ArticleJournal of the American Society of Nephrology : JASN2011
Myeloperoxidase-specific plasma cell depletion by bortezomib protects from anti-neutrophil cytoplasmic autoantibodies-induced glomerulonephritis.
Article in Journal of the American Society of Nephrology : JASN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.
- Identification of susceptibility loci and relevant cell type for IgA nephropathy in Han Chinese by integrative genome-wide analysis.Frontiers of medicine · 2024Pooled it
- Evolving Therapeutic Strategies in ANCA-Associated Vasculitis: Current Standards and Emerging Targets for GPA and MPA.Clinical reviews in allergy & immunology · 2026Review
- Depletion of IgG-producing plasma cells in the colon by treatment of proteasome inhibitor ameliorates chronic DSS-induced colitis in mice.Scientific reports · 2026Article
- BAFF and APRIL signaling in the B-cell lineage: implications for the pathogenesis of ANCA-associated vasculitis.Frontiers in immunology · 2026Review
- Chimeric autoantibody receptor T cells for targeted depletion of myeloperoxidase-specific anti-neutrophil cytoplasmic antibody-producing B cells.Frontiers in immunology · 2026Article
- Investigating potential biomarkers associated with antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis using Mendelian randomization and transcriptomic analysis.Arthritis research & therapy · 2025Article
- Review
- A narrative review of potential drug treatments for nephritis in children with IgA vasculitis (HSP).Clinical rheumatology · 2023Review
- Article
- B cells in autoimmune hepatitis: bystanders or central players?Seminars in immunopathology · 2022Review
- High-affinity autoreactive plasma cells disseminate through multiple organs in patients with immune thrombocytopenic purpura.The Journal of clinical investigation · 2022Article
- Diagnostic and Therapeutic Approach in ANCA-Associated Glomerulonephritis: A Review on Management Strategies.Frontiers in medicine · 2022Review
- B Lineage Cells in ANCA-Associated Vasculitis.International journal of molecular sciences · 2021Review
- USP36-Mediated Deubiquitination of DOCK4 Contributes to the Diabetic Renal Tubular Epithelial Cell InjuryFrontiers in cell and developmental biology · 2021Article
- The Multiple Roles of B Cells in the Pathogenesis of Sjögren's Syndrome.Frontiers in immunology · 2021Review
- A case of vasculitis case with unusual renal pathological findings presenting with rapidly progressing renal failure.Clinical case reports · 2020Article
- Animal Models of ANCA Associated Vasculitis.Frontiers in immunology · 2020Review
- The pathogenesis and treatment in antineutrophil cytoplasmic antibody associated vasculitis.American journal of translational research · 2020Review
- Serum 20S proteasome levels are associated with disease activity in MPO-ANCA-associated microscopic polyangiitis.BMC rheumatology · 2020Article
- Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anti-neutrophil cytoplasmic autoantibodies (ANCA) cause vasculitis and necrotizing crescentic glomerulonephritis (NCGN). Steroids and cytotoxic drugs reduce mortality but can cause significant adverse events. The proteasome inhibitor bortezomib (BTZ) prevents glomerulonephritis in mouse models of lupus but its efficacy in ANCA-associated glomerulonephritis is unknown. We induced anti-MPO IgG-mediated NCGN by transplanting wild-type bone marrow (BM) into irradiated MPO-deficient mice immunized with MPO. Four weeks after BM transplantation, we treated mice with steroid/cyclophosphamide (S/CYC) or BTZ. Compared with untreated control mice, both S/CYC and BTZ significantly reduced urine abnormalities, NCGN, and infiltration of neutrophils and macrophages. Response to BTZ depended on timing of administration: BTZ abrogated NCGN if begun 3 weeks, but not 5 weeks, after BM transplantation. BTZ treatment significantly reduced total and MPO-specific plasma cells in both the spleen and bone marrow, resulting in significantly reduced anti-MPO titers. Furthermore, BTZ affected neither B cells nor total CD4 and CD8 T cells, including their naive and effector subsets. In contrast, S/CYC reduced the total number of cells in the spleen, including total and MPO-specific plasma cells and B cells. In contrast to BTZ, S/CYC did not affect total and MPO-specific plasma cells in the bone marrow. Three of 23 BTZ-treated mice died within 36 hours after BTZ administration. In summary, BTZ depletes MPO-specific plasma cells, reduces anti-MPO titers, and prevents NCGN in mice.
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