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具有相同特异性但独特型不同的受体的细胞群体对抗原的竞争。

Competition for antigen by cell populations having receptors with the same specificity but of different idiotype.

作者信息

Bangasser S A, Kapsalis A A, Fraker P J, Nisonoff A

出版信息

J Immunol. 1975 Feb;114(2 Pt 1):610-4.

PMID:47356
Abstract

All normal A/J mice immunized with keyhole limpet hemocyanin-p-azophenylarsonate (KLH-Ar) produce anti-Ar antiboides, some of which share a cross-reactive idiotype. The present results indicate that the biosynthesis of antibody molecules bearing this idiotype does not occur in mice having an excess of lymphoid cells with receptors for Ar that lack the idiotype. This was shown, first, by introducing into normal, nonirradiated mice lymphoid cells from mice which had been suppressed with respect to production of the idiotype and then immunized with KLH-Ar. The recipients failed to express the idiotype upon immunization. Alternatively, cells from suppressed, mice were transferred into lethally irradiated syngeneic recipients, followed 17 days later by normal cells. All recipients expressed the idiotype upon immunization. If, however, the recipients were challenged with antigen between the two cell transfers, antibodies bearing the idiotype were not produced during subsequent immunization. Arguing against active, cell-mediated suppression was the production of the idiotype by normal cells in the presence of cells from a suppressed animal. However, the possibility of active suppression by hyperimmune suppressed cells was not ruled out. On the basis of the present data, the simplest interpretation is that cells with anti-Ar receptors from immune, suppressed animals, being present in larger numbers, compete successfully for antigen with nonimmune cells and thus prevent the expression of the idiotype. The system may provide a basis for quantitative studies of competition among cells for a limited supply of antigen, particularly if B cell populations are utilized.

摘要

所有用钥孔戚血蓝蛋白 - 对 - 偶氮苯胂酸盐(KLH - Ar)免疫的正常A/J小鼠都会产生抗Ar抗体,其中一些抗体具有交叉反应性独特型。目前的结果表明,带有这种独特型的抗体分子的生物合成不会在具有过量带有Ar受体但缺乏该独特型的淋巴细胞的小鼠中发生。首先,通过将来自已被抑制产生独特型然后用KLH - Ar免疫的小鼠的淋巴细胞引入正常、未受辐射的小鼠中,证明了这一点。接受者在免疫后未能表达该独特型。或者,将来自受抑制小鼠的细胞转移到经致死性照射的同基因接受者中,17天后再注入正常细胞。所有接受者在免疫后都表达了该独特型。然而,如果在两次细胞转移之间用抗原攻击接受者,则在随后的免疫过程中不会产生带有该独特型的抗体。正常细胞在存在来自受抑制动物的细胞的情况下产生独特型,这与主动的细胞介导抑制相矛盾。然而,超免疫抑制细胞主动抑制的可能性并未被排除。根据目前的数据,最简单的解释是,来自免疫、受抑制动物的带有抗Ar受体的细胞数量较多,它们与非免疫细胞成功竞争抗原,从而阻止了独特型的表达。该系统可能为细胞间争夺有限抗原供应的竞争的定量研究提供基础,特别是如果利用B细胞群体的话。

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