study:

  • To investigate the role of bone marrow-derived dendritic cells in regulating B cell proliferation.
  • To elucidate the specific mechanisms and ligands involved in DC-mediated B cell inhibition.
  • To differentiate the functions of distinct CD22 ligands in B cell development and maintenance.

Main Methods:

  • Co-culture experiments using bone marrow-derived immature and mature dendritic cells with B cells.
  • Treatment with BAFF to assess its effect on DC-mediated B cell inhibition.
  • Analysis of CD22 and ST6Gal-I knockout mice to examine B cell subsets and development.
  • Biochemical characterization of CD22 ligands, including resistance to enzymatic and chemical treatments.

Main Results:

  • Immature DCs, but not mature DCs, inhibit BCR-induced B cell proliferation in a contact-dependent manner.
  • This inhibition is BAFF-reversible and dependent on CD22, but not on ST6Gal-I-generated glycans.
  • A novel, ST6Gal-I-independent CD22 ligand on DCs was identified, resistant to neuraminidase and periodate oxidation.
  • ST6Gal-I-generated CD22 ligand influences splenic B cell development, while the DC-associated CD22 ligand is essential for long-lived mature B cell maintenance in bone marrow.

Conclusions:

  • Two distinct CD22 ligands exist with differential functions in B cell regulation.
  • The ST6Gal-I-dependent CD22 ligand is important for splenic B cell subset development.
  • The ST6Gal-I-independent CD22 ligand expressed on DCs is critical for maintaining long-lived mature B cells in the bone marrow.

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