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用抗大鼠C3单克隆抗体选择性抑制滤泡树突状细胞对免疫复合物的捕获。

Selective inhibition of immune complex trapping by follicular dendritic cells with monoclonal antibodies against rat C3.

作者信息

Van den Berg T K, Döpp E A, Daha M R, Kraal G, Dijkstra C D

机构信息

Department of Cell Biology, Medical Faculty, Vrije Universiteit, Amsterdam, The Netherlands.

出版信息

Eur J Immunol. 1992 Apr;22(4):957-62. doi: 10.1002/eji.1830220412.

DOI:10.1002/eji.1830220412
PMID:1551408
Abstract

The role of complement component C3 in the trapping of immune complexes by follicular dendritic cells (FDC) was studied in the rat, by means of the C3-specific monoclonal antibody ED11. Immunocytochemistry revealed the presence of C3 on FDC, where it co-localized with trapped peroxidase anti-peroxidase complexes. Furthermore, C3 was detected on reticular cells occupying the T cell areas of peripheral lymphoid organs, which are not involved in the handling of immune complexes. The in vivo administration of anti-C3 abolished the trapping of immune complexes in splenic follicles, but was unable to release preexisting complexes from the FDC. Trapping of immune complexes was also prevented by treatment of rats with cobra venom factor (CoVF). While CoVF caused massive depletion of C3 from serum, ED11 treatment had no such effect. The effect of anti-C3 appeared at least in part to be due to an inhibition of complement activation by immune complexes. We also analyzed earlier stages of the trapping process, with respect to their C3 dependence. Upon systemic injection immune complexes are initially observed in the marginal zone. Administration of anti-C3 reduced this localization, indicating a role for C3 in the entry of immune complexes into the spleen. Our results confirm experiments in CoVF-treated animals and extend the evidence for a role of C3 in the follicular trapping process using anti-C3 in vivo. The mechanism of immune complex trapping and the role of complement therein is discussed.

摘要

利用C3特异性单克隆抗体ED11,在大鼠中研究了补体成分C3在滤泡树突状细胞(FDC)捕获免疫复合物中的作用。免疫细胞化学显示FDC上存在C3,它与捕获的过氧化物酶抗过氧化物酶复合物共定位。此外,在占据外周淋巴器官T细胞区域的网状细胞上也检测到C3,这些细胞不参与免疫复合物的处理。体内给予抗C3可消除脾滤泡中免疫复合物的捕获,但无法从FDC释放预先存在的复合物。用眼镜蛇毒因子(CoVF)处理大鼠也可防止免疫复合物的捕获。虽然CoVF导致血清中C3大量消耗,但ED11处理没有这种效果。抗C3的作用至少部分似乎是由于抑制了免疫复合物对补体的激活。我们还分析了捕获过程的早期阶段,探讨其对C3的依赖性。全身注射后,最初在边缘区观察到免疫复合物。给予抗C3减少了这种定位,表明C3在免疫复合物进入脾脏中起作用。我们的结果证实了在CoVF处理动物中的实验,并扩展了使用体内抗C3研究C3在滤泡捕获过程中作用的证据。本文讨论了免疫复合物捕获的机制及其补体在其中的作用。

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