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Molecular mimicry in Reiter's syndrome: cytotoxicity and ELISA studies of HLA-microbial relationships

Immunology
|July 1, 1986
PubMed

Insights

This study investigated molecular mimicry between HLA B27 and bacteria causing reactive arthritis. Findings do not support molecular mimicry as the cause of HLA B27-associated arthritis.

Area of Science:

  • Immunogenetics
  • Rheumatology
  • Microbiology

Background:

  • The association between HLA B27, bacterial infections, and arthritis is not fully understood.
  • Molecular mimicry between HLA B27 and causative microorganisms is a proposed mechanism for reactive arthritis.

Purpose of the Study:

  • To investigate molecular mimicry between HLA B27 and Yersinia enterocolitica or Chlamydia trachomatis.
  • To determine if this mimicry contributes to immunogenetic susceptibility in reactive arthritis.

Main Methods:

  • Antibodies from patients and rabbits against Y. enterocolitica and C. trachomatis were tested for cytotoxicity against HLA B27 lymphocytes.
  • Monoclonal antibodies against HLA B27 were assessed for reactivity with bacterial antigens using ELISA.

Main Results:

  • Antibacterial antibodies did not show specific cytotoxicity for HLA B27-positive lymphocytes.
  • Monoclonal anti-HLA B27 antibodies did not react with Y. enterocolitica or C. trachomatis antigens.

Conclusions:

  • The study's data do not support molecular mimicry as the basis for HLA B27-associated susceptibility to reactive arthritis.
  • Alternative mechanisms may explain the link between HLA B27, infections, and arthritis.

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