Correlation between the effects of prostaglandins and interferon on B-16 melanoma growth and their modulation on natural killer activity.

We have previously demonstrated that prostaglandins (PGs) are involved in the control of in vivo tumor growth largely by virtue of their effects on the modulation of immune response. The mechanism of action of prostaglandins on the immune system is for the most part unknown. One possibility is that they are effective because the stimulate the T cell maturation. More recently, we extended our study to the effects on PGs on natural killer (NK) activity. Our results show that di.M-PGE2, a long acting syntetic analog ogfPGE2, restores NK activity in melanoma bearing or in cyclophosphamide (CY) suppressed mice. In vitro and in vivo administration of interferon (IFN) has been noted to boost NK activity both in human and murine experimental models. However, treatment of cancer patients with IFN has not always led to an increased NK response. In order to investigate if di-M-PGE2 could cooperate with IFN in boosting NK activity in immunosuppressed animals we examined (a) the effects of di-M-PGE2 in association with IFN on NK activity and on tumor growth in tumor-bearing or CY-suppressed mice and (b) the effects of di-M-PEG2 on the recovery rate of NK activity in bone marrow reconstituded murine chimeras.