Suppressor monocytes have been found in a number of human diseases most of which are associated with lymphopenia and deficiences in cell mediated immunity. In our studies both quantitative and qualitative differences in monocytes were detected in certain patients with advanced Hodgkin's disease or tuberculosis. In certain patients lymphocyte activating factor production by monocytes was severely depressed in part secondary to decreased activation by suppressed T cells, although at times primary impairment of macrophage function was also probably contributory. Mononuclear cell cultures from patients with advanced Hodgkin's disease also manifested excessive prostaglandin secretion; however, the association of this with monocyte suppression and deficient LAF production was inconstant. Furthermore, reversibility of monocyte suppression could not regularly be achieved by inhibition of prostaglandin synthetase with indomethacin suggesting that excessive production of prostaglandins is unlikely to be the sole mechanism of monocyte inhibition of lymphoproliferation. It also remains to be established whether the inhibition of lymphoproliferation in vitro is important to in vivo delayed hypersensitivity or whether the mechanism is related to other macrophage effects such as tumor cytostasis and cytolysis.