EVIDENCE FOR THE INVOLVEMENT OF MONOCYTE-DERIVED TOXIC OXYGEN METABOLITES IN THE LYMPHOCYTE DYSFUNCTION OF HODGKINS-DISEASE

  • 1 January 1981
    • journal article
    • research article
    • Vol. 46  (2) , 313-320
Abstract
Whether adherent cell-derived toxic O2 metabolites contribute to the suppression of mononuclear cell blastogenic responses in Hodgkin''s disease was studied. Peripheral blood mononuclear cells from 10 patients with Hodgkin''s disease were stimulated in culture with the mitogen PHA [phytohemagglutinin] in the presence of the prostaglandin inhibitor indomethacin and the antioxidants catalase or vitamin E. Patient lymphocytes showed significant increases in PHA-induced proliferation at all PHA doses when cultured with indomethacin. Further augmentation of lymphocyte proliferation was achieved with the addition of catalase or vitamin E to indomethacin in the culture system. The increases in proliferation seen on culture with these agents were greatest in patients with more depressed initial PHA responses. When adherent cells were removed before culture, the agents no longer facilitated increases in proliferation. Abnormal lymphocyte proliferative responses seen in Hodgkin''s disease may result in part from the excessive production of toxic O2 metabolites and prostaglandins by adherent cell populations.