A spontaneous model of spondyloarthropathies that develops bone loss and pathological bone formation: A process regulated by IL27RA-/- and mutant-p53

PloS One
Denada DibraShulin Li

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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Citations

Jul 7, 2019·Annals of the Rheumatic Diseases·Dennis G McGonagleRobert Moots
Jan 16, 2021·Seminars in Immunopathology·Maxime BrebanLuiza M Araujo
Jul 17, 2021·Frontiers in Immunology·Mohamed MandourMarleen G H van de Sande
Aug 20, 2021·Expert Review of Clinical Immunology·Stephanie R Harrison, Helena Marzo-Ortega
Aug 26, 2021·Expert Opinion on Therapeutic Targets·Bilade CherqaouiMaxime Breban

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