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Peripheral B lymphocyte tolerance.

Amanda Gavin1, Djemel Aït-Azzouzene, Annica Mårtensson

  • 1Department of Immunology, and Macromolecular Structure and Chemistry Program, The Scripps Research Institute, La Jolla, CA 92037, USA.

The Keio Journal of Medicine
|October 13, 2004
PubMed
Summary

Peripheral B cell tolerance is explained by a novel "missing self" recognition model. A newly discovered BAFF splice isoform, DBAFF, may also regulate B cell activity and autoimmunity.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Autoimmunity

Background:

  • B cell tolerance prevents autoimmune responses.
  • The 2-signal hypothesis explains tolerance but has limitations with T-independent antigens.
  • B cell survival cytokine BAFF/BLyS is linked to autoimmunity.

Purpose of the Study:

  • To propose a novel mechanism for B cell tolerance.
  • To investigate the role of a novel BAFF splice isoform in regulating B cell activity.

Main Methods:

  • Utilizing 3-83 antibody transgenic mice and mice with cognate antigen in the liver.
  • Investigating B cell responses to T-independent type II (TI-2) antigens.
  • Analyzing a novel BAFF splice isoform (DBAFF) and its function.

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Main Results:

  • A "missing self" recognition model is proposed for B cell tolerance.
  • A novel BAFF splice isoform, DBAFF, was discovered.
  • DBAFF can heteromultimerize with BAFF, suppressing its activity.
  • Preliminary studies suggest DBAFF regulates tolerance.

Conclusions:

  • B cells may use NK-like "missing self" recognition for specificity.
  • DBAFF represents a potential regulator of B cell tolerance and autoimmunity.
  • Relative expression of BAFF and DBAFF may control B cell tolerance.