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外周神经CR1原位表达C3b降解的辅助因子活性。

Peripheral nerve CR1 express in situ cofactor activity for degradation of C3b.

作者信息

Vedeler C A, Matre R

机构信息

Broegelmann Research Laboratory for Microbiology, Gade Institute, University of Bergen, Norway.

出版信息

J Neuroimmunol. 1990 Jan;26(1):51-6. doi: 10.1016/0165-5728(90)90119-8.

DOI:10.1016/0165-5728(90)90119-8
PMID:2403574
Abstract

Adsorption of sheep erythrocytes (E) sensitized with IgM antibodies (A) and C3b (EAC3b) to C3b/C4b receptors (CR1) in cryostat sections of human myelinated nerves was studied using the closed chamber technique. The adsorption was stable for at least 3 h at 37 degrees C. In the presence of purified factor I, the indicator cells detached from the sections after 40 min at 37 degrees C. Factor H was not required. The release was not due to loss of CR1 activity in the sections. The detached indicator cells were negative in the immune adherence test and were agglutinated by antibody to C3d, but not by antibody to C3c. Western blot of the detached indicator cells revealed the presence of C3d and C3c was found in the chamber fluid. Accordingly, detachment of the indicator cells was due to degradation of C3b to C3d with the release of C3c into the chamber fluid. Protease inhibitors did not prevent the detachment of the indicator cells. EAC3b incubated with sections of myelinated nerves pre-incubated with anti-CR1 antibody or with sections of unmyelinated nerves which contain functionally inactive CR1 were not degraded. The results therefore indicate that CR1 in situ in myelinated nerves can provide the necessary cofactor activity for factor I-mediated degradation of C3b to C3d and C3c.

摘要

采用封闭室技术研究了用 IgM 抗体(A)和 C3b 致敏的绵羊红细胞(E)(EAC3b)对人有髓神经冰冻切片中 C3b/C4b 受体(CR1)的吸附作用。在 37℃下,这种吸附作用至少稳定 3 小时。在纯化的 I 因子存在的情况下,指示细胞在 37℃下 40 分钟后从切片上脱离。不需要 H 因子。这种释放不是由于切片中 CR1 活性的丧失。脱离的指示细胞在免疫黏附试验中呈阴性,能被抗 C3d 抗体凝集,但不能被抗 C3c 抗体凝集。对脱离的指示细胞进行蛋白质印迹分析显示存在 C3d,并且在室液中发现了 C3c。因此,指示细胞的脱离是由于 C3b 降解为 C3d,同时 C3c 释放到室液中。蛋白酶抑制剂不能阻止指示细胞的脱离。用抗 CR1 抗体预孵育的有髓神经切片或用含有无功能活性 CR1 的无髓神经切片预孵育的 EAC3b 没有被降解。因此,结果表明有髓神经中的原位 CR1 可以为 I 因子介导的 C3b 降解为 C3d 和 C3c 提供必要的辅因子活性。

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Peripheral nerve CR1 express in situ cofactor activity for degradation of C3b.外周神经CR1原位表达C3b降解的辅助因子活性。
J Neuroimmunol. 1990 Jan;26(1):51-6. doi: 10.1016/0165-5728(90)90119-8.
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