Animal models of the spondyloarthropathies

Curr Rheumatol Rep. 2000 Aug;2(4):282-7. doi: 10.1007/s11926-000-0064-0.


Several lines of rats transgenic for human leukocyte antigen (HLA)-B27 spontaneously develop a multisystemic inflammatory disease resembling human spondyloarthropathies. This disease is mediated by cells of the immune system and is dependent on the presence of a normal bacterial flora. Both antigen-presenting cells expressing high levels of HLA-B27 and T cells appear to be of importance in the pathogenesis of this model. HLA-B27 transgenic/b2- microglobulin deficient mice also develop arthritis, under the influence of the bacterial flora. In both types of model, CD8+ T cells appear to be unnecessary, arguing against the "arthritogenic peptide" hypothesis.

Publication types

  • Comparative Study

MeSH terms

  • Animals
  • Animals, Genetically Modified
  • Arthritis, Reactive / etiology
  • Arthritis, Reactive / immunology
  • Bacteria / immunology
  • Cross Reactions
  • Disease Models, Animal*
  • HLA-B27 Antigen / immunology
  • Humans
  • Mice
  • Mice, Transgenic
  • Rats
  • Rats, Inbred F344
  • Rats, Inbred Lew
  • Spondylarthropathies* / etiology
  • Spondylarthropathies* / immunology
  • T-Lymphocytes / immunology


  • HLA-B27 Antigen