Netting neutrophils in autoimmune small-vessel vasculitis

By K. Kessenbrock, M. Krumbholz, U. Schönermarck, W. Back, W. Gross, Zena Werb, H. Gröne, V. Brinkmann, D. Jenne. Nature Medicine, 2009

1,645 citations recorded by the source corpus.

Small-vessel vasculitis (SVV) is a chronic autoinflammatory condition linked to antineutrophil cytoplasm autoantibodies (ANCAs). Here we show that chromatin fibers, so-called neutrophil extracellular traps (NETs), are released by ANCA-stimulated neutrophils and contain the targeted autoantigens proteinase-3 (PR3) and myeloperoxidase (MPO). Deposition of NETs in inflamed kidneys and circulating MPO-DNA complexes suggest that NET formation triggers vasculitis and promotes the autoimmune response against neutrophil components in individuals with SVV.

Subfields: Immunology, Molecular Biology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/d0a62f4b2a6dd7e99be9df480a514f0d9d0d2bb8

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Citations in the corpus

NETosis: how vital is it? (2013, background): “Indeed, Kessenbrock et al revealed that PMN-mediated host defense and the release of NETs is sufficient to induce smallvessel vasculitis.(105) Although nucleosomes were previously known to circulate in vasculitis patients,(106) Kessenbrock directly demonstrated that the circulating DNA was attached ”
Neutrophils in the activation and regulation of innate and adaptive immunity (2011, background): “Interestingly, NETs are produced by ANCA-stimulated neutrophils and were found in glomeruli and in the interstitium of kidney biopsies from patients with SVV, where they may be involved in the damage to glomerular capillarie”
Neutrophil extracellular traps in COVID-19. (2020, methodology): “MPO-DNA complexes were quantified similarly to what has been previously described (68).”
Intravascular neutrophil extracellular traps capture bacteria from the bloodstream during sepsis. (2012, background): “Numerous reports have demonstrated roles for NETs in tissue damage and disease pathology in a number of infectious, inflammatory, and autoimmune diseases (Clark et al., 2007; Fuchs et al., 2010; Kessenbrock et al., 2009; Villanueva et al., 2011).”
Platelets induce neutrophil extracellular traps in transfusion-related acute lung injury. (2012, background): “They have also been observed in inflammatory diseases such as preeclampsia (13), small-vessel vasculitis (14), and systemic lupus erythematosus (15).”
Netting Neutrophils Are Major Inducers of Type I IFN Production in Pediatric Systemic Lupus Erythematosus (2011, background): “TNF-a–activated neutrophils have been recently described to undergo NETosis upon incubation with anti-MPO (myeloperoxidase) antibodies from patients with ANCA-related vasculitis, and NET-related material could be visualized in kidney sections from these patients (40).”
Diverse novel functions of neutrophils in immunity, inflammation, and beyond (2013, result): “These results are also in line with a proposed contribution of NET degradation defects to SLE pathogenesis (Yasutomo et al., 2001; Hakkim et al., 2010), as well as a previous study on the presence of NET formation in autoimmune small vessel vasculitis (Kessenbrock et al., 2009).”
Neutrophils Activate Plasmacytoid Dendritic Cells by Releasing Self-DNA–Peptide Complexes in Systemic Lupus Erythematosus (2011, background): “NETs are induced by autoantibodies against antimicrobial peptides and are released in higher amounts by neutrophils of SLE patients Because anti-neutrophil antibodies have been shown to trigger the formation of NETs (36), we sought to determine whether antibodies against antimicrobial peptides prese”
Dying for a cause: NETosis, mechanisms behind an antimicrobial cell death modality (2011, neutral): “have also been isolated from patients suffering from the autoimmune disease small vessel vasculitis (SVV).(37) Anti-neutrophil antibodies are also generated in other diseases, such as SLE and malaria,(32,38) and so they might trigger NETosis in these conditions as well.”
Neutrophil Extracellular Traps Directly Induce Epithelial and Endothelial Cell Death: A Predominant Role of Histones (2012, background): “as preeclampsia, small-vessel vasculitis and systemic lupus erythematosus [26,28,29,31,60,61].”
NETs are a source of citrullinated autoantigens and stimulate inflammatory responses in rheumatoid arthritis (2013, background): “Recent evidence suggests that, among the various mechanisms by which neutrophils cause tissue damage and promote autoimmunity, aberrant formation of neutrophil extracellular traps (NETs) could play important roles in the pathogenesis of systemic lupus erythematosus (SLE), psoriasis, small vessel vas”
Neutrophils: Between Host Defence, Immune Modulation, and Tissue Injury (2015, background): “Although NET generation has been described initially as an antimicrobial mechanism, recent data suggest that NETs could play a more important role in autoimmune and autoinflammatory pathologies, such as vasculitis [71], lung injury [72,73], atherosclerosis [74], rheumatoid arthritis [75,76], thrombo”