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关于体液免疫反应的反馈调节。I. “B抑制细胞”的证据。

On the feedback regulation of humoral immune response. I. Evidence for 'B suppressor cells'.

作者信息

Stockinger B, Botzenhardt U, Lemmel E M

出版信息

Immunology. 1979 Jan;36(1):87-94.

Abstract

Evidence has been presented that complete and antigen-specific immune inhibition can be obtained by 'B suppressor cells'. Transfer of spleen cells from twice-immunized (SRBC) donors to untreated syngeneic recipients resulted in antigen-specific inhibition of the hosts' immune response. The cell responsible for this phenomenon could be shown to be the 7S-producing B cell; participation of T cells and macrophages could be excluded. After a second immunization of the donors, these B cells remained inhibitory for more than 20 weeks in the donors as well as in the recipients after transfer. Passively administered specific IgG antibody caused a similar inhibition of the hosts' immune response, which, however, lasted for less than 9 weeks only. The extent of inhibition caused by transfer of hyperimmune cells was parallel to the number of transferred 7S producing cells. Since it could be demonstrated that memory cells were present at times when the transferred cell material had lost its inhibitory potency, we concluded that inhibition is not caused by the mere presence of these cells. Since the transferred cells regained their inhibitory capacity after non-specific activation with LPS, we concluded that a product of such activated cells--most likely the specific 7S antibody--was responsible for the observed inhibition. Thus, it is demonstrated that B cells may serve as 'suppressor cells' in appropriate transfer experiments. It is, however, concluded that this effect is basically mediated by produced IgG and may in its mechanism be identical to the phenomenon of antibody-mediated regulation of humoral immune response.

摘要

已有证据表明,“B抑制细胞”可实现完全且抗原特异性的免疫抑制。将经两次免疫(用绵羊红细胞免疫)的供体的脾细胞转移至未经处理的同基因受体,会导致宿主免疫反应受到抗原特异性抑制。可证明负责此现象的细胞是产生7S的B细胞;可排除T细胞和巨噬细胞的参与。在对供体进行第二次免疫后,这些B细胞在供体以及转移后的受体中保持抑制作用超过20周。被动给予的特异性IgG抗体也会对宿主免疫反应产生类似的抑制作用,然而,这种抑制作用仅持续不到9周。超免疫细胞转移所引起的抑制程度与转移的产生7S的细胞数量平行。由于可以证明在转移的细胞物质失去其抑制效力时记忆细胞仍然存在,我们得出结论,抑制作用并非仅仅由这些细胞的存在引起。由于在用脂多糖进行非特异性激活后,转移的细胞恢复了其抑制能力,我们得出结论,这种活化细胞的一种产物——很可能是特异性7S抗体——是观察到的抑制作用的原因。因此,在适当的转移实验中证明了B细胞可能充当“抑制细胞”。然而,可以得出结论,这种效应基本上是由产生的IgG介导的,其机制可能与抗体介导的体液免疫反应调节现象相同。

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