TgA86 mice overexpress mouse transmembraneTNF from a Δ1-12 mTNF-globin transgene. They develop with 100% incidence peripheral and axial joint pathology accompanied by new bone formation features, all characteristic of human SpA pathology.
Histopathology of TgA86 peripherla joints is characterized by synovial hyperplasia, articular cartilage destruction, bone erosion and ectopic cartilage formation while tail vertebrae display signs of bone marrow oedema and intravertebral disc degeneration. Together these features closely resemble those of human spondyloarthropathies.
Preclinical Efficacy evaluation
Preclinical drug efficacy is evaluated either with an early or with a late treatment starting at 3 or 9 weeks of age respectively.
- In vivo body weight measurements for the whole duration of the study
- In vivo evaluation of ankle and paw joint swelling for the whole duration of the study
- In vivo evaluation of tail bending and ankylosis for the whole duration of the study
- Histopathological evaluation of the pathology in ankle joints and tail vertebrae
- µCT analysis
Figure 3: Representative graphs of the progression of the in vivo arthritic score (left panel) and the tail pathology score (right panel) in TgA86 animals. Treatment with etanercept ameliorates the disease symptoms.
1. Alexopoulou L, Pasparakis M, Kollias G., 1997, "A murine transmembrane tumor necrosis factor (TNF) transgene induces arthritis by cooperative p55/p75 TNF receptor signaling", Eur J Immunol, 27(10):2588-92. (view article)
2. Vieira-Sousa E, van Duivenvoorde LM, Fonseca JE, Lories RJ, Baeten DL. 2015 “Review: animal models as a tool to dissect pivotal pathways driving spondyloarthritis” , Arthritis Rheumatol. 67, 2813-27. (view article) (view article)
Biomedcode's disease models are highlighted in a new review discussing animal models of spondyloarthritis.