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对偶氮苯砷酸盐的耐受性:独特型特异性抑制、B细胞优势及克隆清除。

Tolerance to azobenzenearsonate: idiotype-specific suppression, B cell dominance, and clonal elimination.

作者信息

Collins E T, Hershey E D, Benjamin D C

出版信息

J Immunol. 1985 Aug;135(2):886-91.

PMID:3159797
Abstract

Twenty to 70% of the antibody molecules produced by individual A/J mice in response to azobenzenearsonate (ABA) bear a particular idiotype termed the major cross-reactive idiotype (CRI). Mice that were made tolerant to ABA by injection of ABA coupled to human gamma-globulin show a decrease in production of ABA-specific antibody and a preferential loss of the major CRI. In the experiments reported here, we have used adoptive cell transfers and splenic fragment culture assays to study the mechanism(s) involved in the tolerance to ABA, with emphasis on the preferential loss of the CRI. These studies show that the decrease in total anti-ABA after the induction of tolerance is the result of a decrease in the number of ABA-responsive B cells independent of CRI expression. The preferential loss of the CRI is due to idiotype-specific T cell suppression and/or B cell dominance. In addition, it is demonstrated that immunization in the presence of idiotype-specific suppression converts a normally immunogenic stimulus into a tolerogenic signal, resulting in a decrease in the absolute number of CRI+ B cell precursors.

摘要

个体A/J小鼠针对偶氮苯砷酸盐(ABA)产生的抗体分子中,20%至70%带有一种特定的独特型,称为主要交叉反应独特型(CRI)。通过注射与人类γ球蛋白偶联的ABA而对ABA产生耐受的小鼠,其ABA特异性抗体的产生减少,且主要CRI优先丧失。在本文报道的实验中,我们采用了过继性细胞转移和脾细胞片段培养试验来研究ABA耐受所涉及的机制,重点是CRI的优先丧失。这些研究表明,诱导耐受后总抗ABA的减少是ABA反应性B细胞数量减少的结果,与CRI表达无关。CRI的优先丧失是由于独特型特异性T细胞抑制和/或B细胞优势。此外,还证明在独特型特异性抑制存在的情况下进行免疫会将正常的免疫原性刺激转化为致耐受信号,导致CRI+B细胞前体的绝对数量减少。

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