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在BALB/c小鼠中用同源抗独特型抗体抑制苄青霉素酰基(BPO)特异性IgE的形成。

Suppression of the benzylpenicilloyl- (BPO) specific IgE formation with isologous anti-idiotypic antibodies in BALB/c mice.

作者信息

Blaser K, Nakagawa T, de Weck A L

出版信息

J Immunol. 1980 Jul;125(1):24-30.

PMID:7381201
Abstract

In vivo effects of actively produced or passively administered isologous anti-idiotypic antisera (aId) on the benzylpenicilloyl- (BPO) specific IgE and IgG formation in BALB/c mice have been studied. Isologous anti-BPO aId were raised in BALB/c mice by immunization with purified anti-BPO antibodies isolated from ascites induced with BPO-bovine gamma-globulin in the same mouse strain. Mice producing isologous anti-BPO aId exhibited long-term suppression of BPO-specific IgE and IgG antibody responses induced by BPO-ovalbumin (BPO-OVA) in aluminum hydroxide. Simultaneously, they produced increased amounts of anti-BPO aId after each challenge with the BPO-OVA antigens. Passive administration of isologous anti-BPO aId into syngeneic mice previously sensitized with BPO-OVA caused depression of BPO-specific IgE antibody levels for 2 to 3 weeks. When anti-BPO IgE had again reached its previous level, passively administered aId had decreased to the level of untreated mice. Passive administration of anti-BPO aId also depressed the primary anti-BPO IgE formation for 2 to 3 weeks. In all these experiments the IgE antibody formation against the carrier proteins used for BPO-antigens was not affected. These results show that IgE and IgG antibodies share major idiotypic determinants and that IgE production is accessible to regulation by aId.

摘要

研究了主动产生或被动给予的同源抗独特型抗血清(aId)对BALB/c小鼠中苄青霉素酰基-(BPO)特异性IgE和IgG形成的体内效应。同源抗BPO aId是通过用从同一小鼠品系中用BPO-牛γ球蛋白诱导的腹水中分离的纯化抗BPO抗体免疫BALB/c小鼠而产生的。产生同源抗BPO aId的小鼠表现出对由氢氧化铝中的BPO-卵清蛋白(BPO-OVA)诱导的BPO特异性IgE和IgG抗体反应的长期抑制。同时,它们在每次用BPO-OVA抗原攻击后产生的抗BPO aId量增加。将同源抗BPO aId被动给予先前用BPO-OVA致敏的同基因小鼠,导致BPO特异性IgE抗体水平在2至3周内降低。当抗BPO IgE再次达到其先前水平时,被动给予的aId已降至未处理小鼠的水平。被动给予抗BPO aId也使原发性抗BPO IgE形成在2至3周内受到抑制。在所有这些实验中,针对用于BPO抗原的载体蛋白的IgE抗体形成不受影响。这些结果表明,IgE和IgG抗体共享主要的独特型决定簇,并且IgE的产生可通过aId进行调节。

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