抑制细胞对半抗原特异性T细胞和B细胞反应的调控。

Concepts in immunopathology Pub Date : 1986-01-01
P B Hausman, D H Sherr, M E Dorf
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引用次数: 0

摘要

我们描述了一个免疫调节模型系统,其中与H-2和Igh复合物相关的基因产物指导一系列细胞相互作用。Igh限制代表了T细胞识别高链npb相关独特型决定因子的要求。这些数据提供了额外的证据,证明T细胞和B细胞的Igh产物是不同的。免疫球蛋白产物参与T细胞受体的选择;在T抑制细胞中不表达Igh基因。H-2限制通常涉及I-J次区域。这些限制是通过抗原或抑制因子在特定的I-J承载、抗原呈递细胞群上的呈递施加的,从而以类似于诱导辅助性T细胞的方式发挥作用。NP抑制细胞通路由多个细胞元件组成,包括至少3个不同的T细胞群和2个或更多不同的抗原呈递群。一般来说,每个t细胞亚群产生的特异性可溶性抑制因子参与细胞通讯过程。抑制细胞级联的终末阶段涉及抗原依赖的非特异性旁观者机制。表IX和表X总结了我们目前对NP抑制细胞级联的看法。将所有其他涉及抑制细胞相互作用的实验模型纳入上述方案仍然是不可能的。然而,不同系统之间的差异在某些情况下已经缩小,在其他情况下表明多种免疫调节机制可能同时发生。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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Regulation of hapten-specific T and B cell responses by suppressor cells.

We have described a model system of immunoregulation in which gene products associated with both the H-2 and Igh complexes guide a series of cellular interactions. The Igh restriction represents the requirement for T cell recognition of Igh-linked NPb-related idiotypic determinants. The data provide additional evidence that the T and B cell Igh products are distinct. Immunoglobulin products are involved in the selection of T cell receptors; Igh genes are not expressed in T suppressor cell. The H-2 restrictions generally involve the I-J subregion. These restrictions are imposed by the presentation of antigen or suppressor factor on a specialized population of I-J bearing, antigen-presenting cells, thereby functioning in a manner analogous to that proposed for the induction of helper T cells. The NP suppressor cell pathway consists of multiple cellular elements, including at least 3 distinct T cell populations and 2 or more distinct antigen-presenting populations. Generally, specific soluble suppressor factors produced by each Ts cell subset are involved in the cellular communication process. The terminal phases of the suppressor cell cascade involve an antigen dependent non-specific bystander mechanism. Tables IX and X summarize our present view of the NP suppressor cell cascade. It is still not possible to include all the other experimental models involving suppressor cell interactions into the above scheme. However, the disparities between the various systems have in some cases narrowed and in other instances suggested that multiple mechanisms of immune regulation may occur concurrently.

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