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Infections and autoimmune diseases.

Jean-François Bach1

  • 1Laboratoire d'Immunologie, Hôpital Necker, 161 rue de Sèvres, 75743 Paris Cedex 15, France. bach@necker.fr

Journal of Autoimmunity
|November 10, 2005
PubMed
Summary

Infections can trigger autoimmune diseases through mechanisms like molecular mimicry, but also protect against them. The hygiene hypothesis suggests reduced infections increase immune disorders, with mechanisms like antigenic competition and immunoregulation being explored for protection.

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Revisiting the Hygiene Hypothesis in the Context of Autoimmunity.

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Area of Science:

  • Immunology
  • Infectious Diseases
  • Environmental Health

Background:

  • Autoimmune diseases are influenced by environmental factors, as evidenced by discordant monozygotic twins.
  • Infections are implicated as triggers for autoimmune diseases, with animal models showing viruses (e.g., Coxsackie B4, encephalomyocarditis) increasing autoantigen immunogenicity.
  • Mechanisms like molecular mimicry (e.g., Campylobacter jejuni and Guillain-Barré syndrome) and chemical modification (e.g., iodine and thyroiditis) are observed.

Purpose of the Study:

  • To explore the dual role of infections in the etiology of autoimmune diseases, acting as both triggers and protective agents.
  • To investigate the mechanisms underlying infection-induced autoimmunity and infection-mediated protection.
  • To examine the implications of the hygiene hypothesis regarding the rise in immune disorders and the potential protective role of infections.

Main Methods:

  • Review of animal models demonstrating infection-induced autoimmunity (e.g., viral triggers, bacterial mimicry, chemical modifications).
  • Analysis of epidemiological data linking improved socioeconomic status and decreased infection rates to increased immune disorders.
  • Exploration of proposed mechanisms for infection-induced protection, including antigenic competition and immunoregulation via various immune cells and receptors (Toll, TIM).

Main Results:

  • Animal models show infections can trigger autoimmunity via increased autoantigen immunogenicity or molecular mimicry.
  • Epidemiological trends support the hygiene hypothesis: reduced infections correlate with increased autoimmune, allergic, and inflammatory diseases.
  • Several mechanisms for infection-induced protection are under investigation, including competition for immune responses and bystander suppression by regulatory cells.

Conclusions:

  • Infections play a complex role in immune disorders, capable of initiating or preventing autoimmunity.
  • The hygiene hypothesis provides a framework for understanding the rise in immune diseases due to decreased pathogen exposure.
  • Further research into protective infectious agents and their mechanisms is crucial, with potential therapeutic applications in preventing or treating immune disorders.

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