Effect of iron deficiency on the stimulation of natural killer cells by macrophage-produced interferon

Abstract

Spleen natural killer (NK) cell activity and protein synthesis are decreased in iron-deficient rats. Since the protein, interferon (IFN), activates NK cells, production of IFN by macrophages may be low in iron-deficient rats causing impaired NK cell activity. Weanling male rats (n=9/group) were fed ad libitum 5 or 37 mg iron/kg diet for eight weeks. Pair-fed rats (n=6) were fed control diet as consumed by iron-deficient rats. Hemoglobin and hematocrit levels were lower in iron-deficient rats than in other rats. Spleen NK cell activity was measured by Cr-51 release from labeled Yac-1 cells after NK cells were activated by macrophage-produced IFN. Macrophage were stimulated in vitro with poly inosinic:cytidilic acid to produce IFN. NK cell cytotoxicity after incubation with macrophage-produced IFN was decreased in iron-deficient rats (13.4±1.5%) compared to control rats (19.0±1.9%), while increased NK activity was found in pair-fed rats (25.5±1.9%) compared to control and irondeficient rats. IFN production or ability to stimulate NK cells was decreased by iron deficiency, but syngeneic B cells compensated for the decreased activity. IFN plays a role in decreasing NK cell activity during iron deficiency. Other cellular cellular mechanisms contributing to the impairment remain unknown.