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Editing disease-associated autoantibodies

C Chen1, E L Prak, M Weigert

  • 1Department of Molecular Biology, Princeton University, New Jersey 08544, USA.

Immunity
|January 1, 1997
PubMed
Summary
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Transgenic mice models reveal how B cells with anti-DNA antibodies avoid self-destruction. These models show that receptor editing, primarily through light chain inactivation, helps manage autoreactive B cells in systemic lupus erythematosus (SLE).

Area of Science:

  • Immunology
  • Autoimmunity
  • Genetics

Background:

  • Autoantibodies against DNA are hallmarks of systemic lupus erythematosus (SLE).
  • B cells expressing self-reactive receptors are typically eliminated or inactivated through central and peripheral tolerance mechanisms.
  • Receptor editing is a key process where B cells modify their antibody receptors to reduce self-reactivity.

Purpose of the Study:

  • To generate and characterize site-directed transgenic mouse models expressing anti-DNA antibodies.
  • To investigate the B cell receptor editing phenotypes in response to self-antigen recognition.
  • To clarify the interplay between receptor editing and other tolerance mechanisms in preventing autoimmunity.

Main Methods:

  • Generation of site-directed transgenic mice with combined immunoglobulin heavy (H) and light (L) chains encoding anti-DNA antibodies.

Related Experiment Videos

  • Phenotypic characterization of B cells in these transgenic models, focusing on receptor editing mechanisms.
  • Analysis of B cell tolerance induction, including deletion, inactivation, and receptor editing.

    • Main Results:

    • One model (3H9R/Vkappa4R) exhibited a deletion-prone phenotype with significant receptor editing, primarily via light chain inactivation through leap-frogging.
    • A second model (3H9R/Vkappa8R) showed B cells susceptible to anergy, retaining most of their original H and L chains.
    • These distinct phenotypes highlight different B cell tolerance outcomes in the presence of pathogenic autoantibodies.

    Conclusions:

    • Site-directed transgenic mice provide valuable models for studying B cell tolerance in autoimmunity.
    • Receptor editing, particularly light chain modification, is a crucial mechanism for managing autoreactive B cells.
    • The findings elucidate the complex relationships between receptor editing, anergy, and B cell deletion in preventing self-reactivity.