| First Author | Dibra D | Year | 2018 |
| Journal | PLoS One | Volume | 13 |
| Issue | 3 | Pages | e0193485 |
| PubMed ID | 29494633 | Mgi Jnum | J:258747 |
| Mgi Id | MGI:6147475 | Doi | 10.1371/journal.pone.0193485 |
| Citation | Dibra D, et al. (2018) A spontaneous model of spondyloarthropathies that develops bone loss and pathological bone formation: A process regulated by IL27RA-/- and mutant-p53. PLoS One 13(3):e0193485 |
| abstractText | Spondyloarthropathies, the second most frequently occurring form of chronic inflammatory arthritis, affects young adults in particular. However, a proper model with which to study the biology of this disease and to develop therapeutics is lacking. One of the most accepted animal models for this disease uses HLA-B27/Hu-beta2m transgenic rats; however, only 30%-50% of male HLA-B27/Hu-beta2m rats develop spontaneous, clinically apparent spondylitis and have a variable time until disease onset. Here, we report a high-incidence, low-variation spontaneous mouse model that delineates how the combination of inflammatory cytokine interleukin-27 (IL-27) signaling deficiency and mitogenic signaling (mutant p53R172H) in vivo, leads to bone loss in the vertebral bodies and ossification of the cartilage in the intervertebral discs. In this human disease-like mouse model, bone loss and pathogenic bone development are seen as early as 4 months of age in the absence of inflammatory aggregates in the enthesis or intervertebral disc. |
