血型抗原CD59与疾病的关系

IF 1.9 4区 医学 Q3 HEMATOLOGY
C. Weinstock
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引用次数: 9

摘要

2014年,膜结合蛋白CD59成为一种血型抗原。几十年来,CD59一直被认为是补体系统的抑制剂,位于红细胞和许多其他细胞类型上。在阵发性夜间血红蛋白尿(PNH)中,获得性缺乏表达gpi锚定分子(包括补体抑制剂CD59)的干细胞克隆可导致严重和危及生命的疾病。CD59是膜攻击复合物的唯一膜结合抑制剂,缺乏CD59是PNH患者血管内溶血的主要原因。CD59在PNH疾病中的关键作用促使研究调查其在其他疾病中的作用。在这篇综述中,CD59在炎症、风湿性疾病和年龄相关性黄斑变性中的作用被研究。进一步,对CD59在PNH和先天性CD59缺乏症中的关键作用进行了综述。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Association of Blood Group Antigen CD59 with Disease
In 2014, the membrane-bound protein CD59 became a blood group antigen. CD59 has been known for decades as an inhibitor of the complement system, located on erythrocytes and on many other cell types. In paroxysmal nocturnal haemoglobinuria (PNH), a stem cell clone with acquired deficiency to express GPI-anchored molecules, including the complement inhibitor CD59, causes severe and life-threatening disease. The lack of CD59, which is the only membrane-bound inhibitor of the membrane attack complex, contributes a major part of the intravascular haemolysis observed in PNH patients. This crucial effect of CD59 in PNH disease prompted studies to investigate its role in other diseases. In this review, the role of CD59 in inflammation, rheumatic disease, and age-related macular degeneration is investigated. Further, the pivotal role of CD59 in PNH and congenital CD59 deficiency is reviewed.
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来源期刊
CiteScore
4.00
自引率
9.10%
发文量
47
审稿时长
6-12 weeks
期刊介绍: This journal is devoted to all areas of transfusion medicine. These include the quality and security of blood products, therapy with blood components and plasma derivatives, transfusion-related questions in transplantation, stem cell manipulation, therapeutic and diagnostic problems of homeostasis, immuno-hematological investigations, and legal aspects of the production of blood products as well as hemotherapy. Both comprehensive reviews and primary publications that detail the newest work in transfusion medicine and hemotherapy promote the international exchange of knowledge within these disciplines. Consistent with this goal, continuing clinical education is also specifically addressed.
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