title: Animal models of the spondyloarthropathies.
abstract: 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.
authors: INSERM U477 and Service de Rhumatologie B, Hôpital Cochin, AP-HP, Université René Descartes, 27 rue du Faubourg Saint-Jacques, 75014 Paris, France.
authors: M
authors: M
authors: Breban
authors: G
authors: G
authors: Falgarone
authors: H
authors: H
authors: Blanchard
authors: E
authors: E
authors: Dernis-Labous
authors: D
authors: D
authors: Lamarque
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D016918:Arthritis, Reactive / Q000209:etiology / Q000276:immunology; D001419:Bacteria / Q000276:immunology; D003429:Cross Reactions; D004195:Disease Models, Animal; D015796:HLA-B27 Antigen / Q000276:immunology; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D051381:Rats; D011916:Rats, Inbred F344; D011917:Rats, Inbred Lew; D025242:Spondylarthropathies / Q000209:etiology / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D015796:HLA-B27 Antigen