Neutrophil priming and apoptosis in anti-neutrophil cytoplasmic autoantibody-associated vasculitis
- 1 May 2001
- journal article
- Published by Elsevier BV in Kidney International
- Vol. 59 (5), 1729-1738
- https://doi.org/10.1046/j.1523-1755.2001.0590051729.x
Abstract
No abstract availableKeywords
This publication has 37 references indexed in Scilit:
- The activation of the neutrophil respiratory burst by anti-neutrophil cytoplasm autoantibody (ANCA) from patients with systemic vasculitis requires tyrosine kinases and protein kinase C activationClinical and Experimental Immunology, 1999
- Macrophages that have ingested apoptotic cells in vitro inhibit proinflammatory cytokine production through autocrine/paracrine mechanisms involving TGF-beta, PGE2, and PAF.JCI Insight, 1998
- Antineutrophil Cytoplasmic Autoantibodies Interact with Primary Granule Constituents on the Surface of Apoptotic Neutrophils in the Absence of Neutrophil PrimingThe Journal of Experimental Medicine, 1996
- Reactive oxygen intermediate(s) (ROI): Common mediator(s) of poly(ADP‐ribose)polymerase (PARP) cleavage and apoptosisFEBS Letters, 1996
- Reactive oxygen species and programmed cell deathTrends in Biochemical Sciences, 1996
- CD36 gene transfer confers capacity for phagocytosis of cells undergoing apoptosis.The Journal of Experimental Medicine, 1995
- Methylprednisolone normalizes superoxide anion production by polymorphs from patients with ANCA-positive vasculitidesKidney International, 1993
- Thrombospondin cooperates with CD36 and the vitronectin receptor in macrophage recognition of neutrophils undergoing apoptosis.JCI Insight, 1992
- Vitronectin receptor-mediated phagocytosis of cells undergoing apoptosisNature, 1990
- Macrophage phagocytosis of aging neutrophils in inflammation. Programmed cell death in the neutrophil leads to its recognition by macrophages.JCI Insight, 1989