ArticlePloS one2018
A spontaneous model of spondyloarthropathies that develops bone loss and pathological bone formation: A process regulated by IL27RA-/- and mutant-p53.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Have Therapeutics Enhanced Our Knowledge of Axial Spondyloarthritis?Current rheumatology reports · 2023Review
- Dysregulation of ribosome-related genes in ankylosing spondylitis: a systems biology approach and experimental method.BMC musculoskeletal disorders · 2021Article
- Lessons on SpA pathogenesis from animal models.Seminars in immunopathology · 2021Review
- The Role of the IL-23/IL-17 Axis in Disease Initiation in Spondyloarthritis: Lessons Learned From Animal Models.Frontiers in immunology · 2021Review
- The role of IL-17A in axial spondyloarthritis and psoriatic arthritis: recent advances and controversies.Annals of the rheumatic diseases · 2019Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
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-β2m transgenic rats; however, only 30%-50% of male HLA-B27/Hu-β2m 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.
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Registered trials
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