HLA-B27 transgenic rats model

Ann Med Interne (Paris). 1998 Apr;149(3):139-41.

Abstract

To investigate the role of HLA-B27 in the pathogenesis of spondylarthropathies, rats transgenic for HLA-B27 and human beta 2-microglobulin were produced. Several lines of B27 transgenic rats spontaneously develop a multisystem inflammatory disorder reminiscent of human spondylarthropathies, with gut, joint, skin and male genital lesions. The role of HLA-B27 in this model was studied and it was found that a high expression level of the transgene in cells of hematopoietic origin was critical to induce inflammatory manifestations. Furthermore, a combined implication of CD4+ T cells and antigen presenting cells in this model is suspected, based on passive transfer studies, although a specific influence of HLA-B27 upon T cell education in the thymus is unlikely to be important. Beside the immune system, bacterial flora exerts an important influence in this model, as a triggering agent of gut and joint inflammation. Finally, endogenous rat genetic factors are suspected to be involved in this model.

MeSH terms

  • Animals
  • Animals, Genetically Modified
  • Antigen-Presenting Cells / immunology
  • CD4-Positive T-Lymphocytes / immunology
  • Female
  • Gene Expression / physiology
  • HLA-B27 Antigen / genetics*
  • Humans
  • Male
  • Rats
  • Rats, Inbred Strains
  • Risk Factors
  • Spondylitis, Ankylosing / genetics*
  • Spondylitis, Ankylosing / immunology
  • beta 2-Microglobulin / genetics

Substances

  • HLA-B27 Antigen
  • beta 2-Microglobulin