Effects of rat interleukin-2 and rat interferon on the natural killer cell activity of rat spleen cells after thermal injury.

The natural killer cell activity of splenocytes from rats with scald injury was observed to be significantly suppressed at 7 days after injury compared with that of normal nonburned controls. Incubation of splenocytes from normal rats or rats with burn injury with either rat interleukin-2 or rat interferon (IFN-alpha and IFN-beta) significantly increased the natural killer cell activity. Addition of a rabbit anti-rat interferon antibody to spleen cells incubated with interleukin-2 did not produce any significant alteration in interleukin-2-related enhancement of natural killer cell activity. These results suggest that enhancement of natural killer cell activity after incubation of splenocytes with interleukin-2 is not due to interferon production but is an independent event. Preincubation of spleen cells with a mouse monoclonal antibody to rat interleukin-2 receptor was observed to abolish the interleukin-2-related enhancement of natural killer cell activity completely, whereas it partially blocked the interferon-related enhancement. These results were also confirmed by enhancement of natural killer cell activity of burned rats after in vivo administration of interleukin-2. Our studies thus indicate that after thermal injury, the observed decrease of natural killer cell activity can be enhanced by both interleukin-2 and interferon independently of each other. The decreased natural killer cell activity may be due to a decrease in interleukin-2 production or availability and not to an interleukin-2 receptor defect. These studies thus point toward a potential therapeutic significance of interleukin-2 in enhancing immune function after thermal injury.