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Autoimmunity, polyclonal B-cell activation and infection.

N A Granholm1, T Cavallo

  • 1Department of Pathology, Brown University, Providence, Rhode Island.

Lupus
|February 1, 1992
PubMed
Summary
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Polyclonal B-cell activation, not just loss of self-tolerance, is central to autoimmune disease development. Infectious agents and other factors can trigger this activation, leading to systemic autoimmune disease.

Area of Science:

  • Immunology
  • Pathogenesis of Autoimmune Disease

Background:

  • Autoimmunity is considered an integral part of the immune system.
  • Autoimmune diseases result from genetic, immunologic, hormonal, and environmental factors.
  • Autoimmune disease may represent abnormal immune function rather than a loss of self-tolerance.

Purpose of the Study:

  • To review factors contributing to autoimmune disease development.
  • To examine mechanisms of polyclonal B-cell activation, focusing on infectious agents.
  • To highlight the central role of polyclonal B-cell activation in systemic autoimmune disease pathogenesis.

Main Methods:

  • Review of existing literature on autoimmunity and B-cell activation.
  • Emphasis on infectious agents as triggers for polyclonal B-cell activation.

Related Experiment Videos

  • Use of systemic lupus erythematosus as a prototypic model.

    • Main Results:

    • Polyclonal B-cell activation is central to systemic autoimmune disease pathogenesis.
    • Lipopolysaccharide-induced polyclonal B-cell activation can cause autoimmune disease in normal hosts.
    • Suppression of polyclonal B-cell activation can arrest, while enhancement can exacerbate, autoimmune disease.

    Conclusions:

    • Polyclonal B-cell activation is a key mechanism in the development and exacerbation of systemic autoimmune disease.
    • Various factors contribute to autoimmune disease by inducing polyclonal B-cell activation.
    • Polyclonal B-cell activation can be a sufficient cause of autoimmune disease.