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Initiation of autoimmunity.

Urs Christen1, Matthias G von Herrath

  • 1Immune Regulation Laboratory, Department of Developmental Immunology, La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, California 92121, USA. christen@liai.org

Current Opinion in Immunology
|October 30, 2004
PubMed
Summary

Initiating autoimmunity requires genetic predisposition, reactive lymphocytes, and a trigger. Disease manifestation depends on the quantity of cell destruction and the balance of immune cell functions, not just the presence of autoreactive cells.

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Area of Science:

  • Immunology
  • Autoimmunity Research
  • Disease Pathogenesis

Background:

  • Autoimmunity initiation is multifactorial, involving genetic susceptibility, autoreactive lymphocytes, and environmental triggers.
  • The complexity of autoimmune diseases stems from inter-individual variations in these initiating factors.
  • Clinical manifestation requires significant tissue damage, highlighting quantitative aspects beyond mere lymphocyte presence.

Purpose of the Study:

  • To elucidate the critical factors and conditions necessary for the initiation of autoimmune responses.
  • To explain the variability and complexity observed in human autoimmune diseases.
  • To differentiate between subclinical autoimmunity and overt disease based on immune cell dynamics.

Main Methods:

  • Review and synthesis of current understanding of autoimmunity initiation.

Related Experiment Videos

  • Analysis of the interplay between genetic predisposition, lymphocyte reactivity, and precipitating events.
  • Conceptual modeling of quantitative factors influencing disease progression.

    • Main Results:

    • Autoimmunity initiation requires a confluence of genetic predisposition, naive lymphocytes reactive to autoantigens, and a triggering event for T and/or B cell activation.
    • Inter-individual differences in these factors contribute to the complexity of autoimmune diseases.
    • Clinical disease is contingent upon sufficient cellular destruction, influenced by the kinetics of autoreactive cell generation, their numbers, and regulatory versus destructive effector functions.

    Conclusions:

    • The presence of autoreactive lymphocytes alone does not guarantee autoimmune disease.
    • The balance between destructive and regulatory immune responses, alongside quantitative cellular dynamics, dictates whether autoimmunity remains subclinical or progresses to disease.
    • Understanding these quantitative and regulatory aspects is crucial for comprehending and potentially treating autoimmune conditions.