Madi N, Paccaud J P, Steiger G, Schifferli J A
Department of Medicine, Hôpital Cantonal Universitaire, Geneva, Switzerland.
Clin Exp Immunol. 1991 Apr;84(1):9-15. doi: 10.1111/j.1365-2249.1991.tb08116.x.
C3b-coated immune complexes adhere to the complement receptor 1 (CR1, CD35) on human erythrocytes. This multi-valent binding might be favoured by the known clustering of CR1 and by the multiple C3b-binding sites on each CR1. The size of the CR1 clusters correlates directly with the number of CR1/erythrocytes, and the different structural CR1 alleles bear between two and five C3b-binding sites. Using radiolabelled hepatitis B surface antigen-antibody complexes, we investigated whether CR1 numbers and structural alleles modulate the ability of erythrocytes to bind immune complexes, and assessed if any reorganization of immune complexes takes place at the erythrocyte surface after the initial binding reaction. The binding efficiency (immune complexes/CR1) correlated with CR1 number as determined by the maximal binding at 4 degrees C, the kinetics of binding at 37 degrees C, and the binding in the presence of excess immune complexes and of immune complexes of small size. Binding efficiencies were similar for erythrocytes with low CR1 from normal subjects and patients with AIDS or SLE. A monoclonal antibody blocking the C3b-binding sites (3D9) of CR1 interfered with binding efficiency at a lower concentration on cells bearing low CR1 numbers, suggesting that CR1 clustering is essential. The larger alleles of CR1 (DD and BB) were more efficient than AA alleles. The distribution of immune complexes, visualized by immunofluorescence, was heterogeneous on erythrocytes: about two out of three cells bore between one and 12 immune complexes. No visible immune complex reorganization took place after initial binding, as prefixed erythrocytes displayed the same immune complex distribution and number/erythrocytes as unfixed erythrocytes. The contribution of CR1 alleles in immune complex binding efficiency was confirmed by morphological analysis. These results demonstrate that immune adherence efficiency is the resultant of the CR1 clustering, as well as the particular alleles carried by erythrocytes. Moreover, there is little or no immune complexes surface reorganization after the initial binding reaction.
包被有C3b的免疫复合物可黏附于人类红细胞表面的补体受体1（CR1，CD35）。这种多价结合可能得益于已知的CR1聚集以及每个CR1上多个C3b结合位点。CR1簇的大小与CR1/红细胞数量直接相关，不同结构的CR1等位基因带有2至5个C3b结合位点。我们使用放射性标记的乙肝表面抗原-抗体复合物，研究了CR1数量和结构等位基因是否会调节红细胞结合免疫复合物的能力，并评估了在初始结合反应后免疫复合物在红细胞表面是否会发生任何重组。结合效率（免疫复合物/CR1）与CR1数量相关，这通过4℃下的最大结合量、37℃下的结合动力学以及在过量免疫复合物和小尺寸免疫复合物存在下的结合情况来确定。正常受试者以及艾滋病或系统性红斑狼疮患者中CR1含量低的红细胞，其结合效率相似。一种阻断CR1的C3b结合位点（3D9）的单克隆抗体，在较低浓度下就能干扰CR1数量低的细胞的结合效率，这表明CR1聚集至关重要。CR1的较大等位基因（DD和BB）比AA等位基因更有效。通过免疫荧光观察到的免疫复合物在红细胞上的分布是不均匀的：约三分之二的细胞带有1至12个免疫复合物。初始结合后未观察到明显的免疫复合物重组，因为预先固定的红细胞与未固定的红细胞显示出相同的免疫复合物分布和数量/红细胞。形态学分析证实了CR1等位基因在免疫复合物结合效率中的作用。这些结果表明，免疫黏附效率是CR1聚集以及红细胞所携带的特定等位基因共同作用的结果。此外，初始结合反应后免疫复合物在表面几乎没有或没有重组。
