Abstract
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-α and IFN-(β) 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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 617-622 |
| Number of pages | 6 |
| Journal | Journal of Burn Care and Rehabilitation |
| Volume | 13 |
| Issue number | 6 |
| DOIs | |
| State | Published - 1992 |
ASJC Scopus subject areas
- Surgery
- General Nursing
- Emergency Medicine
- Rehabilitation
- General Health Professions