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Naloxone at concentrations 10(-6) M to 10(-10) M modulated endogenous NK-activity in 11 of 14 samples of human peripheral blood lymphocytes after 18-hour incubation. The dose response usually showed two peaks, which varied with the donor. Enhancement was obtained in 6, suppression in 4, and both effects (depending on naloxone concentration) in 1 example; 3 donors were nonresponders. However, the overall effect of naloxone on endogenous NK activity was not statistically significant in the population as a whole. IL-2-stimulated NK-activity, was also altered by naloxone. The direction of the alteration depended on the degree of IL-2-induced NK-stimulation, and was donor-dependent. For example, naloxone enhanced NK-activity that had been stimulated by low IL-2 concentration (3 U/ml), but decreased NK-activity which had been stimulated by high (50 U/ml) IL-2 concentration. Naloxone 10(-7) M significantly reversed medium stimulation of NK activity, induced by 25 U/ml, in a group as a whole. Naloxone (10(-7) M to 10(-12) M) also modulated NK-activity stimulated by exogenous IFN alpha, as well as by endogenous, Poly-I.C-induced IFN. Decrease, or enhancement, depended on the degree of baseline NK-stimulation and varied with the donor. Short (2-hours) incubation with naloxone also resulted in the modulation of basal and IFN-stimulated NK-activity. Again, the effect varied with the donor and with the degree of lymphocyte activation. Thus, naloxone, the opioid receptor antagonist, modulated the NK-cell activity like opioid peptides, i.e. resembled an opioid agonist, in an individual, donor dependent fashion.