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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Animal models of spondyloarthritis.

PURPOSE OF REVIEW: The aim of this article is to review new insights into spondyloarthritis obtained in animal models during the last year. RECENT FINDINGS: HLA-B27 misfolding has been demonstrated in HLA-B27/human beta2-microglobulin transgenic rats. HLA-B27 misfolding is associated with a typical unfolded protein stress response and with an interferon-response signature. Prebiotic treatment of these rats reduced colitis and arthritis. Proteoglycan-induced spondylitis is distinct from proteoglycan-induced arthritis. Specific susceptibility loci for proteoglycan-induced spondylitis have been demonstrated. Bone morphogenetic proteins are important in new cartilage and bone formation in ankylosing enthesitis. Psoriasis and psoriatic arthritis-like disease develops in conditional double JunB/c-Jun knockout mice. SUMMARY: Insights into the molecular signaling pathways driving HLA-B27 associated spondylitis, autoimmune spondylitis, ankylosing enthesitis and psoriasis, resulting from animal models, identify new and specific therapeutic targets in spondyloarthritis.[1]


  1. Animal models of spondyloarthritis. Lories, R.J. Current opinion in rheumatology. (2006) [Pubmed]
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