Regulation of human natural killer cell activity by interferon-gamma: lack of a role in interleukin 2-mediated augmentation.

Abstract
Natural killer cell activity was consistently increased after overnight incubation with recombinant IL 2. Recombinant IFN-gamma, on the other hand, increased NK activity only in three out of 25 preparations of donor lymphocytes. No synergy was observed when suboptimal amounts of recombinant (r)IL 2 and rIFN-gamma were added to donor lymphocytes, with any increase in activity attributable to additive effects of the two lymphokines. Three antibodies to IFN-gamma could not block the rIL 2 induction of NK activity, further suggesting that IFN-gamma was not involved in the enhancement of NK activity by IL 2. Two other anti-IFN-gamma antibody preparations showed significant inhibition of rIL 2-induced augmentation of NK activity, but the inhibition was found to be attributable to antibody-unrelated factors in the antiserum or ascites fluid. Our results suggest that IFN-gamma produced by rIL 2 treatment of human PBL does not play an essential role in increasing NK activity in most donors and that IL 2-induced augmentation of NK activity is due to the direct action of IL 2 on LGL.

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