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通过B细胞优势机制完全抑制独特型的表达。

Complete inhibition of the expression of an idiotype by a mechanism of B-cell dominance.

作者信息

Eig B M, Ju S T, Nisonoff A

出版信息

J Exp Med. 1977 Dec 1;146(6):1574-84. doi: 10.1084/jem.146.6.1574.

Abstract

Mice of the C.AL-20 strain, which express genes controlling CH regions of the AL/N strain on a BALB/c background, normally synthesize antibodies to the p-azophenylarsonate group (anti-Ar antibodies) with an idiotype characteristic of the A strain. The synthesis of the idiotype, as quantitated by a sensitive assay, can be completely inhibited by the transfer of leukocytes from BALB/c mice producing anti-Ar antibodies, which lack the idiotype. A number of control experiments show that the inhibition is not attributable to suppressor T cells and that the synergistic action of such cells is not required. The results indicate that B-cell dominance, mediated by secondary cells, can completely prevent the expression of unprimed cells with receptors of the same specificity. It is uncertain whether this effect is due entirely to selective capture of antigen by the secondary cells, or whether some type of active suppression by B cells is involved.

摘要

C.AL-20品系的小鼠在BALB/c背景上表达控制AL/N品系CH区域的基因,通常会合成具有A品系独特型特征的针对对氨基苯砷酸盐基团的抗体(抗Ar抗体)。通过一种灵敏的检测方法定量的独特型合成,可被产生抗Ar抗体但缺乏该独特型的BALB/c小鼠的白细胞转移完全抑制。多项对照实验表明,这种抑制并非归因于抑制性T细胞,且不需要此类细胞的协同作用。结果表明,由次级细胞介导的B细胞优势可完全阻止具有相同特异性受体的未致敏细胞的表达。尚不确定这种效应是否完全归因于次级细胞对抗原的选择性捕获,或者是否涉及B细胞的某种类型的主动抑制。

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