We examined the role of a prostaglandin producing suppressor cell in the hyporesponsiveness to phytohemagglutinin seen in Hodgkin's disease. Addition of indomethacin to phytohemagglutinin cultures of lymphocytes from six patients with Hodgkin's disease resulted in an increase of 182±60 per cent in 3H-thymidine incorporation versus a 44±18 per cent increase in 29 controls (mean ± S.D., P<0.001). Without indomethacin the mean response of the lymphocytes in Hodgkin's disease was 48 per cent of that of control. With indomethacin it was 94 per cent of the control value. Phytohemagglutinin cultures of Hodgkin-disease lymphocytes produced approximately fourfold more prostaglandin E2 after 48 hours than did normal lymphocytes (P<0.02). Removal of glass-adherent cells markedly decreased the enhancement seen with indomethacin; it reduced prostaglandin E2 production by more than 80 per cent and eliminated the differences in response to phytohemagglutinin between Hodgkin-disease and normal lymphocytes. Thus, a glass-adherent, prostaglandin-producing suppressor cell is responsible for the hyporesponsiveness to phytohemagglutinin seen with Hodgkin-disease lymphocytes. (N Engl J Med 297:963–968, 1977) Patients with Hodgkin's disease have depressed cellular immunity, manifested by skin-test anergy or hyporesponsiveness,1,2 decreased homograft rejection,3 increased susceptibility to certain infections4 and impaired response in vitro to T-cell mitogens.5 Two general mechanisms could account for the T-cell defect. Anergy could exist on the basis of loss of effector cells or could be due to an active suppression of the effector cells by so-called suppressor cells. This second possibility is intriguing because it offers possibilities for therapeutic intervention by “turning off” the suppressor. Investigations by others in our laboratory,6 as well as work by Twomey et al.,7 have suggested that.
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