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单克隆抗独特型抗体调节病毒诱导的小鼠心肌炎的表达。

Monoclonal anti-idiotypic antibodies regulate the expression of virus-induced murine myocarditis.

作者信息

Paque R E, Miller R

机构信息

Department of Microbiology, University of Texas Health Science Center, San Antonio 78284.

出版信息

Infect Immun. 1989 Sep;57(9):2864-71. doi: 10.1128/iai.57.9.2864-2871.1989.

DOI:10.1128/iai.57.9.2864-2871.1989
PMID:2547722
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC313539/
Abstract

A monoclonal anti-idiotypic antibody (anti-Id), produced by electrofusion and designated anti-Id88, was able to modulate expression of murine autoimmune myocarditis mediated by coxsackievirus B3 (CVB3). The anti-Id was characterized as an immunoglobulin G2b species possessing kappa light chains and was able to reduce expression of inflammatory myocarditis in anti-Id-pretreated mice challenged with CVB3. Anti-Id88 was able to stimulate specific cell-mediated immunity against anti-Id88, as well as CVB3, and exerted a suppressive effect on the proliferation of mixed spleen cell populations from virus-exposed mice. Anti-Id stimulated an anti-anti-Id antibody 3 population able to bind antibody 2 F(ab')2 fragments or virus antigen in an indirect enzyme-linked immunosorbent assay. Western blot (immunoblot) analysis of anti-Id88 exhibited binding of syngeneic anti-Id antibody to idiotypes present on immunoglobulin G molecules from virus-immunized mice.

摘要

通过电融合产生的一种单克隆抗独特型抗体(抗Id),命名为抗Id88,能够调节由柯萨奇病毒B3(CVB3)介导的小鼠自身免疫性心肌炎的表达。该抗Id被鉴定为具有κ轻链的免疫球蛋白G2b类型,并且能够在接受CVB3攻击的抗Id预处理小鼠中降低炎症性心肌炎的表达。抗Id88能够刺激针对抗Id88以及CVB3的特异性细胞介导免疫,并对来自接触病毒小鼠的混合脾细胞群体的增殖产生抑制作用。抗Id刺激了一个抗抗Id抗体群体,该群体在间接酶联免疫吸附测定中能够结合抗体2 F(ab')2片段或病毒抗原。抗Id88的蛋白质印迹(免疫印迹)分析显示,同基因抗Id抗体与来自病毒免疫小鼠的免疫球蛋白G分子上存在的独特型发生结合。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7387/313539/e555ab0386de/iai00069-0291-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7387/313539/e555ab0386de/iai00069-0291-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7387/313539/e555ab0386de/iai00069-0291-a.jpg

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