NO INHIBITION OF INTERFERON-GAMMA RELEASE IN HUMAN-LYMPHOCYTES BY CIAMEXONE

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 mu-g/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 <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 mu-g/ml hydrocortisone was added (P <0.05). At 10 mu-g/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.