Abstract

The suppressive mechanism of Interleukin 2 (IL-2) production was investigated in cancer patients.
IL-2 production of peripheral blood mononuclear cells (PBMC) derived from control subjects and patients with non-treated advanced carcinoma were 524.1±250.4 nano Jurkat Units (nJ. U.)/cell and 139.3±85.4 nJ. U./cell, respectively. The mean value of IL-2 production in cancer patients was significantly lower than that of normal subjects. IL-1 release from bacterial lipopolysaccharide-stimulated monocytes in cancer patients was significantly higher than that of normal subjects and the supplementation of IL-1 did not restore the IL-2 production, suggesting that the impairment of IL-1 release was not responsible for the decrease of IL-2 production in cancer bearers.
On the other hand, monocyte depletion increased the IL-2 release in PBMC of cancer patients. Moreover, the monocytes derived from cancer patients possessed a higher suppressive activity on IL-2 production than those of normal subjects. These results suggest that the increase of the suppressive monocytes is responsible for the impairment of IL-2 production. However, this suppression was not abolished by treatment with indomethacin, a inhibitor of prostaglandin synthesis, but was restored by treatment with phorbol myristate acetate (PMA).
Our experiments suggest that the IL-2 decrease in cancer patients is chiefly mediated through a suppressive monokine which is diminished by treatment with PMA rather than indomethacin.