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Antigenic mimicry and autoimmune diseases.

C Nickerson1, H Luthra, C David

  • 1Department of Immunology, Mayo Clinic, Rochester, Minnesota.

International Reviews of Immunology
|January 1, 1991
PubMed
Summary

Molecular mimicry and cross-reactive autoantibodies do not automatically indicate disease. Autoimmune disease requires antibodies targeting critical host proteins, not just sequence homology.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Autoimmune Diseases

Background:

  • Cross-reactive autoantibodies and sequence homology are often found but may not be biologically significant.
  • Natural antibodies to cellular components can be present in healthy individuals.
  • Autoimmune disease pathogenesis requires antibodies targeting functionally important host protein domains.

Purpose of the Study:

  • To evaluate the biological significance of molecular mimicry in autoimmune disease.
  • To determine the criteria for cross-reactive immune responses to be pathologically relevant.

Main Methods:

  • Review of existing literature on autoantibodies, sequence homology, and molecular mimicry.
  • Analysis of cases with shared sequences between host proteins and microbial antigens (e.g., HLA-B27 and EBV).
  • Assessment of antibody binding to target proteins based on sequence similarity and amino acid substitutions.

Main Results:

  • High incidence of autoantibodies in relatives of patients and elderly individuals does not correlate with autoimmune disease.
  • Extensive sequence homology does not always elicit a cross-reactive immune response.
  • Even with identical amino acid sequences (e.g., HLA-B27 and EBV protein), cross-reactive antibodies may not be detected.
  • Antibody binding to whole proteins can be abrogated by single amino acid substitutions in synthetic peptides.

Conclusions:

  • Molecular mimicry alone is insufficient to cause autoimmune disease.
  • Cross-reactive immune responses must target biologically important host proteins involved in disease pathogenesis to be relevant.
  • The presence of autoantibodies or sequence homology does not necessarily imply a role in disease development.

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