2001
DOI: 10.1002/1529-0131(200107)44:7<1698::aid-art294>3.0.co;2-j
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Antineutrophil cytoplasmic antibodies induce human monocytes to produce oxygen radicals in vitro

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Cited by 82 publications
(52 citation statements)
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“…antigens, [29][30][31] are activated by ANCA, and are consistently detected in ANCA-induced NCGN, their role is less well understood. 31,32 In addition, although ANCA-induced neutrophil and monocyte activation has been extensively characterized in vitro, the effector mechanisms that actually cause the in vivo damage are not yet characterized. It is hypothesized that in a cytokine-rich milieu, ANCAs bind to cell surface membrane-expressed antigens on neutrophils and monocytes, leading to cellular activation and adhesion to the endothelium, the generation of reactive oxygen species, and the release of proteases and other toxic granule proteins, the cumulative effects of which result in small-vessel vasculitis, including NCGN.…”
Section: Discussionmentioning
confidence: 99%
“…antigens, [29][30][31] are activated by ANCA, and are consistently detected in ANCA-induced NCGN, their role is less well understood. 31,32 In addition, although ANCA-induced neutrophil and monocyte activation has been extensively characterized in vitro, the effector mechanisms that actually cause the in vivo damage are not yet characterized. It is hypothesized that in a cytokine-rich milieu, ANCAs bind to cell surface membrane-expressed antigens on neutrophils and monocytes, leading to cellular activation and adhesion to the endothelium, the generation of reactive oxygen species, and the release of proteases and other toxic granule proteins, the cumulative effects of which result in small-vessel vasculitis, including NCGN.…”
Section: Discussionmentioning
confidence: 99%
“…Furthermore, production of oxygen radicals by TNF-α-primed monocytes in response to MPO or PR3-ANCA has been described (13). In addition to a pathogenic role for ANCA, cellular immunity is also considered to be important in ANCA vasculitis, with a role for effector CD4 + cells demonstrated in a murine model (14).…”
Section: Introductionmentioning
confidence: 99%
“…3,4 At first, ANCAs were regarded only as clinical markers of disease activity, but it is now apparent that they have direct biologic effects on neutrophils 5,6 and monocytes. 7 The binding of ANCAs to antigen expressed on the leukocyte cell surface following cytokine priming is followed by the activation of an array of intracellular signaling pathways, 8 with resultant degranulation and dysregulated apoptosis. 9 Granulocyte infiltration and fibrinoid necrosis of the vessel wall are the pathologic hallmarks of SVV.…”
Section: Introductionmentioning
confidence: 99%