Evidence for the involvement of monocyte-derived toxic oxygen metabolites in the lymphocyte dysfunction of Hodgkin's disease

R. D. Deshazo, C. Ewel, S. Londono, Z. Metzger, J. T. Hoffeld, J. J. Oppenheim

Research output: Contribution to journalArticlepeer-review

Abstract

This study was performed to see if adherent cell-derived toxic oxygen metabolites contribute to the suppression of mononuclear cell blastogenic response in Hodgkin's disease. Peripheral blood mononuclear cells from 10 patients with Hodgkin's disease were stimulated in culture with the mitogen PHA 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. These data suggest that abnormal lymphocyte proliferative responses seen in Hodgkin's disease may result in part from the excessive production of toxic oxygen metabolites as well as prostaglandins by adherent cell populations.

Original languageEnglish
Pages (from-to)313-320
Number of pages8
JournalClinical and Experimental Immunology
Volume46
Issue number2
StatePublished - 1981

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