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补体参与了志贺毒素相关性溶血尿毒综合征的发病机制。

Complement contributes to the pathogenesis of Shiga toxin-associated hemolytic uremic syndrome.

机构信息

Department of Pediatrics, Clinical Sciences Lund, Lund University, Lund, Sweden.

Department of Pediatrics, Clinical Sciences Lund, Lund University, Lund, Sweden.

出版信息

Kidney Int. 2016 Oct;90(4):726-9. doi: 10.1016/j.kint.2016.07.002.

DOI:10.1016/j.kint.2016.07.002
PMID:27633864
Abstract

Complement is activated during Shiga toxin-producing Escherichia coli-associated hemolytic uremic syndrome (STEC-HUS). There is evidence of complement activation via the alternative pathway in STEC-HUS patients as well as from in vivo and in vitro models. Ozaki et al. demonstrate activation of the mannose-binding lectin (MBL) pathway in Shiga toxin-treated mice expressing human MBL2, but lacking murine Mbls. Treatment with anti-human MBL2 antibody was protective, suggesting that MBL pathway activation also contributes to Shiga toxin-mediated renal injury.

摘要

补体在产志贺样毒素大肠杆菌相关性溶血尿毒症综合征(STEC-HUS)中被激活。有证据表明,STEC-HUS 患者以及体内和体外模型中存在补体通过替代途径的激活。Ozaki 等人证明,在表达人 MBL2 但缺乏鼠 Mbls 的 Shiga 毒素处理的小鼠中,甘露糖结合凝集素(MBL)途径被激活。用抗人 MBL2 抗体治疗具有保护作用,表明 MBL 途径的激活也有助于 Shiga 毒素介导的肾损伤。

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