Animal models and in vitro models for the study of aetiopathogenesis of spondyloarthropathies

Among several animal models, HLA-B27 transgenic rodents proved useful for investigating the interplay between genetic factors and the bacterial environment in the aetiopathogenesis of the spondyloarthropathies (SpA). HLA-B27 transgenic rats spontaneously develop a multisystemic inflammatory disease resembling human SpA. This disease is dependent on the presence of a normal bacterial flora and implicates the immune system. The presence of both T cells and antigen-presenting cells expressing high levels of HLA-B27 seems of critical importance in its pathogenesis. HLA-B27 transgenic mice also develop arthritis, under the influence of the bacterial flora. In both types of model, CD8+ T cells seem not to be necessary, arguing against the 'arthritogenic peptide' hypothesis. In vitro models have been used to study the immune response against bacterial agents and the role of HLA-B27 in human SpA. It appears that an impaired immune response against bacteria could be involved in the triggering of human SpA. HLA-B27 could be implicated at the level of interaction between host cells and bacteria in the driving of a specific immune response against bacterial antigens or as a target of an autoimmune response.