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脂质体对人补体的激活:替代途径膜激活的模型。

Activation of human complement by liposomes: a model for membrane activation of the alternative pathway.

作者信息

Cunningham C M, Kingzette M, Richards R L, Alving C R, Lint T F, Gewurz H

出版信息

J Immunol. 1979 Apr;122(4):1237-42.

PMID:448089
Abstract

Liposomal model membranes were found to activate the alternative pathway of human complement. Activation was measured by C3 conversion and component consumption in serum that had been incubated with liposomes. C3 conversion did not require C1 or C2 of the classical pathway, since it was observed in serum from a C1r-deficient patient, serum from a C2-dificient patient, and normal serum in buffer containing EGTA and MgCl2. The incubation of liposomes with C2-deficient serum resulted in consumption of components C3 through C9 with no consumption of C1 or C4 in a profile typical of alternative pathwya activation. The reaction was further shown to require alternative pathway factor D, and to be independent of antibody. Activation of the alterative pathway was dependent on the membrane composition of the liposomes. A positive charge was required for liposomes to produce C3 conversion. Liposomal cholesterol concentration and phospholipid fatty acyl chain length and unsaturation all influenced activation, suggesting the importance of membrane fluidity. Positively charged liposomes containing dimyristoyl phosphatidylcholine and cholesterol required the presence of certain glycolipids for C3 conversion. The activation of the alternative complement pathway by liposomes of defined membrane composition may provide a suitable model for the study of alternative pathway activation by cellular membranes.

摘要

发现脂质体模型膜可激活人补体的替代途径。通过与脂质体孵育的血清中的C3转化和成分消耗来测定激活情况。C3转化不需要经典途径的C1或C2,因为在C1r缺陷患者的血清、C2缺陷患者的血清以及含有EGTA和MgCl2的缓冲液中的正常血清中均观察到了C3转化。脂质体与C2缺陷血清孵育导致C3至C9成分的消耗,而C1或C4无消耗,这是替代途径激活的典型特征。进一步表明该反应需要替代途径因子D,且与抗体无关。替代途径的激活取决于脂质体的膜组成。脂质体产生C3转化需要正电荷。脂质体胆固醇浓度、磷脂脂肪酰链长度和不饱和度均影响激活,表明膜流动性的重要性。含有二肉豆蔻酰磷脂酰胆碱和胆固醇的带正电荷脂质体需要某些糖脂的存在才能进行C3转化。具有确定膜组成的脂质体对替代补体途径的激活可能为研究细胞膜对替代途径的激活提供合适的模型。

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1
Activation of human complement by liposomes: a model for membrane activation of the alternative pathway.脂质体对人补体的激活:替代途径膜激活的模型。
J Immunol. 1979 Apr;122(4):1237-42.
2
Effect of membrane phospholipids on activation of the alternative complement pathway.膜磷脂对替代补体途径激活的影响。
J Immunol. 1989 Sep 1;143(5):1663-8.
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[Formation of classical C3 convertase during the alternative pathway of human complement activation].[人类补体激活替代途径中经典C3转化酶的形成]
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In vitro activation of complement by isolated human heart subcellular membranes.人心脏亚细胞膜对补体的体外激活作用
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Persistently circulating C3 nephritic factor (C3 NeF)-stabilized alternative pathway C3 convertase (C3 CoF) in serum of an 11-year-old girl with meningococcal septicemia--simultaneous occurrence with free C3 NeF.一名11岁患脑膜炎球菌败血症女孩血清中持续循环的C3肾炎因子(C3 NeF)稳定化替代途径C3转化酶(C3 CoF)——与游离C3 NeF同时出现
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The functional inhibition of activated C1 inhibitor in normal human serum causes spontaneous consumption of the complement components C2, C3, C4, and factor B.正常人血清中活化的C1抑制剂的功能抑制会导致补体成分C2、C3、C4和B因子的自发消耗。
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Alternative complement pathway activation by C4b deposited during classical pathway activation.经典途径激活过程中沉积的C4b对替代补体途径的激活。
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Activation of the classical pathway of complement by Hageman factor fragment.凝血因子片段激活补体经典途径。
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Surface modulation of classical pathway activation: C2 and C3 convertase formation and regulation on sheep, guinea pig, and human erythrocytes.经典途径激活的表面调节:绵羊、豚鼠和人红细胞上C2和C3转化酶的形成与调节
J Immunol. 1983 Jul;131(1):403-8.

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