This newest addition in our collection of humanized mouse disease models integrates characteristics of the human Systemic Lupus Erythematosus complexity and develops a chronic multiorgan autoimmune disease marked by proteinuria, anti-dsDNA antibodies, severe inflammatory lesions in the skin and milder pathologies in the kidneys and lungs.

This novel model of lupus can prove to be an invaluable translational tool for studying the aetiopathogenic role of the IL23 cytokine in SLE and for use as a preclinical tool to assess the efficacy of novel  lupus  therapeutics.

Published in Arthritis Rheumatol. 2024 Feb 15. doi: 10.1002/art.42830.

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With a new publication in Arthritis Research and Therapy, entitled “Ectopic bone formation and systemic bone loss in a transmembrane TNF-driven model of human spondyloarthritis”, Biomedcode in collaboration with George Kollias Lab at BSRC Al. Fleming, introduce the TgA86 transmembrane TNF transgenic mouse as a novel model of human spondyloarthritis (SpA).

The authors show that the TgA86 mouse model develops spontaneously peripheral arthritis and axial pathologies that closely reproduce key pathogenic features of human SpA, including distinct stages of inflammation and ectopic new bone formation. This is a chronic and complex disease model that similar to human patients also develops extraarticular comorbidities such as heart valve pathology and systemic bone loss. As with human patients in the clinic, all the pathologies of the TgA86 mouse model are reversed following early treatment with anti-hTNF therapeutics.

This novel model of SpA that captures not only specific features, but also the complexity of human disease, can prove to be an invaluable translational tool in the study of SpA pathogenesis as well as in the evaluation of human therapeutics.

Published in Arthritis Research and Therapy 2020 Oct 6;22(1):232. doi: 10.1186/s13075-020-02327-4.

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