ArticleClinical and experimental immunology2010
Anti-PR3 immune responses induce segmental and necrotizing glomerulonephritis.
Article in Clinical and experimental immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 72 citations in OpenAlex.
- Clinical Utility of Serial Measurements of Antineutrophil Cytoplasmic Antibodies Targeting Proteinase 3 in ANCA-Associated Vasculitis.Frontiers in immunology · 2020Trial
- Immunopathology of Antineutrophil Cytoplasmic Antibody (ANCA)-Associated Vasculitis.International journal of molecular sciences · 2025Review
- Differential roles of human CD4Nature immunology · 2025Article
- Animal models for anti-neutrophil cytoplasmic antibody-associated vasculitis: Are current models good enough?Animal models and experimental medicine · 2023Review
- Proteinase 3 promotes formation of multinucleated giant cells and granuloma-like structures in patients with granulomatosis with polyangiitis.Annals of the rheumatic diseases · 2023Article
- Increased Circulating PD-1 hi CXCR5 - Peripheral T Helper Cells are Associated with Disease Activity of ANCA-Associated Vasculitis.Clinical and experimental immunology · 2022Article
- Dynamic Changes in the Nasal Microbiome Associated With Disease Activity in Patients With Granulomatosis With Polyangiitis.Arthritis & rheumatology (Hoboken, N.J.) · 2021Article
- Pathogenesis and pathology of anti-neutrophil cytoplasmic antibody（ANCA）-associated vasculitis.Journal of translational autoimmunity · 2021Review
- Different Types of ANCA Determine Different Clinical Phenotypes and Outcome in ANCA-Associated Vasculitis (AAV).Frontiers in medicine · 2021Article
- Animal Models of ANCA Associated Vasculitis.Frontiers in immunology · 2020Review
- Pathogenesis and therapeutic interventions for ANCA-associated vasculitis.Nature reviews. Rheumatology · 2019Review
- Milk fat globule-EGF factor 8 suppresses the aberrant immune response of systemic lupus erythematosus-derived neutrophils and associated tissue damage.Cell death and differentiation · 2017Article
- Updates in ANCA-associated vasculitis.European journal of rheumatology · 2016Review
- Factors Determining the Clinical Utility of Serial Measurements of Antineutrophil Cytoplasmic Antibodies Targeting Proteinase 3.Arthritis & rheumatology (Hoboken, N.J.) · 2016Article
- IgA- and SIgA anti-PR3 antibodies in serum versus organ involvement and disease activity in PR3-ANCA-associated vasculitis.Clinical and experimental immunology · 2016Article
- Induction of proteinase 3-anti-neutrophil cytoplasmic autoantibodies by proteinase 3-homologous bacterial protease in mice.Immunologic research · 2016Article
- Overview of the Pathogenesis of ANCA-Associated Vasculitis.Kidney diseases (Basel, Switzerland) · 2016Review
- Innate immune cells in the pathogenesis of primary systemic vasculitis.Rheumatology international · 2016Review
- Proteinase 3-ANCA Vasculitis versus Myeloperoxidase-ANCA Vasculitis.Journal of the American Society of Nephrology : JASN · 2015Review
- Vasculitis: do we know more to classify better?Pediatric nephrology (Berlin, Germany) · 2015Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Wegener's granulomatosis (WG) is a life-threatening autoimmune vasculitis that affects lungs, kidneys and other organs. A hallmark of WG is the presence of classic anti-neutrophil cytoplasmic antibodies (c-ANCA) against self-proteinase 3 (PR3). Little is known about the role of these antibodies and PR3-specific immune responses in disease development. In this study, we demonstrate that PR3-specific autoimmune responses are pathogenic in non-obese diabetic (NOD) mice with an impaired regulatory arm of the immune response. Immunization of autoimmunity prone NOD mice with rmPR3 (recombinant mouse PR3) in complete Freund's adjuvant (CFA) resulted in high levels of c-ANCA, without detectable disease development. However, when splenocytes from these immunized mice were transferred into immunodeficient NOD-severe combined immunodeficiency (SCID) mice, the recipient mice developed vasculitis and severe segmental and necrotizing glomerulonephritis. No disease developed in NOD-SCID mice that received splenocytes from the CFA-alone-immunized donors (controls), indicating that disease development depends upon PR3-specific immune responses. In contrast to the pathology observed in NOD-SCID mice, no disease was observed when splenocytes from rmPR3-immunized C57BL/6 mice were transferred into immunodeficient C57BL/6-RAG-1(-/-) mice, suggesting that complex and probably multi-genetic factors play a role in the regulation of disease development.
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