Epitope studies with anti-β2-glycoprotein I antibodies from autoantibody and immunized sources
Epitope studies with anti-β2-glycoprotein I antibodies from autoantibody and immunized sources
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DOI：
10.1006/jaut.2000.0427
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发表时间：
2000-09-01
影响因子：
12.8
通讯作者：
Krilis, SA
中科院分区：
文献类型：
--
作者：
Reddel, SW;Wang, YX;Krilis, SA
本文探讨了抗β（2）-糖蛋白I（β（2）-GPI）表位测定的方法，并提供了使用含有抗β（2）-GPI自身抗体的人血清进行的进一步表位研究。该领域的研究可能会产生误导，因为使用突变形式的β（2）-GPI的抗原包被密度可能低于低亲和力抗β（2）-GPI自身抗体单配二价结合所需的阈值，而容易被免疫动物的高亲和力抗β（2）-GPI检测到。在来自人的抗β（2）-GPT自身抗体和来自具有自身免疫性疾病模型的小鼠的单克隆抗β（2）-GPI中发现抗原密度阈值效应。来自自身免疫小鼠和来自18/21人血清的抗-β（2）-GPI不与高于背景水平的结构域I缺失突变体结合。此外，结构域I中的单点突变导致许多含有抗β（2）-GPI的人血清的结合发生显著变化。这些发现支持β 2-GPI结构域I含有抗磷脂综合征中抗β 2-GPI抗体的重要表位的结论。(C)北京大学出版社.
This paper examines the methodology of anti-beta(2)-glycoprotein I (beta(2)-GPI) epitope determination and provides further epitope studies using human sera containing anti-beta(2)-GPI autoantibodies. Studies in this field may be misleading as the antigen coating density using mutant forms of beta(2)-GPI may be below the threshold required for monogamous divalent binding by low affinity anti-beta(2)-GPI autoantibodies, while being easily detected by high affinity anti-beta(2)-GPI from immunized animals. The antigen density threshold effect is found in anti-beta(2)-GPT autoantibodies from humans and from monoclonal anti-beta(2)-GPI derived from mice with models of autoimmune disease. Anti-beta(2)-GPI from an autoimmune mouse and from 18/21 human sera did not bind above background levels to a domain-I-deleted mutant. In addition, single point mutations in domain I result in dramatic changes in the binding of many human sera containing anti-beta(2)-GPI. These findings support a conclusion that domain I of beta(2)-GPI contains significant epitopes for the anti-beta(2)-GPI antibodies found in the antiphospholipid syndrome. (C) 2000 Academic Press.