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    Anti-proteinase 3 anti-neutrophil cytoplasm autoantibodies recapitulate systemic vasculitis in mice with a humanized immune system.

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    Authors
    Little, Mark A
    Al-Ani, Bahjat
    Ren, Shuyu
    Al-Nuaimi, Hamad
    Leite, Maurilo
    Alpers, Charles E
    Savage, Caroline O
    Duffield, Jeremy S
    Affiliation
    Centre for Nephrology, Royal Free Hospital, University College London, London, United Kingdom. mark.little@ucl.ac.uk
    Issue Date
    2012
    MeSH
    Animals
    Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis
    Antibodies, Antineutrophil Cytoplasmic
    Autoantibodies
    Female
    Flow Cytometry
    Hematopoietic Stem Cells
    Hematuria
    Hemorrhage
    Humans
    Immune System
    Immunoenzyme Techniques
    Leukocytes
    Mice
    Mice, Inbred NOD
    Mice, SCID
    Myeloblastin
    Receptors, Interleukin-2
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    Citation
    Anti-proteinase 3 anti-neutrophil cytoplasm autoantibodies recapitulate systemic vasculitis in mice with a humanized immune system. 2012, 7 (1):e28626 PLoS ONE
    Journal
    PloS one
    URI
    http://hdl.handle.net/10147/237978
    DOI
    10.1371/journal.pone.0028626
    PubMed ID
    22247758
    Additional Links
    http://www.ncbi.nlm.nih.gov/pubmed?term=Anti-proteinase%203%20anti-neutrophil%20cytoplasm%20autoantibodies%20recapitulate%20systemic%20vasculitis%20in%20mice%20with%20a%20humanized%20immune%20system
    Abstract
    Evidence is lacking for direct pathogenicity of human anti-proteinase-3 (PR3) antibodies in development of systemic vasculitis and granulomatosis with polyangiitis (GPA, Wegener's granulomatosis). Progress in study of these antibodies in rodents has been hampered by lack of PR3 expression on murine neutrophils, and by different Fc-receptor affinities for IgG across species. Therefore, we tested whether human anti-PR3 antibodies can induce acute vasculitis in mice with a human immune system. Chimeric mice were generated by injecting human haematopoietic stem cells into irradiated NOD-scid-IL2Rγ⁻/⁻ mice. Matched chimera mice were treated with human IgG from patients with: anti-PR3 positive renal and lung vasculitis; patients with non-vasculitic renal disease; or healthy controls. Six-days later, 39% of anti-PR3 treated mice had haematuria, compared with none of controls. There was punctate bleeding on the surface of lungs of anti-PR3 treated animals, with histological evidence of vasculitis and haemorrhage. Anti-PR3 treated mice had mild pauci-immune proliferative glomerulonephritis, with infiltration of human and mouse leukocytes. In 3 mice (17%) more severe glomerular injury was present. There were no glomerular changes in controls. Human IgG from patients with anti-PR3 autoantibodies is therefore pathogenic. This model of anti-PR3 antibody-mediated vasculitis may be useful in dissecting mechanisms of microvascular injury.
    Item Type
    Article
    Language
    en
    ISSN
    1932-6203
    ae974a485f413a2113503eed53cd6c53
    10.1371/journal.pone.0028626
    Scopus Count
    Collections
    Tallaght University Hospital

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