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Differential effects of recombinant interferons alpha, beta, and gamma on induction of human lymphokine
13rd Department of Internal Medicine, University of Tokushima School of Medicine, Japan.
The effects of three classes of recombinant interferons (IFN-alpha A, IFN-beta, and IFN-gamma) on maximal induction of lymphokine (IL-2)-activated killer (LAK) activity were studied. Highly purified lymphocytes (greater than 99%) were obtained by counter-flow centrifugal elutriation from peripheral blood of healthy donors. After incubation for 4 days with IL-2 (1 U/ml), purified lymphocytes showed maximal LAK activity against NK cell-resistant target (Daudi) cells, as assessed by 4-hour 51Cr release assay. Addition of exogenous IFN-alpha A or IFN-beta to cultures of lymphocytes plus IL-2 resulted in significant inhibition of LAK activity, but addition of IFN-gamma had no effect on LAK induction by IL-2. IFN-alpha A caused greatest inhibition of LAK activity when added at the start of culture of lymphocytes with IL-2, and was less inhibitory when added 1 day later. Similar inhibition by IFN-alpha A or IFN-beta was observed with nine lines of human tumorigenic cells as targets of LAK activity. IFN-alpha A and IFN-beta also inhibited the proliferative responses of lymphocytes to IL-2 stimulation, and the expression of IL-2 receptors on their surface, whereas IFN-gamma did not. These results suggest that IFN-alpha A and IFN-beta may be important in in situ regulation of LAK cell induction against neoplasms.
The effects of three classes of recombinant interferons (IFN-alpha A, IFN-beta, and IFN-gamma) on maximal induction of lymphokine (IL-2)-activated killer (LAK) activity were studied. Highly purified lymphocytes (greater than 99%) were obtained by counter-flow centrifugal elutriation from peripheral blood of healthy donors. After incubation for 4 days with IL-2 (1 U/ml), purified lymphocytes showed maximal LAK activity against NK cell-resistant target (Daudi) cells, as assessed by 4-hour 51Cr release assay. Addition of exogenous IFN-alpha A or IFN-beta to cultures of lymphocytes plus IL-2 resulted in significant inhibition of LAK activity, but addition of IFN-gamma had no effect on LAK induction by IL-2. IFN-alpha A caused greatest inhibition of LAK activity when added at the start of culture of lymphocytes with IL-2, and was less inhibitory when added 1 day later. Similar inhibition by IFN-alpha A or IFN-beta was observed with nine lines of human tumorigenic cells as targets of LAK activity. IFN-alpha A and IFN-beta also inhibited the proliferative responses of lymphocytes to IL-2 stimulation, and the expression of IL-2 receptors on their surface, whereas IFN-gamma did not. These results suggest that IFN-alpha A and IFN-beta may be important in in situ regulation of LAK cell induction against neoplasms.