Pathogenic role of antimyeloperoxidase antibodies

被引:5
|
作者
Guilpain, P. [1 ,2 ]
Maldini, C. [1 ]
Guillevin, L. [1 ]
机构
[1] Univ Paris 05, Hop Cochin, AP HP, Fac Med,Ctr Natl Reference Malad Autoimmunes & Sy, F-75679 Paris 14, France
[2] Univ Paris 05, Hop Cochin, AP HP, Fac Med,EA 1833,IFR Alfred Jost,Lab Immunol, F-75014 Paris, France
来源
REVUE DE MEDECINE INTERNE | 2011年 / 32卷 / 07期
关键词
Antineutrophil cytoplasm antibodies; Anca; Myeloperoxidase; Vasculitis; Hypochlorous acid; Neutrophil; ANTINEUTROPHIL CYTOPLASMIC AUTOANTIBODIES; SMALL-VESSEL VASCULITIS; MPO-ANCA; MICROSCOPIC POLYANGIITIS; MYELOPEROXIDASE; GLOMERULONEPHRITIS; NEUTROPHILS; PROPYLTHIOURACIL; INHIBITION; CELLS;
D O I
10.1016/j.revmed.2010.05.005
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Antirnyeloperoxidase antibodies are a variety of antineutrophil cytoplasm antibodies (Anca), which can be detected in systemic small-sized vessel vasculitides such as microscopic polyangiitis, Wegener's granulomatosis and Churg-Strauss syndrome. Antimyeloperoxidase antibodies have been also associated with the development of lung fibrosis. Their pathogenic role has been well established, both in vitro and in vivo. These autoantibodies can activate neutrophils and trigger their oxidative burst leading to the release of free oxygen species and cytotoxic proteins. The oxidative burst is deleterious for the endothelium. Another mechanism by which antimyeloperoxidase may act is the activation of myeloperoxydase leading to an increased production of hypochlorous acid, which is highly toxic for the endothelial cells. These mechanisms contribute to the development of vasculitis. (C) 2010 Societe nationale francaise de medecine interne (SNFMI). Published by Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:411 / 415
页数:5
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