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Infectious agents and B cell tolerance breakdown.

S Jung1, A Kern, A S Korganow

  • 1CNRS UPR 9021 Therapeutic Immunology and Chemistry, Molecular and Cellular Biology Institute (IBMC), Strasbourg, France. s.jung@unistra.fr

Bulletin Du Groupement International Pour La Recherche Scientifique En Stomatologie & Odontologie
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PubMed
Summary
This summary is machine-generated.

Infections can break B cell tolerance, enabling low-affinity autoreactive B cells to mature and produce autoantibodies. This study shows infections can drive affinity maturation in autoreactive B cells, potentially linking infections to autoimmune diseases.

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Area of Science:

  • Immunology
  • Autoimmunity
  • Infectious Diseases

Background:

  • Infectious agents are debated triggers for autoimmune diseases.
  • Mechanisms linking infections to autoimmunity, particularly autoantibody production, are unclear.
  • Low-affinity autoreactive B cells may undergo affinity maturation during infections.

Purpose of the Study:

  • To investigate B cell tolerance breakdown during infections.
  • To determine if low-affinity autoreactive B cells can undergo affinity maturation.
  • To explore the link between infection, B cell tolerance, and autoimmunity.

Main Methods:

  • Developed an intermediate-affinity autoreactive B cell model (SWHEL X HEL2x).
  • Analyzed B cell tolerance phenotypes in the model.
  • Infected mice with Borrelia burgdorferi to induce immune responses.
  • Assessed B cell proliferation, activation, autoantibody production, and somatic mutation.

Main Results:

  • Autoreactive B cells in the model exhibited partial tolerance.
  • Infection led to B cell proliferation, activation, and autoantibody production (IgM, IgG).
  • Produced IgG autoantibodies showed somatic mutations in the auto-antigen binding site.

Conclusions:

  • Infections can induce a breakdown of B cell tolerance.
  • Intermediate-affinity autoreactive B cells can undergo affinity maturation during infection.
  • Somatic mutations in autoantibodies suggest a potential pathogenic role in autoimmune diseases.