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Avoiding autoimmune disease--T cells know their limits.

Stephen M Anderton1

  • 1University of Edinburgh, Institute of Immunology and Infection Research, School of Biological Sciences, Kings Buildings, West Mains Road, Edinburgh EH9 3JT, UK. steve.anderton@ed.ac.uk

Trends in Immunology
|April 4, 2006
PubMed
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Molecular mimicry explains autoimmune diseases by infection-triggered T-cell responses. However, immune tolerance mechanisms, including deletion, anergy, and regulation, prevent T-cell receptor cross-reactivity from causing widespread autoimmunity.

Area of Science:

  • Immunology
  • Autoimmunity
  • T-cell biology

Background:

  • The molecular mimicry theory posits that infections can trigger autoimmune diseases.
  • This occurs when T lymphocytes, activated by foreign antigens, cross-react with similar self-antigens.
  • Autoreactive T cells are common, and T-cell receptor (TCR) cross-reactivity is extensive.

Purpose of the Study:

  • To explore the mechanisms by which the immune system prevents autoimmunity despite the prevalence of autoreactive T cells.
  • To challenge the notion that molecular mimicry inevitably leads to autoimmune disease.

Main Methods:

  • Review and synthesis of existing evidence on T-cell tolerance and TCR cross-reactivity.
  • Theoretical modeling of immune responses to self and non-self antigens.

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Main Results:

  • The strength of TCR stimulation by self and non-self antigens typically differs significantly.
  • Evidence supports a model where immune tolerance mechanisms actively limit autoimmune responses.
  • These mechanisms include deletion of autoreactive T cells, induction of anergy, and active regulation.

Conclusions:

  • Immune tolerance, encompassing deletion, anergy, and regulation, is crucial in preventing autoimmune disease development from molecular mimicry.
  • The immune system possesses robust safeguards against self-attack, even in the presence of cross-reactive T cells.