We are excited to introduce a new addition to our collection of genetically modified mice used in human disease modelling. We have now developed and characterized a proprietary Rag1KO/BMC mouse line that either alone or in combination with our collection of proprietary mouse lines allows us to offer a new series of anti-CD40 colitis mouse models that can serve as invaluable preclinical tools to better understand and treat the pathogenic mechanisms involved in the development and progression of Inflammatory Bowel Disease (IBD).

💉 The anti-CD40 model of colitis is a valuable model to study innate immune responses in colon inflammation and to evaluate the therapeutic effect of TNF, IFNγ or IL-12/IL-23 p40 inhibition 💊

What is the anti-CD40 induced colitis model?
Activation of CD40 by an agonistic anti-CD40 antibody in mice lacking T and B cells, as the Rag1 or Rag2 knockout mice, leads to the activation of innate immune responses, the excessive production of IL-23, IL-1β and IL-12 and the development of inflammation in the colon.
The anti-CD40 induced colitis pathology is characterized by body weight loss, increased levels of circulating cytokines, reduced colon length and increased colon weight,  accompanied by relevant histopathological signs of gut inflammation and extensive crypt destruction.

 

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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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