ArticleJournal of the American Society of Nephrology : JASN2012
Neutrophil serine proteases promote IL-1β generation and injury in necrotizing crescentic glomerulonephritis.
Article in Journal of the American Society of Nephrology : JASN, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 129 citations in OpenAlex.
- Immature leukocyte and plasma-induced cell death reveal subclinical immune activation in EGPA patients in remission.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Cathepsin C-driven enhancement of neutrophil extracellular trap formation contributes to acute lung injury.iScience · 2025Article
- CAR-T cells targeting CD19 for the treatment of ANCA vasculitis.Clinical kidney journal · 2025Article
- Dipeptidyl peptidase 1 inhibitors and neutrophilic inflammation in bronchiectasis: a narrative review.Journal of thoracic disease · 2025Review
- NLRP3 inflammasome activity and pyroptosis are involved in CD206Acta biochimica et biophysica Sinica · 2025Article
- Exploring the involvement of serine proteases in neutrophil extracellular traps: a review of mechanisms and implications.Cell death & disease · 2025Review
- Role of the RAB27/SYTL Axis in Tumor Microenvironment Construction.Cancer science · 2025Review
- CCL23 is a potential biomarker for antineutrophil cytoplasmic antibody-associated vasculitis.Arthritis research & therapy · 2025Article
- Neutralizing the Th1 effector cytokines, IFN-γ and TNF-α, attenuates established experimental autoimmune anti-myeloperoxidase glomerulonephritis.Frontiers in immunology · 2025Article
- Neutrophil extracellular traps and interleukin-1β in cystic fibrosis lung disease.Frontiers in immunology · 2025Review
- Drug repurposing for glomerular diseases: an underutilized resource.Nature reviews. Nephrology · 2024Review
- Cathepsin C from extracellular histone-induced M1 alveolar macrophages promotes NETosis during lung ischemia-reperfusion injury.Redox biology · 2024Article
- Autoinflammatory diseases and the kidney.Immunologic research · 2023Review
- Epigenetic regulation of chemokine (CC-motif) ligand 2 in inflammatory diseases.Cell proliferation · 2023Review
- Cysteine Cathepsins as Therapeutic Targets in Immune Regulation and Immune Disorders.Biomedicines · 2023Review
- Dipeptidyl peptidase 1 inhibition as a potential therapeutic approach in neutrophil-mediated inflammatory disease.Frontiers in immunology · 2023Review
- Myeloid expression of the anti-apoptotic protein Mcl1 is required in anti-myeloperoxidase vasculitis but myeloperoxidase inhibition is not protective.Kidney international · 2023Article
- Protective α1-antitrypsin effects in autoimmune vasculitis are compromised by methionine oxidation.The Journal of clinical investigation · 2022Article
- CSF2-dependent monocyte education in the pathogenesis of ANCA-induced glomerulonephritis.Annals of the rheumatic diseases · 2022Article
- Glomerulonephritis and autoimmune vasculitis are independent of P2RX7 but may depend on alternative inflammasome pathways.The Journal of pathology · 2022Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The pathogenesis of anti-neutrophil cytoplasmic antibody (ANCA)-associated necrotizing crescentic GN (NCGN) is incompletely understood. Dipeptidyl peptidase I (DPPI) is a cysteine protease required for the activation of neutrophil serine proteases (NSPs) cathepsin G, neutrophil elastase, and proteinase 3, which are enzymes that modulate inflammation. We used a mouse model of anti-myeloperoxidase (MPO) antibody-induced NCGN to determine whether active NSPs contribute to its pathogenesis. MPO-deficient animals immunized with murine MPO, irradiated, and transplanted with wild-type bone marrow developed NCGN. In contrast, transplantation with bone marrow that lacked DPPI or lacked both neutrophil elastase and proteinase 3 protected mice from NCGN induced by anti-MPO antibody. The kidneys of mice reconstituted with DPPI-deficient bone marrow generated significantly less IL-1β than did those of mice reconstituted with wild-type bone marrow; similarly, in vitro, DPPI-deficient monocytes produced significantly less IL-1β in response to anti-MPO antibody than did wild-type monocytes. This reduction in IL-1β was NSP dependent; exogenous addition of PR3 restored IL-β production in DPPI-deficient monocytes. Last, the IL-1 receptor antagonist anakinra protected animals against anti-MPO antibody-induced NCGN (16.7%±6.0% versus 2.4%±1.7% crescents), suggesting that IL-1β is a critical inflammatory mediator in this model. These data suggest that the development of anti-MPO antibody-induced NCGN requires NSP-dependent IL-1β generation and that these processes may provide therapeutic targets for ANCA-mediated diseases in humans.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.