Tissue factor expression in neutrophil extracellular traps and neutrophil derived microparticles in antineutrophil cytoplasmic antibody associated vasculitis may promote thromboinflammation and the thrombophilic state associated with the disease

Kambas, Konstantinos; Chrysanthopoulou, Akrivi; Vassilopoulos, Dimitrios; Apostolidou, Eirini; Skendros, Panagiotis; Girod, Andreas; Arelaki, Stella; Froudarakis, Marios; Nakopoulou, Lydia; Giatromanolaki, Alexandra; Sidiropoulos, Prodromos; Koffa, Maria; Boumpas, Dimitrios T.; Ritis, Konstantinos; Mitroulis, Ioannis

doi:10.1136/annrheumdis-2013-203430

Cited by 234 publications

(240 citation statements)

References 44 publications

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“…Deregulated NET formation/degradation represents a source of intracellular antigens that can be presented in inflammatory contexts that favour their immunogenicity. Indeed, deregulated NET generation and processing have been associated with several autoimmune diseases [8][9][10][11][12][13][14]. Here, we report evidence that supports the existence of a finely tuned regulatory loop by which neutrophils that had successfully phagocytosed apoptotic cells lose their ability to respond to inflammatory stimuli and in particular to generate NETs.…”

Section: Introductionsupporting

confidence: 55%

Instructive influences of phagocytic clearance of dying cells on neutrophil extracellular trap generation

Manfredi

Covino²,

Rovere‐Querini

et al. 2014

Clinical and Experimental Immunology

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Instructive influences of phagocytic clearance of dying cells on neutrophil extracellular trap generation OTHER ARTICLES PUBLISHED IN THIS SERIESDying autologous cells as instructors of the immune system. Clinical and Experimental Immunology 2015, 179: 1-4. Anti-dsDNA antibodies as a classification criterion and a diagnostic marker for systemic lupus erythematosus: critical remarks. Clinical and Experimental Immunology 2015, 179: 5-10. The effect of cell death in the initiation of lupus nephritis. Clinical and Experimental Immunology 2015, 179: 11-16

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Section: Introductionsupporting

confidence: 55%

Instructive influences of phagocytic clearance of dying cells on neutrophil extracellular trap generation

Manfredi

Covino²,

Rovere‐Querini

et al. 2014

Clinical and Experimental Immunology

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“…In a similar manner, an increase in the amount of proinflammatory, procoagulant platelet-derived EVs in patients with Crohn's disease compared with that in healthy subjects was observed, implicating these EVs in disease progression (80). Both neutrophil-derived and platelet-derived EVs were shown to increase in patients with an anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) compared with that in remittent AAV subjects (81)(82)(83). Furthermore, platelet-derived EVs associated with oxidized high-mobility group box 1 protein (HMGB1) were shown to increase neutrophil activation, which could be responsible for phenotypes associated with systemic sclerosis.…”

Section: Immune Regulation By Circulating Endogenous Evsmentioning

confidence: 56%

Regulation of chronic inflammatory and immune processes by extracellular vesicles

Robbins

Dorronsoro

Booker

2016

Journal of Clinical Investigation

236

195

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“…44 On the other hand, expression of ADAM17 is increased in activated leukocytes, and release of neutrophil microparticles is also strongly enhanced in AAV. 45,46 Moreover, expression of ADAM17, but not of ADAM10, is strongly enhanced in blood cells of patients with active AAV. It is therefore likely that ADAM17-bearing microparticles originated from both endothelial cells and leukocytes.…”

Section: Discussionmentioning

confidence: 99%

Circulating ADAM17 Level Reflects Disease Activity in Proteinase-3 ANCA-Associated Vasculitis

Bertram

Lovric

Engel

et al. 2015

Journal of the American Society of Nephrology

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ANCA-associated vasculitides are characterized by inflammatory destruction of small vessels accompanied by enhanced cleavage of membrane-bound proteins. One of the main proteases responsible for ectodomain shedding is disintegrin and metalloproteinase domain-containing protein 17 (ADAM17). Given its potential role in aggravating vascular dysfunction, we examined the role of ADAM17 in active proteinase-3 (PR3)-positive ANCA-associated vasculitis (AAV). ADAM17 concentration was significantly increased in plasma samples from patients with active PR3-AAV compared with samples from patients in remission or from other controls with renal nonvascular diseases. Comparably, plasma levels of the ADAM17 substrate syndecan-1 were significantly enhanced in active AAV. We also observed that plasmaderived ADAM17 retained its specific proteolytic activity and was partly located on extracellular microparticles. Transcript levels of ADAM17 were increased in blood samples of patients with active AAV, but those of ADAM10 or tissue inhibitor of metalloproteinases 3, which inhibits ADAMs, were not. We also performed a microRNA (miR) screen and identified miR-634 as significantly upregulated in blood samples from patients with active AAV. In vitro, miR-634 mimics induced a proinflammatory phenotype in monocyte-derived macrophages, with enhanced expression and release of ADAM17 and IL-6. These data suggest that ADAM17 has a prominent role in AAV and might account for the vascular complications associated with this disease.

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Tissue factor expression in neutrophil extracellular traps and neutrophil derived microparticles in antineutrophil cytoplasmic antibody associated vasculitis may promote thromboinflammation and the thrombophilic state associated with the disease

Abstract: Expression of TF in NETs and neutrophil derived MPs proposes a novel mechanism for the induction of thrombosis and inflammation in active AAV.

Cited by 234 publications

References 44 publications

Instructive influences of phagocytic clearance of dying cells on neutrophil extracellular trap generation

Instructive influences of phagocytic clearance of dying cells on neutrophil extracellular trap generation

Regulation of chronic inflammatory and immune processes by extracellular vesicles

Circulating ADAM17 Level Reflects Disease Activity in Proteinase-3 ANCA-Associated Vasculitis

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