Mechanisms of suppression in the transfer of contact sensitivity. Analysis of an I-J+ molecule required for Ly2 suppressor cell activity.
Mechanisms of suppression in the transfer of contact sensitivity. Analysis of an I-J+ molecule required for Ly2 suppressor cell activity.
复制标题
接触灵敏度转移的抑制机制。分析LY2抑制细胞活性所需的I-J+分子。
DOI：
10.1084/jem.158.6.1822
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发表时间：
1983-12-01
影响因子：
15.3
通讯作者：
Flood, P M
中科院分区：
文献类型：
--
作者：
Ptak, W;Gershon, R K;Flood, P M
免疫细胞的接触敏感性 (CS) 被动转移可以通过抗原特异性 T 抑制因子来抑制。该因子由两个子因子组成：由 Ly1+ 细胞 (PC1-F) 产生的抗原特异性亚因子和由 Ly2+ T 细胞 (TNBSA-F) 产生的抗原非特异性亚因子。完全因子的抑制活性可以通过耗尽 Ly2+ 细胞的检测群体来消除，即使是群体中的 Ly1+ 细胞传递过继免疫。这表明检测群体中的 Ly2+ 细胞需要将抑制信号转导至 DTH 的 Ly1+ 效应细胞。我们发现来自免疫动物的 Ly2+ 细胞可以被诱导产生一种无细胞亚因子，该亚因子克服了 TsF 抑制 CS 时对这种 Ttrans 细胞的需求。诱导仅需要 PC1-F、TNP 偶联的脾细胞，并导致免疫 Ly2+、I-J+ 细胞产生抗原非特异性 I-J+ 亚因子。对 Ly2+ 转导细胞的需求也可以通过添加对 SRBC 进行超免疫的 Ly1 T 细胞分泌的 I-J+ 分子来克服。由 I-J+ 分子与 TNBSA-F 混合制成的抑制复合物可以直接抑制免疫 T 细胞的功能活性，不仅可以转移 CS，还可以在体外 PFC 反应中向 B 细胞提供帮助。这种抑制复合物是抗原非特异性的，并且不需要检测群体中的 Ly2+ T 细胞来发挥抑制活性。这些结果表明抑制电路的效应因子需要两个分子；一种包含功能性抑制材料，另一种充当“schlepper”，一种将抑制传递到适当靶细胞所需的分子。使用不同的免疫程序，从针对不同抗原产生的两个亚因子构建功能性抑制复合物的能力，这些亚因子是从表现出不同功能活性的因子中分离出来的，这表明免疫系统的某些细胞可能在“转导”抑制信号中发挥普遍作用。
The passive transfer of contact sensitivity (CS) by immune cells can be inhibited with an antigen-specific T suppressor factor. This factor is composed of two subfactors: an antigen-specific subfactor made by an Ly1+ cell (PC1-F) and a antigen nonspecific subfactor made by an Ly2+ T cell (TNBSA-F). The suppressive activity of the complete factor can be eliminated by depleting the assay population of Ly2+ cells, even though it is the Ly1+ cell in the population that transfers the adoptive immunity. This suggests that the Ly2+ cell in the assay population is needed to transduce the suppressive signal to the Ly1+ effector cell of DTH. We found that an Ly2+ cell from immune animals could be induced to produce a cell free subfactor that overcame the requirement for this Ttrans cell in the suppression of CS by TsF. The induction required only PC1-F, TNP-coupled spleen cells, and resulted in the production of an antigen-nonspecific I-J+ subfactor by immune Ly2+, I-J+ cells. The need for the Ly2+ transducer cell could also be overcome by addition of an I-J+ molecule secreted by Ly1 T cells hyperimmunized to SRBC. A suppressor complex made from mixing the I-J+ molecule with TNBSA-F could directly suppress the functional activity of immune T cells not only to transfer CS, but also to deliver help to B cells in an in vitro PFC response. This suppressive complex is antigen-nonspecific and does not require Ly2+ T cells in the assay population for suppressive activity. These results indicate that effector factors of the suppressor circuit require two molecules; one that contains the functional suppressor material and one that serves as a "schlepper," a molecule needed to deliver the suppression to the appropriate target cell. The ability to construct a functional suppressor complex from two subfactors raised against different antigens, using different immunization procedures, which were isolated from factors exhibiting different functional activities suggests that certain cells of the immune system may play a universal role in "transducing" the suppressive signal.