Braun D P, Harris Z L, Harris J E, Sandler S, Khandekar J, Locker G, Haid M, Gordon L, Shaw J, Cobleigh M
J Biol Response Mod. 1983;2(3):251-62.
The effect of interferon (IFN) therapy on prostaglandin (PGE)-synthesizing immunoregulatory cell function was assessed in the peripheral blood mononuclear cells of renal cell carcinoma patients. Ten patients were treated daily for 28 days with either 1 X 10(6) IU (five patients) or 10 X 10(6) IU (five patients) of leukocyte IFN. Patient cells were assessed for phytohemagglutinin (PHA) responsiveness in the presence and absence of the PGE synthetase inhibitor indomethacin. Progressive impairment in PHA responsiveness was found in all patients by the end of 28 days of therapy. It was associated with increased levels of indomethacin-sensitive suppressor function. Change in any of the patients studied was not correlated with IFN dose level. There was no correlation between clinical response to IFN and alterations in these parameters of immune function. In co-culture experiments, preincubation of glass-adherent cells with IFN led to increased indomethacin-sensitive regulatory function. These results suggest that IFN can produce progressive impairment of PHA-induced lymphoproliferation by increasing PGE-synthesizing immunoregulatory cell activity.
