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Nephrol Dial Transplant (2002) 17: 1725-1728
© 2002 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

Apoptosis: the central actor in the three hits that trigger anti-neutrophil cytoplasmic antibody-related systemic vasculitis

Vincent L. M. Esnault

Nephrology–Clinical Immunology Department, Nantes University Hospital, Nantes, France

The first 10% of the full text of this article appears below.

Small vessel vasculitis is associated with harmful anti-neutrophil cytoplasmic antibodies directed against sheltered antigens

Wegener's granulomatosis and microscopic polyangiitis are small vessel systemic vasculitides characterized by the presence of anti-neutrophil cytoplasmic antibodies (ANCA) and a high frequency of rapidly progressive glomerulonephritis. The main target antigens for ANCA are proteinase 3 (PR3) and myeloperoxidase (MPO). Both antigens are tightly sheltered from the immune system (cryptic). Indeed, they are stored in cytoplasmic granules of neutrophils, and are very rapidly scavenged after degranulation at the inflammatory site by specific inhibitors: {alpha}1-antitrypsin for PR3 [1] and ceruloplasmin for MPO [2]. However, both antigens are exposed at the cell surface after neutrophil priming by a proinflammatory cytokine [tumour necrosis factor {alpha} (TNF{alpha})], and this allows neutrophil activation by ANCA in vitro, with production of toxic oxygen species, degranulation of proteolytic enzymes and endothelial cell lysis [3]. This activation process of neutrophils by ANCA is highly regulated, . . . [Full Text of this Article]

Neutrophil apoptosis: saviour or villain?

The development of ANCA positive systemic vasculitis may require a three step pathological process

(i) An exogenous stimulus increases neutrophil and macrophage apoptosis
(ii) Increased apoptotic neutrophil exposure together with ‘danger signals’ induces ANCA production
(iii) Environmental and genetic factors amplify disease expression
Conclusion


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[Abstract] [Full Text] [PDF]