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系统性坏死性血管炎致病机制的最新进展

Update on pathogenic mechanisms of systemic necrotizing vasculitis.

作者信息

Danila Maria I, Bridges S Louis

机构信息

Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham, 1530 3rd Avenue South, 805 FOT, Birmingham, AL 35294, USA.

出版信息

Curr Rheumatol Rep. 2008 Dec;10(6):430-5. doi: 10.1007/s11926-008-0070-1.

DOI:10.1007/s11926-008-0070-1
PMID:19007531
Abstract

Systemic necrotizing vasculitis is rare but can have serious sequelae. Despite recent advances in cellular and molecular immunology and genetics, the causes of vasculitic syndromes remain largely undefined. Although mechanisms of blood vessel damage in systemic necrotizing vasculitis are complex, recent studies have provided significant insights.

摘要

系统性坏死性血管炎较为罕见,但可产生严重的后遗症。尽管细胞和分子免疫学以及遗传学方面近来有所进展,但血管炎综合征的病因在很大程度上仍不明确。虽然系统性坏死性血管炎中血管损伤的机制很复杂,但最近的研究已提供了重要的见解。

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Update on pathogenic mechanisms of systemic necrotizing vasculitis.系统性坏死性血管炎致病机制的最新进展
Curr Rheumatol Rep. 2008 Dec;10(6):430-5. doi: 10.1007/s11926-008-0070-1.
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Involvement of regulatory T cells in the pathogenesis of Churg-Strauss syndrome.调节性T细胞在变应性肉芽肿性血管炎发病机制中的作用
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Antibodies to proteinase 3 prime human oral, lung, and kidney epithelial cells to secrete proinflammatory cytokines upon stimulation with agonists to various Toll-like receptors, NOD1, and NOD2.蛋白酶3抗体促使人类口腔、肺和肾上皮细胞在受到各种Toll样受体、NOD1和NOD2激动剂刺激时分泌促炎细胞因子。
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Neutrophil surface presentation of the anti-neutrophil cytoplasmic antibody-antigen proteinase 3 depends on N-terminal processing.抗中性粒细胞胞浆抗体-抗原蛋白酶3在中性粒细胞表面的呈递取决于N端加工。
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