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Department of Microbiology and Immunology * Division of Nutrition, Department of Physiology and Biochemistry, The Medical College of Pennsylvania, Philadelphia, PA 19129
We examined the effect of vitamin A deficiency on natural killer (NK) cell activity and interferon (IFN) production. Rats were weaned at 16 or 21 d of age onto semisynthetic diets containing either 0 or 4 µg retinol/g diet. At the time of study, retinol-depleted rats had serum vitamin A concentrations < 7% of those of pair-fed controls. In two studies, rats exhibited no external signs of retinol deficiency, but with further depletion some symptoms were observed. Splenic NK cell activity against chromium-51-labeled YAC-1 cells was significantly decreased in vitamin A-depleted rats (2280% of values for control rats, depending on the degree of retinol deficiency), regardless of the ratio of effector to target cells used. When vitamin A-depleted rats were repleted orally with retinol, NK cell activity was consistently normalized. To understand the possible mechanisms involved in decreasing NK cell activity, we investigated IFN production by concanavalin A-stimulated spleen cells from vitamin A-depleted, from repleted and from control animals. IFN titers were significantly decreased (2233% of values for control rats) in supematants of spleen cell cultures of the vitamin A-depleted rats. Repletion with vitamin A resulted in IFN activities ranging from 80 to 130% of controls. Adding
/ß IFN in vitro to the spleen cells of vitamin A-depleted animals increased their NK cell activity. The number of spleen cells reacting with a monoclonal antibody specific for rat NK cells was slightly lower in retinol-depleted rats, but not enough to account for the differences in NK cell and IFN activities. These data suggest that vitamin A deficiency affects the nonspecific arm of the immune system, possibly by altering the functional capacity of cells to produce lymphokines needed for the generation of an appropriate cytolytic response.
KEY WORDS: retinol YAC-1 cells rats
1 This research was supported by U.S. Department of Agriculture grant 86 CRCR-1 1980, National Institutes of Health grants DE-07686, HD-00691 and DK-41479, and funds from the Howard Heinz Endowment.
2 Author to whom all correspondence should be addressed.
3 Present address: NIAID Twinbrook II Research Facility, 12441 Park Lawn Drive, Rockville, MD 20852.
Manuscript received 18 December 1989. Revision accepted 26 April 1990.