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Related Experiment Videos

Cutting edge: Complement (C3d)-linked antigens break B cell anergy.

Taras Lyubchenko1, Joseph M Dal Porto, V Michael Holers

  • 1Division of Rheumatology, Department of Medicine, University of Colorado School of Medicine, Denver, CO 802602, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|August 22, 2007
PubMed
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Complement receptor type 2 (CR2) can overcome B cell anergy by amplifying B cell receptor signals. This interaction, using complement-opsonized antigens, may increase autoimmunity risk in certain individuals.

Area of Science:

  • Immunology
  • Molecular Biology

Background:

  • Complement receptor type 2 (CR2; CD21) and the B cell antigen receptor (BCR) can be co-ligated by C3dg-adducted antigens.
  • This co-ligation amplifies BCR-mediated signals, significantly lowering the threshold for B cell activation and humoral immune responses in naive mice.

Purpose of the Study:

  • To investigate whether CR2-mediated complementation of BCR signals can overcome B cell anergy.
  • To explore the potential of cross-reactive, complement-opsonized antigens in triggering responses from anergic B cells.

Main Methods:

  • Utilized Ars-CCG/C3dg complexes for BCR/CR2 co-stimulation of anergic Ars/A1 B cells in vitro and in vivo.
  • Assessed calcium (Ca2+) mobilization in vitro and autoantibody production in vivo.

Main Results:

Related Experiment Videos

  • BCR/CR2 co-stimulation, but not antigen alone, induced Ca2+ mobilization in anergic B cells.
  • In vivo, BCR/CR2 co-stimulation led to autoantibody production from anergic B cells without germinal center formation.

Conclusions:

  • CR2-mediated signal complementation can overcome B cell anergy.
  • Complement-opsonized, cross-reactive antigens can activate anergic B cells, potentially increasing autoimmunity risk following exposure to complement-fixing bacteria.