Neutrophil priming and apoptosis in anti-neutrophil cytoplasmic autoantibody-associated vasculitis

Kidney International

Volumn 59, Issue 5, 2001, Pages 1729-1738

  Harper, L ^a   Cockwell, P ^a   Adu, D ^a   Savage, C O S ^a  

^a UNIVERSITY OF BIRMINGHAM   (United Kingdom)

Author keywords

Anti neutrophil cytoplasmic antibodies; Apoptosis; Inflammatory response; Small vessel vasculitis; Superoxide

Indexed keywords

APOPTOSIS; ARTICLE; CONTROLLED STUDY; HUMAN; HUMAN CELL; IMMUNE RESPONSE; LEUKOCYTE ACTIVATION; MACROPHAGE; NEPHRITIS; PRIORITY JOURNAL; VASCULITIS;

EID: 0035053871     PISSN: 00852538     EISSN: None     Source Type: Journal    
DOI: 10.1046/j.1523-1755.2001.0590051729.x     Document Type: Article

References (45)

1. Overview of vasculitis: Classification and pathogenesis
2. Activated neutrophils express PR3 on their plasma membrane in vitro and in vivo
3. Endothelial-borne platelet-activating factor and interleukin-8 rapidly immobilize rolling neutrophils
4. A large subset of neutrophils expressing membrane proteinase 3 is a risk factor for vasculitis and rheumatoid arthritis
5. Leucocyte membrane expression of proteinase 3 correlates with disease activity in patients with Wegener's granulomatosis
6. Methylprednisolone normalises superoxide anion production by the polymorphs from patients with ANCA-positive vasculitis
7. Anti-neutrophil cytoplasmic autoantibodies induce neutrophils to degranulate and produce oxygen radicals in vitro
8. Reactivity of antineutrophil cytoplasmic antibodies with mononuclear phagocytes
9. Reactive oxygen species and programmed cell death
10. Involvement of reactive oxygen intermediaries in spontaneous and CD95 (Fas/APO-1)-mediated apoptosis of neutrophils
11. Reactive oxygen intermediate(s) (ROI): Common mediators of poly (ADP-ribose) polymerase (PARP) cleavage and apoptosis
12. Dysregulated neutrophil apoptosis in systemic vasculitis
13. Macrophage phagocytosis of ageing neutrophils in inflammation: Programmed cell death in the neutrophil leads to its recognition by macrophages
14. Glomerular mesangial cells and inflammatory macrophages ingest neutrophils undergoing apoptosis
15. Granulocyte clearance by apoptosis in the resolution of inflammation
16. Resolution of acute inflammation and the role of apoptosis in tissue fate of granulocytes
17. Macrophage engulfment of apoptotic neutrophils contributes to the resolution of acute pulmonary inflammation in vivo
18. Phagocytosis of apoptotic neutrophils does not induce macrophage release of thromboxane B2
19. Human glomerular mesangial cell phagocytosis of apoptotic neutrophils: Mediation by a novel CD36-independent vitronectin receptor/thrombospondin recognition mechanism that is uncoupled from chemokine secretion
20. Different populations of macrophages use either the vitronectin receptor or the phosphatidylserine receptor to recognise and remove apoptotic cells
21. Exposure of phosphatidylserine on the surface of apoptotic lymphocytes triggers specific recognition and removal by macrophages
22. Phagocytosis of aged neutrophils by macrophages is mediated by a novel "charge-sensitive" recognition mechanism
23. Vitronectin receptor mediated phagocytosis of cells undergoing apoptosis
24. Thrombospondin cooperates with CD36 and the vitronectin receptor in macrophage recognition of neutrophils undergoing apoptosis
25. Macrophages that have ingested apoptotic cells in vitro inhibit proinflammatory cytokine production through autocrine/paracrine mechanisms involving TGF-β, PGE2 and PAF
26. Immunosuppressive effects of apoptotic cells
27. Antineutrophil cytoplasmic autoantibodies interact with primary granule constituents on the surface of apoptotic neutrophils in the absence of neutrophil priming
28. Impairment of function in ageing neutrophils is associated with apoptosis
29. IL-1β production by human polymorphonuclear leukocytes stimulated by anti-neutrophil cytoplasmic autoantibodies: Relevance to systemic vasculitis
30. 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 activation
31. The end of the (cell) line: Methods for the study of apoptosis in vitro
32. Pro-inflammatory cytokines potentiate thrombospondin-mediated phagocytosis of cells undergoing apoptosis
33. Interleukin-8: A pathogenetic role in antineutrophil cytoplasmic autoantibody (ANCA)-associated glomerulonephritis
34. Involvement of caspases in neutrophil apoptosis: Regulation off reactive oxygen species
35. Inhibition of neutrophil apoptosis by antioxidants in culture medium
36. Are circulating neutrophils intravascularly activated in patients with anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides?
37. Antibodies against granule proteins activate neutrophils in vitro
38. Interactive role of nitric oxide and superoxide anion in neutrophil-mediated endothelial cell injury
39. Cytokine-induced neutrophil-mediated injury of human endothelial cells
40. New mechanism for glomerular injury: Myeloperoxidase-hydrogen peroxide-halide system
41. Apoptotic cell clearance in systemic lupus erythematosus. I. Opsonisation by antiphospholipid antibodies
42. In situ production of TNF-α, IL-1β and IL-2R in ANCA-positive glomerulonephritis
43. Intraglomerular and interstitial leukocyte infiltration, adhesion molecules, and interleukin-1 alpha expression in 15 cases of antineutrophil cytoplasmic autoantibody-associated renal vasculitis
44. Dendritic cell presentation of antigens from apoptotic cells in a pro-inflammatory context: Role of opsonising anti-β2-glycoprotein I antibodies
45. Bronchoalveolar lavage analysis in Wegener's granulomatosis: A method to study disease pathogenesis