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抗髓过氧化物酶抗体可诱导中性粒细胞黏附于培养的人内皮细胞。

Antimyeloperoxidase antibodies induce neutrophil adherence to cultured human endothelial cells.

作者信息

Ewert B H, Becker M E, Jennette J C, Falk R J

机构信息

Department of Medicine, University of North Carolina--Chapel Hill, USA.

出版信息

Ren Fail. 1995 Mar;17(2):125-33. doi: 10.3109/08860229509026249.

Abstract

Antimyeloperoxidase autoantibodies are found in the sera of some patients with glomerulonephritis and systemic vasculitis. Previously, we demonstrated that they were able to stimulate neutrophils to damage cultured human endothelial cells. We now report that antimyeloperoxidase antibodies are able to stimulate neutrophils to adhere to cultured human endothelial cells. Immunoglobulin G purified from myeloperoxidase-antineutrophil cytoplasmic autoantibody positive sera increased adherence to 331 +/- 60% of unstimulated controls. In a similar manner, rabbit antimyeloperoxidase enhanced neutrophil adherence. Stimulating the endothelial cells with 10 micrograms/mL endotoxin enhanced antimyeloperoxidase stimulated adherence. In the presence of a CD18 blocking antibody (MoAb 60.3), antimyeloperoxidase-stimulated adherence was significantly decreased. These results add further understanding to the antimyeloperoxidase-stimulated neutrophil-endothelial cell interaction and further support the hypothesis that antimyeloperoxidase autoantibodies are of pathogenic import in glomerulonephritis and vasculitis.

摘要

抗髓过氧化物酶自身抗体在一些肾小球肾炎和系统性血管炎患者的血清中被发现。此前,我们证明它们能够刺激中性粒细胞损伤培养的人内皮细胞。我们现在报告抗髓过氧化物酶抗体能够刺激中性粒细胞黏附于培养的人内皮细胞。从髓过氧化物酶-抗中性粒细胞胞浆自身抗体阳性血清中纯化的免疫球蛋白G使黏附增加至未刺激对照的331±60%。以类似方式,兔抗髓过氧化物酶增强了中性粒细胞黏附。用10微克/毫升内毒素刺激内皮细胞增强了抗髓过氧化物酶刺激的黏附。在存在CD18阻断抗体(单克隆抗体60.3)的情况下,抗髓过氧化物酶刺激的黏附显著降低。这些结果进一步加深了对抗髓过氧化物酶刺激的中性粒细胞-内皮细胞相互作用的理解,并进一步支持了抗髓过氧化物酶自身抗体在肾小球肾炎和血管炎中具有致病重要性的假说。

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