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免疫活性淋巴细胞上的细胞相互作用分子。F1杂种小鼠中抗亲本细胞相互作用分子受体反应的发展以及相互作用细胞独特F1杂种亚群的证据。

Cell-interaction molecules on immunocompetent lymphocytes. Development of anti-parent cell-interaction-molecule-receptor reactions in F1 hybrid mice and evidence for a unique F1 hybrid subset of interacting cells.

作者信息

Katz D H, Katz L R, Bogowitz C A

出版信息

J Exp Med. 1981 Feb 1;153(2):407-22. doi: 10.1084/jem.153.2.407.

Abstract

The experiments presented herein demonstrate that F1-parent T-B cell cooperation in vivo is significantly diminished by the addition of lymphoid cells of opposite parental type. This inhibition phenomenon is not a straightforward allosuppression mechanism as (a) it can be induced by parental lymphoid cells depleted by T cells, (b) it does not operate on cooperative interactions between homologous T and B cells of opposite parental type, and (c) absolutely requires the presence of F1 cells as participants in the reactions generated. The possible involvement of alloantibodies produced aberrantly under the experimental conditions employed has been ruled out by direct macrophage/antigen-presenting cell components of the reactions has been excluded. Because the presence of parental lymphoid cells only affects cooperative interactions between F1 T cells and B lymphocytes of opposite parental type but has no inhibitory effect on cooperative interactions between homologous F1, T and B cells, this (and other points discussed herein) strongly argues for the existence of one or more subsets of F1 interacting partner cells that are uniquely specific for F1, as distinct from either parental type cell interaction determinants. For reasons discussed, it appears that the most likely mechanism underlying such parental cell-induced inhibitory effects on F1-parent partner cell interactions is the development of anti-self cell interaction structure responses by F1 cells against the relevant self-specific cell-interaction structures of the parental partner cells involved.

摘要

本文所呈现的实验表明,在体内,加入相反亲本类型的淋巴细胞会显著削弱F1亲本T细胞与B细胞之间的协作。这种抑制现象并非简单的同种异体抑制机制,因为:(a)它可由T细胞耗尽的亲本淋巴细胞诱导产生;(b)它对相反亲本类型的同源T细胞和B细胞之间的协作相互作用不起作用;(c)绝对需要F1细胞作为反应的参与者。在所用实验条件下异常产生的同种异体抗体的可能参与已被排除,反应中直接的巨噬细胞/抗原呈递细胞成分也已被排除。由于亲本淋巴细胞的存在仅影响F1 T细胞与相反亲本类型的B淋巴细胞之间的协作相互作用,而对同源F1 T细胞和B细胞之间的协作相互作用没有抑制作用,这一点(以及本文讨论的其他要点)有力地支持了存在一个或多个F1相互作用伙伴细胞亚群的观点,这些亚群对F1具有独特的特异性,与任何一种亲本类型细胞相互作用决定簇不同。出于所讨论的原因,亲本细胞对F1亲本伙伴细胞相互作用产生这种抑制作用的最可能机制似乎是F1细胞针对所涉及的亲本伙伴细胞的相关自身特异性细胞相互作用结构产生抗自身细胞相互作用结构反应。

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