Baier J, Neumann H A, Ricken O
Medizinische Klinik der Ruhr-Universität Bochum, St. Josef Hospital, Federal Republic of Germany.
Cancer Immunol Immunother. 1991;32(5):311-4. doi: 10.1007/BF01789049.
In previous experiments Ciamexone, derivative of 2-cyan-aziridine, was able to influence T-cell-mediated regulatory mechanisms but seemed to have no or only little effect on T cell effector mechanisms. On the basis of these observations Ciamexone seems to be a highly selective immunosuppressive agent. In order to evaluate further possible mechanisms of Ciamexone it was the aim of our investigation to study its influence on interferon gamma (IFN gamma) production in phytohaemogglutinin (PHA)-stimulated T lymphocytes of 15 tumour patients and 12 healthy reference subjects. The IFN gamma concentration of the cell supernatant was measured using an enzyme-linked immunosorbent assay. When the cells were stimulated with PHA at 7.5 micrograms/ml the IFN gamma concentration rose to significantly different values in the reference group (1.0 ng/ml) as compared to the tumour patients (0.4 ng/ml) (P less than 0.05). An addition of Ciamexone (at any of the concentrations administered) to PHA stimulation of peripheral blood mononuclear cells (PBMC) showed no influence on the IFN gamma release in either test group. The influence of hydrocortisone on the stimulation of PBMC with PHA resulted in a dose-dependent suppression of IFN gamma production in both test groups, again with significant differences between them. The IFN gamma concentration was 0.95 ng/ml in the reference group and 0.2 ng/ml in the tumour patients when 0.01 micrograms/ml hydrocortisone was added (P less than 0.05). At 10 micrograms/ml hydrocortisone suppressed IFN gamma production completely in both groups. Our results corroborate those investigations that showed no influence of the compound on T cell effector mechanisms. The attenuation of humoral immunophenomena, however, suggest a very specific point of action within the immune system by Ciamexone.
在之前的实验中,2-氰基氮丙啶衍生物西阿美酮能够影响T细胞介导的调节机制,但似乎对T细胞效应机制没有影响或只有很小的影响。基于这些观察结果,西阿美酮似乎是一种高度选择性的免疫抑制剂。为了进一步评估西阿美酮可能的作用机制,我们研究的目的是探讨其对15名肿瘤患者和12名健康对照者的植物血凝素(PHA)刺激的T淋巴细胞中γ干扰素(IFNγ)产生的影响。使用酶联免疫吸附测定法测量细胞上清液中的IFNγ浓度。当细胞用7.5微克/毫升的PHA刺激时,与肿瘤患者(0.4纳克/毫升)相比,健康对照组的IFNγ浓度显著升高至不同的值(1.0纳克/毫升)(P<0.05)。在PHA刺激外周血单核细胞(PBMC)时添加西阿美酮(在任何给药浓度下)对两个测试组中的IFNγ释放均无影响。氢化可的松对PHA刺激PBMC的影响导致两个测试组中IFNγ产生的剂量依赖性抑制,两组之间再次存在显著差异。当添加0.01微克/毫升氢化可的松时,健康对照组的IFNγ浓度为0.95纳克/毫升,肿瘤患者为0.2纳克/毫升(P<0.05)。在10微克/毫升时,氢化可的松在两组中完全抑制了IFNγ的产生。我们的结果证实了那些表明该化合物对T细胞效应机制没有影响的研究。然而,体液免疫现象的减弱表明西阿美酮在免疫系统内有一个非常特殊的作用点。