ArticleRheumatology international2013
PR3 antibodies do not induce renal pathology in a novel PR3-humanized mouse model for Wegener's granulomatosis.
Article in Rheumatology international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Animal models for anti-neutrophil cytoplasmic antibody-associated vasculitis: Are current models good enough?Animal models and experimental medicine · 2023Review
- Animal Models of ANCA Associated Vasculitis.Frontiers in immunology · 2020Review
- Pathogenesis of antineutrophil cytoplasmic autoantibody-associated small-vessel vasculitis.Annual review of pathology · 2013Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Different murine models have been used as basis for Proteinase 3 (PR3)-associated vasculitis models, but sufficient reproduction of the human clinical manifestation has failed to this date. As a reliable animal model is needed to further elucidate the pathological value of PR3-ANCA, we developed a PR3-humanized transgenic mouse model, in order to induce a glomerulonephritis. Our huPR3-transgenic mice were injected i.v. with our monoclonal antibodies, either unlabeled or directly labeled by fluorescein isothiocyanate. For a period of 5 days, proteinuria and erythrocyte count were measured with urine dip sticks. None of the mice exhibited proteinuria and/or an abnormal number of erythrocytes in the urine. Five days after antibody treatment, the mice were killed and different organs were fixed and immunohistochemically assessed. In the case of the kidney, we could detect a glomerulonephritis. Our study is able to show that although a direct renal target was given in transgenic human PR3 mice, no renal pathology was detectable. Multifactorial mechanisms for PR3-ANCA involvement in the development of Wegener's granulomatosis must be hypothesized.
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