Adult male mallards were treated with dexamethasone (DEX) to observe the impact of glucocorticoids (GC) upon natural killer cell activity, humoral antibody response to sheep erythrocytes (SRBC), and other physiologic parameters. Results showed that DEX caused significant decreases in total and 2-mercaptoethanol-resistant antibody responses, while a separate experiment showed that DEX resulted in consistent elevation of NKC activity. In-vitro studies showed that DEX and indomethacin were protective of NKC activity in the presence of monocytes, and that prostaglandin-E2 was highly suppressive when added to non-adherent NKCs. Furthermore, DEX caused only a slight loss in lymphocyte viability in-vitro at 10 to the minus fifth M but significantly reduced phagocytic ability of mature monocytes. From these results, mallard lymphocytes and NKC activity appear refractory to glucocorticoid-mediated suppression, and it is suggested that the elevation in activity observed is likely due to an inhibition of prostaglandin production by monocytes.