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Retroviral Overexpression of CXCR4 on Murine B-1a Cells and Adoptive Transfer for Targeted B-1a Cell Migration to the Bone Marrow and IgM Production
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Oxysterols direct B-cell migration through EBI2.

Changlu Liu1, Xia V Yang, Jiejun Wu

  • 1Johnson & Johnson Pharmaceutical Research & Development, L.L.C., 3210 Merryfield Row, San Diego, California 92121, USA. cliu9@its.jnj.com

Nature
|July 29, 2011
PubMed
Summary
This summary is machine-generated.

Oxysterols, like 7α,25-dihydroxycholesterol, are identified as endogenous ligands for the EBI2 receptor, controlling B-cell migration and immune responses. This discovery reveals a new role for oxysterols in the immune system.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Cholesterol Metabolism

Background:

  • EBI2 (GPR183) is an orphan G-protein-coupled receptor crucial for B-cell migration and antibody production.
  • Oxysterols influence immune responses and cholesterol metabolism, primarily through nuclear hormone receptors.

Purpose of the Study:

  • To identify endogenous ligands for EBI2.
  • To elucidate the role of oxysterols in EBI2-mediated immune functions.

Main Methods:

  • Isolation of oxysterols from porcine spleen extracts.
  • In vitro migration assays using EBI2-expressing and deficient cells.
  • In vivo studies involving EBI2-deficient mice and CYP7B1 inhibition.

Main Results:

  • 7α,25-dihydroxycholesterol (OHC) identified as a potent endogenous ligand for EBI2 (Kd = 450 pM).
  • 7α,25-OHC stimulates EBI2-dependent migration of B and T cells in vitro.
  • In vivo, EBI2 deficiency or 7α,25-OHC desensitization impairs B-cell homing to splenic follicles.

Conclusions:

  • Establishes a direct link between EBI2 and oxysterols, specifically 7α,25-OHC.
  • Uncovers a novel role for oxysterols as signaling molecules in EBI2-mediated immune cell trafficking.
  • Highlights a new pathway regulating immune responses and B-cell localization within lymphoid organs.