Nepom G T, Hellström I, Hellström K E
Experientia. 1983 Mar 15;39(3):235-42. doi: 10.1007/BF01955286.
There are many parallels between T cell-mediated suppression of tumor immunity and suppression of immune responses to haptens and polypeptides. We propose a cell interaction model which takes this into account and outlines a regulatory pathway for suppression of immunity to tumor antigens. Free antigen or antigen/antibody complexes trigger an inducer T cell subset, Tsi, which is tumor-specific. This cell activates a non-immune T cell population, pre Tse, to generate effector suppressor cells, Tse. The Tse are specific for either the idiotype of Tsi or for antigen complexed with a soluble factor made by the Tsi, but the suppression they mediate is antigenically nonspecific. Tumor antigen-specific suppressor factors, TsF, play a major role in the communication between different suppressor cells. Characterization of polyclonal and monoclonal factors produced by Tsi, called TsFi, indicates that they both bind to tumor antigen and contain tumor-specific (idiotypic?) determinants.
T细胞介导的肿瘤免疫抑制与对半抗原和多肽的免疫反应抑制之间存在许多相似之处。我们提出了一个细胞相互作用模型,该模型考虑到了这一点,并概述了一条抑制对肿瘤抗原免疫的调节途径。游离抗原或抗原/抗体复合物触发一个诱导性T细胞亚群Tsi,它是肿瘤特异性的。该细胞激活一个非免疫性T细胞群体pre Tse,以产生效应性抑制细胞Tse。Tse对Tsi的独特型或与Tsi产生的可溶性因子复合的抗原具有特异性,但它们介导的抑制在抗原方面是非特异性的。肿瘤抗原特异性抑制因子TsF在不同抑制细胞之间的通讯中起主要作用。对由Tsi产生的多克隆和单克隆因子(称为TsFi)的特性分析表明,它们都与肿瘤抗原结合并含有肿瘤特异性(独特型?)决定簇。