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1
Increased enzymatic activity of the alternative pathway convertase when bound to the erythrocytes of paroxysmal nocturnal hemoglobinuria.当与阵发性夜间血红蛋白尿症的红细胞结合时，替代途径转化酶的酶活性增加。
J Clin Invest. 1982 Feb;69(2):337-46. doi: 10.1172/jci110457.
2
Abnormality of glycophorin-alpha on paroxysmal nocturnal hemoglobinuria erythrocytes.阵发性夜间血红蛋白尿症红细胞上血型糖蛋白α的异常。
J Clin Invest. 1984 Apr;73(4):1130-43. doi: 10.1172/JCI111299.
3
Protection of the classical and alternative complement pathway C3 convertases, stabilized by nephritic factors, from decay by the human C3b receptor.由肾炎因子稳定的经典和替代补体途径C3转化酶免受人类C3b受体介导的衰变作用。
Eur J Immunol. 1984 Dec;14(12):1111-4. doi: 10.1002/eji.1830141209.
4
Paroxysmal nocturnal hemoglobinuria: deficiency in factor H-like functions of the abnormal erythrocytes.阵发性夜间血红蛋白尿：异常红细胞中类似补体因子H功能的缺陷。
J Exp Med. 1983 Jun 1;157(6):1971-80. doi: 10.1084/jem.157.6.1971.
5
Deficiency of an erythrocyte membrane protein with complement regulatory activity in paroxysmal nocturnal hemoglobinuria.阵发性夜间血红蛋白尿中具有补体调节活性的红细胞膜蛋白缺乏。
Proc Natl Acad Sci U S A. 1983 Sep;80(17):5430-4. doi: 10.1073/pnas.80.17.5430.
6
Affected erythrocytes of patients with paroxysmal nocturnal hemoglobinuria are deficient in the complement regulatory protein, decay accelerating factor.阵发性夜间血红蛋白尿患者的受累红细胞缺乏补体调节蛋白衰变加速因子。
Proc Natl Acad Sci U S A. 1983 Aug;80(16):5066-70. doi: 10.1073/pnas.80.16.5066.
7
Stabilization of the amplification convertase of complement by monoclonal antibodies directed against human factor B.针对人B因子的单克隆抗体对补体扩增转化酶的稳定作用
J Immunol. 1984 May;132(5):2538-42.
8
Regulation of the C3 nephritic factor stabilized C3/C5 convertase of complement by purified human erythrocyte C3b receptor.纯化的人红细胞C3b受体对补体C3肾炎因子稳定的C3/C5转化酶的调节作用。
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9
A circulating inhibitor of fluid-phase amplification. C3 convertase formation in systemic lupus erythematosus.液相放大的循环抑制剂。系统性红斑狼疮中C3转化酶的形成。
J Clin Invest. 1985 Jun;75(6):1786-95. doi: 10.1172/JCI111891.
10
Enhanced reactive lysis of paroxysmal nocturnal hemoglobinuria erythrocytes by C5b-9 does not involve increased C7 binding or cell-bound C3b.C5b-9对阵发性夜间血红蛋白尿红细胞的反应性溶解增强并不涉及C7结合增加或细胞结合的C3b增加。
J Immunol. 1985 Jan;134(1):506-11.

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1
Anti-Complement Treatment in Paroxysmal Nocturnal Hemoglobinuria: Where we Stand and Where we are Going.阵发性睡眠性血红蛋白尿症的抗补体治疗：我们的现状与未来走向
Transl Med UniSa. 2014 Feb 4;8:43-52. eCollection 2014 Jan.
2
Advances in the diagnosis and therapy of paroxysmal nocturnal hemoglobinuria.阵发性睡眠性血红蛋白尿症的诊断与治疗进展
Blood Rev. 2008 Mar;22(2):65-74. doi: 10.1016/j.blre.2007.10.002. Epub 2007 Dec 3.
3
Effects of two types of cobra venom factor on porcine complement activation and pulmonary artery pressure.两种眼镜蛇毒因子对猪补体激活及肺动脉压的影响。
Clin Exp Immunol. 1989 Nov;78(2):299-306.
4
Activation of human complement by immunoglobulin G antigranulocyte antibody.免疫球蛋白G抗粒细胞抗体对人补体的激活作用。
J Clin Invest. 1982 Dec;70(6):1137-47. doi: 10.1172/jci110712.
5
Affected erythrocytes of patients with paroxysmal nocturnal hemoglobinuria are deficient in the complement regulatory protein, decay accelerating factor.阵发性夜间血红蛋白尿患者的受累红细胞缺乏补体调节蛋白衰变加速因子。
Proc Natl Acad Sci U S A. 1983 Aug;80(16):5066-70. doi: 10.1073/pnas.80.16.5066.
6
Characterization of alternative pathway inhibition by a serum derived, low molecular weight complement inhibitor.一种血清来源的低分子量补体抑制剂对替代途径抑制作用的表征
Clin Exp Immunol. 1984 Jan;55(1):166-76.
7
The role of complement in immune clearance of blood cells.补体在血细胞免疫清除中的作用。
Springer Semin Immunopathol. 1983;6(4):373-98. doi: 10.1007/BF02116281.
8
Increased efficiency of binding of nascent C3b to the erythrocytes of chronic cold agglutinin disease.慢性冷凝集素病患者新生C3b与红细胞结合效率增加。
J Clin Invest. 1984 Sep;74(3):1050-62. doi: 10.1172/JCI111472.
9
Abnormality of glycophorin-alpha on paroxysmal nocturnal hemoglobinuria erythrocytes.阵发性夜间血红蛋白尿症红细胞上血型糖蛋白α的异常。
J Clin Invest. 1984 Apr;73(4):1130-43. doi: 10.1172/JCI111299.
10
Deficiency of an erythrocyte membrane protein with complement regulatory activity in paroxysmal nocturnal hemoglobinuria.阵发性夜间血红蛋白尿中具有补体调节活性的红细胞膜蛋白缺乏。
Proc Natl Acad Sci U S A. 1983 Sep;80(17):5430-4. doi: 10.1073/pnas.80.17.5430.

本文引用的文献

1
Paroxysmal nocturnal hemoglobinuria. II. Erythrocyte acetylcholinesterase defect.阵发性夜间血红蛋白尿。II. 红细胞乙酰胆碱酯酶缺陷。
Am J Med. 1959 Sep;27:401-10. doi: 10.1016/0002-9343(59)90005-1.
2
Inhibitors of complement derived from the erythrocyte membrane in paroxysmal nocturnal hemoglobinuria.阵发性夜间血红蛋白尿中源自红细胞膜的补体抑制剂。
Blood. 1980 May;55(5):772-6.
3
Activation of the alternative complement pathway: recognition of surface structures on activators by bound C3b.替代补体途径的激活：结合的C3b识别激活物上的表面结构。
J Immunol. 1980 Feb;124(2):977-82.
4
Identification of the membrane glycoprotein that is the C3b receptor of the human erythrocyte, polymorphonuclear leukocyte, B lymphocyte, and monocyte.鉴定作为人类红细胞、多形核白细胞、B淋巴细胞和单核细胞C3b受体的膜糖蛋白。
J Exp Med. 1980 Jul 1;152(1):20-30. doi: 10.1084/jem.152.1.20.
5
Current concepts in immunology: the alternative pathway of complement--a system for host resistance to microbial infection.免疫学的当前概念：补体替代途径——宿主抵抗微生物感染的系统
N Engl J Med. 1980 Jul 31;303(5):259-63. doi: 10.1056/NEJM198007313030505.
6
Release of endogenous C3b inactivator from lymphocytes in response to triggering membrane receptors for beta 1H globulin.响应β1H球蛋白的触发膜受体，淋巴细胞释放内源性C3b灭活剂。
J Exp Med. 1980 Dec 1;152(6):1625-44. doi: 10.1084/jem.152.6.1625.
7
Immune lysis of normal human and paroxysmal nocturnal hemoglobinuria (PNH) red blood cells. I. The sensitivity of PNH red cells to lysis by complement and specific antibody.正常人及阵发性睡眠性血红蛋白尿症（PNH）红细胞的免疫溶解作用。I. PNH红细胞对补体和特异性抗体介导的溶解作用的敏感性。
J Clin Invest. 1966 May;45(5):736-48. doi: 10.1172/JCI105388.
8
Erythrocyte acetylcholinesterase deficiency in paroxysmal nocturnal hemoglobinuria (PNH). A comparison of the complement-sensitive and insensitive populations.阵发性夜间血红蛋白尿（PNH）中的红细胞乙酰胆碱酯酶缺乏。补体敏感和不敏感群体的比较。
Blood. 1969 Apr;33(4):607-16.
9
Immune lysis of normal human and paroxysmal nocturnal hemoglobinuria (PNH) red blood cells. II. The role of complement components in the increased sensitivity of PNH red cells to immune lysis.正常人及阵发性睡眠性血红蛋白尿（PNH）红细胞的免疫溶解。II. 补体成分在PNH红细胞对免疫溶解敏感性增加中的作用。
J Clin Invest. 1966 May;45(5):749-57. doi: 10.1172/JCI105389.
10
Molecular weight estimation of polypeptide chains by electrophoresis in SDS-polyacrylamide gels.通过SDS-聚丙烯酰胺凝胶电泳对多肽链进行分子量估计
Biochem Biophys Res Commun. 1967 Sep 7;28(5):815-20. doi: 10.1016/0006-291x(67)90391-9.

当与阵发性夜间血红蛋白尿症的红细胞结合时，替代途径转化酶的酶活性增加。

Increased enzymatic activity of the alternative pathway convertase when bound to the erythrocytes of paroxysmal nocturnal hemoglobinuria.

作者信息

Parker C J, Baker P J, Rosse W F

出版信息

J Clin Invest. 1982 Feb;69(2):337-46. doi: 10.1172/jci110457.

DOI:10.1172/jci110457
PMID:6915939
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC370983/
Abstract

To investigate the greater fixation of C3 to the erythrocytes of patients with paroxysmal nocturnal hemoglobinuria (PNH) upon activation of complement, we have examined the formation and the reaction of the C3 nephritic factor-stabilized alternative pathway convertase made with purified components on normal and PNH erythrocytes. Each convertase complex converts four to five times more fluid-phase C3 to C3b when affixed to a PNH cell than when affixed to a normal cell. The greater activity of the convertase on PNH cells is not due to differences in the intrinsic or extrinsic stability of the convertase complex. The excessive binding of C3 to PNH cell si due to this increased conversion of fluid-phase C3, because the efficiency of binding of nascent C3b was identical for the two cell types. This is the first instance in which the enzyme activity of a complement complex has been shown to be increased by being affixed to an abnormal surface.

摘要

为了研究阵发性夜间血红蛋白尿（PNH）患者补体激活后C3与红细胞的结合增强情况，我们检测了用纯化成分在正常和PNH红细胞上形成的C3肾炎因子稳定的替代途径转化酶的形成及反应。当固定在PNH细胞上时，每个转化酶复合物将液相C3转化为C3b的能力比固定在正常细胞上时高4至5倍。转化酶在PNH细胞上的活性更高并非由于转化酶复合物内在或外在稳定性的差异。C3与PNH细胞的过度结合是由于液相C3转化增加，因为两种细胞类型新生C3b的结合效率相同。这是首次证明补体复合物的酶活性通过附着于异常表面而增强。