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氧化应激后的补体激活。

Complement activation following oxidative stress.

作者信息

Collard C D, Lekowski R, Jordan J E, Agah A, Stahl G L

机构信息

Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

出版信息

Mol Immunol. 1999 Sep-Oct;36(13-14):941-8. doi: 10.1016/s0161-5890(99)00116-9.

Abstract

It is clear that complement plays an important role in the inflammatory process following oxidative stress in cellular and animal models. Clinical trials underway with novel complement inhibitors will establish the potential therapeutic benefit of complement inhibition in human disease. For as much as we understand about the role of complement in disease states, many questions remain. How is complement activated on endothelial cells following oxidative stress? What is the ligand for MBL on endothelial cells following oxidative stress? Will inhibition of MBL provide tissue protection to the extent observed with other complement inhibitors such as sCR1 or anti-C5 mAbs? These questions and more will undoubtedly be answered in the next millennium.

摘要

显然,在细胞和动物模型中,补体在氧化应激后的炎症过程中发挥着重要作用。正在进行的新型补体抑制剂临床试验将确定补体抑制在人类疾病中的潜在治疗益处。尽管我们对补体在疾病状态中的作用了解颇多,但仍有许多问题存在。氧化应激后内皮细胞上的补体是如何被激活的?氧化应激后内皮细胞上MBL的配体是什么?抑制MBL是否能像其他补体抑制剂(如sCR1或抗C5单克隆抗体)那样提供同等程度的组织保护?毫无疑问,这些问题以及更多问题将在未来千年内得到解答。

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